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43 publications mentioning hsa-mir-198

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-198. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 379
The data presented above demonstrate that miR-198 can target sequences in the Cyclin T1 mRNA 3′UTR and can repress expression of endogenous Cyclin T1 protein expression when ectopically expressed. [score:9]
Although the pre-miR-198 was able to reduce expression of the p198T reporter plasmid about 20-fold relative to the pre-miR control, it had no inhibitory effect on Cyclin T1 expression and even appeared to stimulate Cyclin T1 expression. [score:9]
Inhibition of Cyclin T1 up-regulation by miR-198 in a monocytic cell line also resulted in decreased HIV-1 proviral gene expression and HIV-1 replication, indicating that miR-198 possesses an anti-HIV-1 function that appears to function through the repression of an essential cellular cofactor. [score:8]
Down-regulation of Cyclin T1 by miR-198 inhibits HIV-1 proviral gene expression and HIV-1 replication. [score:8]
We found that inhibition of miR-198 function in primary monocytes resulted in increased Cyclin T1 protein levels, and overexpression of miR-198 in differentiating monocytes repressed the normal Cyclin T1 up-regulation. [score:8]
To verify that repression of Cyclin T1 protein expression by miR-198 requires target sequences in the Cyclin T1 3′UTR, we carried out a plasmid transfection experiment with a HA-tagged Cyclin T1 expression plasmid lacking the Cyclin T1 3′UTR. [score:7]
In addition, mutation of three nucleotides in the site 6502 which are complementary to the mRNA seed sequence abolished the inhibition by shmiR-198 (Figures 4C and 5A), strongly suggesting the direct targeting of miR-198 to site 6502 and highlighting the importance of the seed match present in site 6502 during miRNA -mediated repression. [score:7]
miR-198 inhibitor (anti-miR-198) or control miRNA inhibitor (anti-miR-Control) was transfected into primary monocytes (250 pmole inhibitors/3×10 [6] cells) obtained from healthy donors using the Amaxa Nucleofector system. [score:7]
Down-regulation of miR-198 and up-regulation of Cyclin T1 during monocyte differentiation. [score:7]
Because Cyclin T1 is a component of P-TEFb, a general RNA polymerase II elongation factor, miR-198 is likely to broadly regulate gene expression in monocytes through its own targeting functions and through indirect effects on Cyclin T1 -dependent genes. [score:7]
The expression levels of miR-198 are greatly reduced in macrophages, and this appears to allow translation of Cyclin T1 mRNA and expression of Cyclin T1 protein. [score:7]
Because the ectopic expression of miR-198 reduces Cyclin T1 protein levels without affecting Cyclin T1 mRNA levels, it is likely that miR-198 acts through translational inhibition as is common for miRNAs. [score:7]
Because overexpression of PTEN enhances HIV-1 expression [45], it is possible that the anti-HIV-1 function of miR-198 involves targeting cellular cofactors in addition to Cyclin T1. [score:7]
These data demonstrate that miR-198, a miRNA which is down-regulated during monocyte to macrophage differentiation, is capable of down -regulating Cyclin T1 protein expression. [score:7]
Our finding that miR-198 represses Cyclin T1 protein expression in monocytes provides mechanistic insight into previous observations that translation of Cyclin T1 mRNA is inhibited in these cells [10], [14]. [score:7]
To examine if HIV-1 proviral gene expression is affected by the down-regulation of Cyclin T1 by miR-198, a HIV-1 NL4-3 luciferase proviral reporter plasmid was co -transfected with shGFP or shmiR-198 plasmid into MM6 cells. [score:6]
This analysis identified miR-198 as a negative regulator of Cyclin T1 protein expression through targeting sequences in the 3′UTR of Cyclin T1 mRNA. [score:6]
Ectopic expression of miR-198 in MM6 cells from a transfected shmiR-198 plasmid, followed by PMA treatment, largely prevented Cyclin T1 up-regulation (Figure 7A, right panel). [score:6]
Ectopic expression of miR-198 down-regulates endogenous Cyclin T1 protein levels without affecting its mRNA levels. [score:6]
In hepatic tumors, expression of miR-198 was found to be down-regulated relative to normal liver parenchyma [38]. [score:6]
We therefore examined if down-regulation of Cyclin T1 by miR-198 could result in decreased HIV-1 proviral expression. [score:6]
To examine whether miR-198 regulates Cyclin T1 expression in primary monocytes, we isolated primary monocytes and macrophages from two donors (Donor3 and Donor4) and first re-examined the correlation between miR-198 expression and Cyclin T1 protein levels. [score:6]
Ectopic expression of miR-198 down-regulates endogenous Cyclin T1 without affecting the mRNA levels. [score:6]
Because HIV-1 infection induces Cyclin T1 protein expression in macrophages [12], it is possible that following up-regulation of Cyclin T1 mRNA and protein by infection, a cellular negative-feed back loop is activated that results in elevated levels of miR-198 and a subsequent dampening of the induction of Cyclin T1. [score:6]
As quantified by TaqMan MicroRNA assays (Applied Biosystems), miR-198 was expressed >400-fold in cell pools expressing shmiR-198 relative to pools expressing shGFP. [score:6]
It appears therefore that target sites for miR-198 reside in these two fragments, consistent with recent findings that miRNA target sites are generally locate away from the center of a 3′UTR [23]. [score:5]
Expression pattern of miR-198 and other potential mRNA targets. [score:5]
We used both PicTar [40] and TargetScan [41], [42] to identity mRNAs that are predicted to be targets of miR-198. [score:5]
Interestingly, the HIV-1 Tat protein has been shown to decrease expression of PTEN in primary human macrophages [44], which is consistent with our findings that HIV-1 infection induces miR-198 expression in macrophages (Figure 8). [score:5]
An shRNA strategy was utilized to express miR-198 (shmiR-198) or a control shRNA designed to target GFP (shGFP) from a pCL -based retroviral vector [51]. [score:5]
These data indicate that the repression of Cyclin T1 protein expression by miR-198 requires target sequences in the Cyclin T1 mRNA 3′UTR. [score:5]
These data in primary monocytes further support the proposal that miR-198 plays a role in repressing Cyclin T1 protein expression in monocytes, and the reduction in miR-198 levels during macrophage differentiation contributes to induction of Cyclin T1 protein expression. [score:5]
In loss-of-function experiments, we examined the effects of a miR-198 inhibitor on Cyclin T1 expression in monocytes. [score:5]
The greater inhibition of proviral reporter plasmid expression by miR-198 in Figure 7B than in the HIV-1 infection in Figure 7C is likely the result of transfection efficiency. [score:5]
These data suggest that miR-198 is capable of repressing HIV-1 proviral expression by targeting its cellular cofactor Cyclin T1. [score:5]
Expression of pU3-full was also repressed by ∼40%, suggesting that there are miR-198 target sites in the Cyclin T1 3′UTR. [score:5]
Although expression in monocytes was not examined in a previous study in 40 normal human tissues, miR-198 expression was found to be generally low and restricted to only a few tissues [37]. [score:5]
The data in Figure 7C further suggest that miR-198 is capable of repressing HIV-1 replication through down-regulation of the essential cofactor Cyclin T1. [score:4]
These data suggest that HIV-1 infection up-regulates miR-198 levels in macrophages. [score:4]
A topic for future research will be the study of signals and mechanisms that lead to the down-regulation of miR-198 in macrophages. [score:4]
We selected several down-regulated miRNAs, including miR-15b, miR-26a, and miR-198, for initial experiments. [score:4]
miR-198 regulates Cyclin T1 protein expression during in vitro monocyte to macrophage differentiation. [score:4]
Furthermore, genes involved in immune responses are overrepresented in the set of Cyclin T1 -dependent mRNAs in macrophages [13], suggesting that proper macrophage function may require the down-regulation of miR-198. [score:4]
An intriguing predicted target for miR-198 is in the 3′UTR of PTEN, a negative regulator of the PI3-kinase pathway, and PTEN is involved in LPS signaling in monocytes/macrophages [43]. [score:4]
This analysis identified 41 mRNAs in common between the two programs that are potential targets for miR-198. [score:3]
The reduction of expression of miR-198 is therefore likely to be important for monocyte differentiation. [score:3]
Therefore, we wished to examine if HIV-1 infection affects miR-198 expression in macrophages. [score:3]
Because Tat is essential for HIV-1 replication [6] and Cyclin T1 is a critical Tat cofactor, miR-198 can function in monocytes as an additional repressor of viral gene expression and replication (Figure 6B and 6C). [score:3]
miR-198 functions to repress Cyclin T1 protein expression in primary monocytes. [score:3]
The active translation of Cyclin T1 mRNA following the relief of repression by miR-198 may reduce the mRNA half-life, and if a transcriptional induction of the Cyclin T1 gene does not occur, a decrease in the amount of Cyclin T1 mRNA will result. [score:3]
However, site 6502 contains additional eight nucleotides at its 3′ end complementary to the miR-198 seed sequence (Figure 4C), which closely resembles the structure of the 5′-dominant canonical miRNA target site [24]. [score:3]
Because miR-198 restricts Cyclin T1 expression in monocytes, this miRNA may contribute to the prevention of a transcriptional program of differentiation. [score:3]
We identified a microRNA (miRNA) named miR-198 that represses the expression of Cyclin T1 in monocytes. [score:3]
An shRNA vector was generated to express miR-198 (shmiR-198) from the pCL -based retroviral vector. [score:3]
Pre-miR-198 or pre-miR-Control was also transfected with the Amaxa system into primary monocytes (250 pmole inhibitors/3×10 [6] cells) and cells were treated with GM-CSF to induce differentiation for 48 hours. [score:3]
In an additional gain-of-function experiment, transfection of pre-miR-198 to overexpress miR-198 in monocytes induced to differentiate with GM-CSF treatment resulted in about a 3-fold decrease in Cyclin T1 protein levels (Figure 6C, right panel). [score:3]
Three predicted miR-198 target sequences, site 2478, site 2867, and site 6502, are shown and named according to the position of their first nucleotide in Cyclin T1 mRNA. [score:3]
1000263.g003 Figure 3 (A) 293T cells were transfected with 150 pmole of pre-miR-198, pre-miR-15b, or siRNA against Cyclin T1 (siCyclin T1) and examined for Cyclin T1 and β-actin protein expression at 72 hours after transfection. [score:3]
miR-198 represses HIV-1 proviral expression and HIV-1 replication. [score:3]
Finally, given the ∼5 kb of 3′UTR sequence in Cyclin T1 mRNA, it is possible if not likely that miRNAs in addition to miR-198 are involved in repression of Cyclin T1 expression in monocytes and other cell types. [score:3]
To examine if HIV-1 replication is also repressed by ectopic expression of miR-198, MM6 cells were transfected with a shGFP control or shmiR-198 plasmid and cells were treated with PMA immediately after transfection. [score:3]
All three predicted targets show extensive of complementarity with miR-198 at their 5′ ends. [score:3]
Identification of functional miR-198 target sites in Cyclin T1 3′UTR. [score:3]
To further validate the effect of miR-198 on Cyclin T1 protein expression, increasing amounts of pre-miR-198 were transfected into HeLa cells, and a dose -dependent reduction in Cyclin T1 protein level was seen (Figure 3B). [score:3]
The effects of miR-198 on Cyclin T1 expression are consistent with recent quantitative proteomic studies that have shown that in most cases miRNAs influence proteins levels about 1.5- to 2-fold [25], [26]. [score:3]
miR-198 target sequences in the Cyclin T1 mRNA 3′UTR. [score:3]
Little information is available concerning potential functions and mRNA targets for miR-198. [score:3]
We transfected a chemically modified single-stranded nucleic acid inhibitor of miR-198 (anti-miR-198) into freshly isolated monocytes. [score:3]
We found that miR-198 is predicted to have >10 potential target sites in the 3′UTR of Cyclin T1 mRNA with mfe lower than −20 kcal/mol (see ). [score:3]
The levels of β-actin and GAPDH mRNAs also remained unchanged following transfection of pre-miR-198, suggesting that miR-198 overexpression has no impact on overall mRNA levels. [score:3]
Identification of miR-198 target sites in the 3′UTR of Cyclin T1 mRNA. [score:3]
We observed that HIV-1 infection of macrophages modestly induces both miR-198 and Cyclin T1 mRNA expression levels (Figure 7). [score:3]
Effects of HIV-1 infection on miR-198 expression in macrophages. [score:3]
1000263.g008 Figure 8 Macrophages were infected with HIV-1 SF162 strain for seven days and total RNA was isolated and assayed for: (A) expression levels of miR-198; (B) Cyclin T1 and α-tubulin mRNAs. [score:2]
To determine if the Cyclin T1 3′UTR can be regulated by miR-198, we inserted the full length 3′UTR between the luciferase coding sequence and the poly(A) signal of the pGL3 firefly luciferase vector driven by CMV immediate early promoter (pU3-full, Figure 4B). [score:2]
Macrophages were infected with HIV-1 SF162 strain for seven days and total RNA was isolated and assayed for: (A) expression levels of miR-198; (B) Cyclin T1 and α-tubulin mRNAs. [score:2]
Ectopic expression of miR-198 and reporter assay. [score:2]
As shown in Figure 8A, miR-198 levels increased modestly to 1.9-fold in Donor 6 and 3.8-fold in Donor 7 when normalized to U6B snRNA. [score:1]
Additionally, p198T, which contains sequences with perfect complementarity to miR-198, was included as a positive control that should be repressed through an siRNA pathway. [score:1]
The correlation between the FSTL1 transcript and miR-198 levels has not yet been established, but FSTL1 transcripts are not detectable in peripheral blood leukocytes [36], suggesting that the processing of the FSTL1 primary transcript for protein production or miR-198 might be mutually exclusive. [score:1]
miR-198 precursor (pre-miR-198) or control precursor (pre-miR-Control) were transfected into freshly isolated monocytes and differentiation was induced with GM-CSF treatment (Donor 5). [score:1]
In the HIV-1 infection experiment, it is likely that a significant portion of infected cells were not transfected with the miR-198 shRNA vector. [score:1]
At day seven post-infection, cells were washed with PBS three times for total RNA isolation for miR-198 quantification and mRNA quantification as described above. [score:1]
U6B snRNA was used for normalization of miR-198 and β-actin mRNA was used for normalization of mRNAs. [score:1]
miR-198 is in the 3′UTR (exon 11) of FSTL1, a gene that has recently been shown to enhance inflammatory cytokine production in a monocytic cell line after mitogen stimulation [35]. [score:1]
In the proviral reporter plasmid experiment, both the reporter plasmid and the miR-198 shRNA vector were co -transfected and it is therefore likely that the majority of transfected cells contained both plasmids. [score:1]
Cyclin T1 protein levels were reduced in 293T cells transfected with the miR-198 precursor (pre-miR-198) relative to mock -transfected cells, while miR-15b precursor (pre-miR-15b) had no significant effect (Figure 3A). [score:1]
The HA-Cyclin T1 plasmid was co -transfected with a precursor for either miR-198 (pre-miR-198) or a pre-miR-Control. [score:1]
Although both Cyclin T1 mRNA and miR-198 levels were decreased in macrophages, the ratio between Cyclin T1 mRNA and miR-198 increased in macrophages. [score:1]
affects miR-198 as well as Cyclin T1 mRNA levels. [score:1]
For the transfection experiment to examine the requirement of the Cyclin T1 3′UTR for repression by miR-198, pHA-Cyclin T1 [4] (50 ng), p198T (50 ng) and pTK-renilla luciferase (10 ng) were co -transfected into HeLa cells with pre-miR-Control (50 nmol), pre-miR-198 (50 nmol) or siCyclin T1 (50 nmol) in a 24-well culture dish using Lipofectamine (Invitrogen). [score:1]
Additionally, miR-198 did not affect Cyclin T1 mRNA levels, which remained constant in cells transfected with pre-miR-198 (Figure 3C). [score:1]
This observation indicates that in macrophages there are more copies of Cyclin T1 mRNA for each copy of miR-198. [score:1]
Therefore, site 2867 in fragment U3-1 and especially site 6502 in fragment U3-4 appear to be responsible for repression mediated by miR-198 in Cyclin T1 mRNA 3′UTR. [score:1]
As shown in Figure 6C, anti-miR-198 was able to induce Cyclin T1 levels from two- to six-fold in two donors examined (Donor 3, 4). [score:1]
The significance in the modest increase in miR-198 levels in HIV-1 infected macrophages remains to be elucidated. [score:1]
A genetic analysis identified a SNP in the miR-198 gene that has a nominally significant allelic association with schizophrenia [39]. [score:1]
miR-198 and HIV-1 replication in monocytes. [score:1]
In agreement with the microarray data shown in Figure 1A, miR-198 levels were reduced in macrophages relative to monocytes, showing a 14-fold reduction in Donor3 and a 19-fold reduction in Donor4. [score:1]
To verify that the transfected pre-miR-198 was biologically active, we co -transfected the p198T luciferase control plasmid (Figure 4C) that is repressed by miR-198 by a siRNA pathway. [score:1]
Macrophages isolated from healthy blood donors were allowed to differentiate for four days, and were infected with a M-tropic HIV-1 SF162 strain for seven days, and RNA was isolated for miR-198 quantification. [score:1]
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[+] score: 135
Overexpression of miR-198 in colorectal cancer cell lines inhibited cell proliferation, invasion, and migration by targeting fucosyl transferase 8 in vitro. [score:7]
GC samples were classified into low miR-198 expression group (n = 53) and high miR-198 expression group (n = 53) according to the median miR-198 expression level (relative to U6) of all GC samples. [score:7]
Yet miR-198 was reported to be upregulated in retinoblastoma and squamous cell carcinoma of the tongue [23, 24], indicating that miR-198 may not behave as a tumor suppressor in all cases. [score:6]
Survival analysis indicated that patients in the high miR-198 expression group had better 5-year overall survival than those in the low miR-198 expression group (p < 0.001, Fig.   2). [score:5]
In addition, Yang et al. reported that miR-198 inhibited proliferation and induced apoptosis of A549 lung cancer cells via targeting FGFR1 [17]. [score:5]
Tan et al. found that miR-198 inhibited hepatocellular carcinoma cell invasion and migration by targeting the HGF/c-MET pathway [19]. [score:5]
These findings suggested that miR-198 downregulation may be associated with progression of GC and that this miR may be an independent prognostic marker for GC patients. [score:4]
In pancreatic cancer, reconstitution of miR-198 resulted in reduced tumor growth and metastasis through direct targeting MSLN, PBX-1, and VCP [20]. [score:4]
In conclusion, our study showed that miR-198 was downregulated in GC tissues and correlated with aggressive clinicopathological features. [score:4]
Downregulation of miR-198 in human GC tissues. [score:4]
Decreased miR-198 expression in colorectal cancer showed a significant association with histological grade, T stage, lymph node invasion, and AJCC stage [18]. [score:3]
We also found that decreased miR-198 expression was significantly correlated with aggressive clinicopathological features. [score:3]
miR-198 expression was detected in 106 pairs of GC and corresponding adjacent noncancerous tissues normalized to U6 small nuclear RNA. [score:3]
Univariate analysis revealed that miR-198 expression (p < 0.001), tumor size (p = 0.006), tumor depth (p = 0.015), lymph node metastasis (p = 0.028), and TNM stage (p < 0.001) were prognostic factors for patient’s overall survival (Table  2). [score:3]
The relationship between miR-198 expression and clinicopathological features and patient’s survival was also analyzed. [score:3]
Fig. 2Kaplan-Meier survival curves of 106 gastric cancer patients based on miR-198 expression status. [score:3]
However, the expression and clinical significance of miR-198 in GC is still unclear. [score:3]
Prognostic values of miR-198 expression in GC patients. [score:3]
The expression levels of miR-198 in GC tissues were significantly lower than those in corresponding noncancerous tissues (p < 0.01). [score:3]
Previous research has demonstrated the tumor-suppressive functions of miR-198 in several human cancers. [score:3]
In the present study, we examined miR-198 expression in GC tissues and paired adjacent noncancerous tissues. [score:3]
The results showed that the relative level of miR-198 expression in GC samples (mean ± SD 7.05 ± 1.98) was significantly lower than that in corresponding adjacent normal tissues (mean ± SD 18.38 ± 4.30; p < 0.01). [score:3]
Multivariate analysis confirmed low miR-198 expression (p = 0.015, RR = 2.52) as an unfavorable prognostic indicator independent of other clinicopathological factors, including depth of infiltration (p = 0.003, HR = 3.17), lymph node status (p = 0.012, HR = 2.79), and TNM stage (p = 0.008, HR = 2.95; Table  2). [score:3]
Then, the associations of miR-198 expression with clinicopathological factors and patient’s survival were determined. [score:3]
In vivo, restoration of miR-198 significantly inhibited xenograft growth and invasion in nude mice. [score:3]
To the author’s knowledge, this is the first study to analyze the expression and clinical significance of miR-198 in GC. [score:3]
Furthermore, low miR-198 expression was an important indicator for unfavorable prognosis of GC patients. [score:3]
Decreased miR-198 expression was significantly associated with larger tumor size, deeper invasion depth, positive lymph node metastasis, advanced tumor-node-metastasis (TNM) stage, and shorter overall survival. [score:3]
Correlation between miR-198 expression and clinical features of GC. [score:3]
In the current study, we found that miR-198 was downregulated in human GC tissues compared with noncancerous tissues. [score:3]
Moreover, Kaplan-Meier analysis showed that GC patients with low miR-198 expression tend to have shorter overall survival. [score:3]
However, the complex molecular mechanisms underlying low miR-198 expression in human cancers and its function are still incompletely known. [score:3]
The multivariate analysis confirmed low miR-198 expression as an independent predictor of poor survival. [score:3]
Moreover, multivariate regression analysis identified low miR-198 expression as an independent predictor of poor survival. [score:3]
As shown in Fig.   1, miR-198 expression in cancer tissues was distinctly decreased compared to noncancerous tissues. [score:2]
Taken together, these research indicated that loss of miR-198 might contribute to cancer formation and progression. [score:1]
miR-198 Gastric cancer Prognosis Overall survival Gastric cancer (GC) is the fourth most prevalent human malignancy and the second leading cause of cancer death worldwide [1]. [score:1]
miR-198 is a recently identified cancer-related miR. [score:1]
However, we did not find any significant correlation between miR-198 levels and other clinicopathological features, such as patient’s gender, age, Lauren type, and cancer differentiation. [score:1]
The association between clinicopathological characteristics and miR-198 expression was summarized in Table  1. We found that miR-198 level was associated with tumor size (p = 0.009), tumor depth (p = 0.005), lymph node metastasis (p = 0.03), and clinical stage (p = 0.02). [score:1]
We further evaluated the association of miR-198 expression level with survival of GC patients. [score:1]
More studies should be applied to clarify the precise mechanisms by which miR-198 exerts antitumor activity. [score:1]
Low miR-198 levels in pancreatic cancer tissue samples predicted shorter overall survival. [score:1]
Our study aims to investigate the expression and clinical significance of miR-198 in GC patients. [score:1]
miR-198 expression levels were calculated by the 2 [−ΔCT] method and normalized to U6 small nuclear RNA We further analyzed the association between miR-198 expression levels and clinicopathological characteristics of GC. [score:1]
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[+] score: 31
As shown by Li et al., “knockdown of SChLAP1 significantly increased the expression of miR-198 and SChLAP1 overexpression markedly decreased it. [score:6]
Thus, SChLAP1 acted as a negative regulator in the expression of miR-198” and subsequently modulated the MAPK1 signaling pathway in PCa (49) (Figure 1). [score:4]
SChLAP1 acts as a negative regulator in the expression of miR-198 and subsequently modulates the MAPK1 signaling pathway in PCa (49). [score:4]
In Pathway 2, miR-198 might exert its anticancer effect through inhibition of MAPKs signaling pathway. [score:3]
miR-198 might exert its anticancer effect through inhibition of MAPKs signaling pathway (49). [score:3]
miR-198 suppress the proliferation and invasion of colorectal carcinoma (48). [score:3]
In PCa tissue, a low expression of miR-198 was found. [score:3]
MiR-198 is downregulated in many cancers, such as gastric cancer, lung cancer, and hepatocellular carcinoma (45– 47). [score:3]
Second Chromosome Locus Associated with Prostate-1. SChLAP1’s Working Mechanisms: Interaction with SWI/SNF Complex and miR-198. [score:1]
Recent studies have shown interaction between SChLAP1 and miR-198. [score:1]
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[+] score: 28
Because knockdown of these miRNAs in monocytes enhanced HIV-1 infection, and miRNA overexpression in MDMs inhibited HIV-1 replication, the authors proposed that the expression levels of these miRNAs determine the susceptibility of monocytes or MDMs to HIV-1. Interestingly, as in the case of resting CD4 [+] T-cells, cyclin T1 expression was shown to be upregulated upon differentiation of monocytes into MDMs, which was accompanied by robust downregulation of the cellular miR-198 [182]. [score:16]
The miR-198 was shown to directly target the 3′UTR of cyclin T1, and miR-198 overexpression or knockdown in monocytes undergoing differentiation decreased or increased the cyclin T1 protein levels, respectively, with concomitant effects on HIV-1 replication. [score:7]
Sung T. L. Rice A. P. miR-198 inhibits HIV-1 gene expression and replication in monocytes and its mechanism of action appears to involve repression of cyclin T1PLoS Pathog. [score:5]
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[+] score: 18
MiR-198 does not target the viral transcripts but targets HIV-1 Tat cofactor, cyclin T1, and overexpression of miR-198 in macrophages suppresses HIV-1 replication [129]. [score:9]
Similarly, the expression of miR-198 is reported to be downregulated during monocytes differentiation into macrophages [129]. [score:6]
The expression of miR-198 is quite low in resting CD4 [+] T cells [130]. [score:3]
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[+] score: 16
Other miRNAs from this paper: hsa-mir-31, hsa-mir-93, hsa-mir-181a-2, hsa-mir-191
This analysis revealed that miR-31 levels were significantly reduced in cells stably overexpressing EMSY, whereas the expression of other miRNAs such as miR-181a-2 and miR-198 remained unchanged (Figure 2C). [score:5]
Conversly, and consistent with these findings, miR-31 was markedly upregulated in EMSY -depleted MCF-7 cells (Figure S2E), in comparison to miR-181a-2 and miR-198 (Figure 2D). [score:4]
Importantly, it did so without affecting the expression of miR-198 and miR-181a-2. To further confirm these results and validate the predictions from the bioinformatic analyses, we tested the ETS-1 motifs in the miR-31 cis-regulatory element in functional transcription assays. [score:3]
Figure 5A shows that putative binding sites for ETS family members (ETS-1 and ETV4/PEA3) can be found in the miR-31 regulatory region but not within the analogous regions of miR-198 and miR-181a-2, whereas a GATA1 site is present within miR-31 and miR-198. [score:2]
This analysis also showed that ETS-1 did not bind to other regions within the miR-31 promoter, nor did it bind to the promoters of miR-181a-2 or miR-198 (Figure S5C). [score:1]
ChIP analyses indicated that EMSY associated with the promoter of miR-31 but did not bind the regions upstream of two control miRNA genes, miR-181a-2 and miR-198 (Figures 4B and S4B). [score:1]
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[+] score: 12
FGFR1 is a direct target of miR-16 (Chamorro-Jorganes et al., 2011), miR-133b (Wen et al., 2013), miR-198 (Yang et al., 2014), (Wang et al., 2013b), miR-382 (Mor et al., 2013), miR-424 (Chamorro-Jorganes et al., 2011), and miR-503 (Kim et al., 2013b). [score:4]
MicroRNA-198 inhibits proliferation and induces apoptosis of lung cancer cells via targeting FGFR1. [score:4]
FGFR1 is a direct target of miR-16, miR-133b, miR-198,, miR-382, miR-424, and miR-503. [score:4]
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[+] score: 12
Additionally, host cell miRNAs were described targeting HDFs important for HIV-1 Tat -mediated LTR activation: PCAF (P300/CBP -associated factor), a histone acetylase is target by hsa-miR-20a and hsa-miR-17-5p (Triboulet et al., 2007); purine-rich element binding protein alpha (PUR-α), is targeted by hsa-miR-15a, hsa-miR-15b, hsa-miR-16, hsa-miR-20a, hsa-miR-93, and hsa-miR-106b (Shen et al., 2012); and cyclin T1 is repressed by hsa- miR-198 and hsa-miR-27b (Sung and Rice, 2009; Chiang et al., 2011). [score:7]
miR-198 inhibits HIV-1 gene expression and replication in monocytes and its mechanism of action appears to involve repression of cyclin T1. [score:5]
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[+] score: 12
miR-198 was found to inhibit the replication of human immunodeficiency virus type 1 (HIV-1) by suppressing Cyclin T1 protein (CCNT1) expression [47]. [score:7]
Sung T. L. Rice A. P. miR-198 inhibits HIV-1 gene expression and replication in monocytes and its mechanism of action appears to involve repression of cyclin T1 PLoS Pathog. [score:5]
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Some of the upregulated miRNAs included, miR-499, miR-372, miR-18a, miR-21 and miR-30d, while let-7c and miR-198 were downregulated. [score:7]
The downregulation of let-7c and miR-198 is supported by other recent findings [10, 28]. [score:4]
html) for the first 789 bp 3’UTR of PDCD4 MicroRNA Fold change miR-372 4.82 miR-499 2.89 miR-18a 2.82 miR-200c 2.69 miR-130a 2.59 miR-21 2.29 miR-30d 2.21 miR-409-5p 2.14 miR-20a 2.12 let-7c 0.45 miR-198 0.40 The array data were then confirmed by QRT-PCR of 4 representative miRNAs using ten tumour and adjacent normal samples. [score:1]
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[+] score: 12
MiR-198 directly targets c-Met via its 3' UTR and consequently its overexpression diminished HGF -induced phosphorylation of p44/42 MAPK in HCC cells, leading to an inhibition of cell migration and invasion in a c-Met -dependent manner [54]. [score:7]
Tan S. Li R. Ding K. Lobie P. E. Zhu T. miR-198 inhibits migration and invasion of hepatocellular carcinoma cells by targeting the HGF/c-MET pathway FEBS Lett. [score:5]
[1 to 20 of 2 sentences]
12
[+] score: 12
Other miRNAs from this paper: hsa-mir-27a, hsa-mir-32, hsa-mir-206
During wound healing, a switch from miR-198 to FSTL1 protein expression is observed without a change in the FSTL1 mRNA level. [score:3]
Contrary to this, miR-198 is expressed in this tissue. [score:3]
MiR-198 is also involved in suppressing colorectal cancer growth [114] and lung adenocarcinoma A549 cell proliferation [115], but the relation between FSTL1 and miR-198 in this cancer type has not yet been studied. [score:3]
Disregulation of the ratio FSTL1 versus miR-198 is observed in head and neck squamous cell carcinoma, in which FSTL1 protein persists with the afore-mentioned consequences [62]. [score:2]
miR-198 is encoded in the 3′UTR of human FSTL1 primary transcript [112]. [score:1]
[1 to 20 of 5 sentences]
13
[+] score: 11
For example, miR-382, miR-198, miR-223, miR-125b, and miR-28 inhibit HIV replication by modulating host cellular factors or by directly targeting the HIV genome (10, 11). [score:6]
Sung TL, Rice AP 2009 miR-198 inhibits HIV-1 gene expression and replication in monocytes and its mechanism of action appears to involve repression of cyclin T1. [score:5]
[1 to 20 of 2 sentences]
14
[+] score: 10
Upper slides, magnification 20×, lower slides, magnification 10× (B) Mean omental adipocyte diameter in a patient with high miRNA-198 expression (miR-198 high) compared to a patient with low miRNA-198 expression (miR-198 low). [score:4]
Relationships between miRNA (miR-132 and miR-198) expression and morphology of adipose tissue. [score:3]
The strongest relationship between mean omental adipocyte diameter and microRNA expression was found for miRNA-198 (Figure 1B, Table 4). [score:3]
[1 to 20 of 3 sentences]
15
[+] score: 8
A549 cells were infected or mock infected with RSV 6340WT virus at an m. o. i. of 1 for 24 h. The data represent the mean qPCR fold change± sem of let-7f (let-7f), miR-337-3p (miR-337), miR-520a-5p (miR-520a), miR-24, miR-26b, miR-198 and miR-595 from three independent experiments relative to mock-infected cells, with values >1.0 considered to be upregulation and values below 1.0 considered to be downregulation. [score:5]
In this mo del, microarray data validated by quantitative real-time PCR (qPCR) showed that a different set of miRNAs (let-7f, miR-337, miR-520a, miR-24, miR-26b, miR-198 and miR-595) was deregulated following RSV infection. [score:2]
The miRNAs miR-24, miR-26b, miR-29a, miR-320a and miR-520a-5p (miR-520a) were also induced ≥1.5-fold, whilst miR-198, miR-224 and miR-595 were repressed by at least 1.5-fold (Table S1). [score:1]
[1 to 20 of 3 sentences]
16
[+] score: 7
In contrast, the expression is up-regulated by miR-198 in hepatocellular carcinoma cells [25]. [score:6]
Elfimova N. Sievers E. Eischeid H. Kwiecinski M. Noetel A. Hunt H. Becker D. Frommolt P. Quasdorff M. Steffen H. M. Control of mitogenic and motogenic pathways by miR-198, diminishing hepatoma cell growth and migration Biochim. [score:1]
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17
[+] score: 7
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-25, hsa-mir-26a-1, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-96, hsa-mir-99a, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-204, hsa-mir-210, hsa-mir-212, hsa-mir-181a-1, hsa-mir-214, hsa-mir-215, hsa-mir-216a, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-224, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-27b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-130a, hsa-mir-132, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-142, hsa-mir-145, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-134, hsa-mir-146a, hsa-mir-150, hsa-mir-186, hsa-mir-188, hsa-mir-193a, hsa-mir-194-1, hsa-mir-320a, hsa-mir-155, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-194-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-219a-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-99b, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-362, hsa-mir-369, hsa-mir-375, hsa-mir-378a, hsa-mir-382, hsa-mir-340, hsa-mir-328, hsa-mir-342, hsa-mir-151a, hsa-mir-148b, hsa-mir-331, hsa-mir-339, hsa-mir-335, hsa-mir-345, hsa-mir-196b, hsa-mir-424, hsa-mir-425, hsa-mir-20b, hsa-mir-451a, hsa-mir-409, hsa-mir-484, hsa-mir-486-1, hsa-mir-487a, hsa-mir-511, hsa-mir-146b, hsa-mir-496, hsa-mir-181d, hsa-mir-523, hsa-mir-518d, hsa-mir-499a, hsa-mir-501, hsa-mir-532, hsa-mir-487b, hsa-mir-551a, hsa-mir-92b, hsa-mir-572, hsa-mir-580, hsa-mir-550a-1, hsa-mir-550a-2, hsa-mir-590, hsa-mir-599, hsa-mir-612, hsa-mir-624, hsa-mir-625, hsa-mir-627, hsa-mir-629, hsa-mir-33b, hsa-mir-633, hsa-mir-638, hsa-mir-644a, hsa-mir-650, hsa-mir-548d-1, hsa-mir-449b, hsa-mir-550a-3, hsa-mir-151b, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-454, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-708, hsa-mir-216b, hsa-mir-1290, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-378b, hsa-mir-3151, hsa-mir-320e, hsa-mir-378c, hsa-mir-550b-1, hsa-mir-550b-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-219b, hsa-mir-203b, hsa-mir-451b, hsa-mir-499b, hsa-mir-378j, hsa-mir-486-2
For example, Glioma Tumor Suppressor Candidate Region Gene 1 (GLTSCR1), Synaptotagmin (STY1), neuronatin (NNAT) and Synaptic Ras GTPase-activating protein 1 (SYNGAP1) are putative targets of miR-126, miR-222, miR-198 and miR-633, respectively [76]. [score:5]
Furthermore, higher expression of miR-7, miR-198 and miR-633 was found in patients with CNS relapse compared with non-CNS-relapsed ALL [76]. [score:2]
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18
[+] score: 7
Different target cells might respond differently to the interaction between the virus and the host cell, although miRNAs that are known to regulate virus replication (e. g., miRNA-198) have been found to be commonly regulated by HIV-1 in both T and monocyte/macrophage targets [80]. [score:7]
[1 to 20 of 1 sentences]
19
[+] score: 7
Emerging evidence indicates that miR-198 is downregulated in hepatocellular carcinoma compared with in normal liver parenchyma, and forced expression of miR-198 inhibited HGF’s promotion of hepatocellular carcinoma cell migration and invasion in a c-MET -dependent manner [19]. [score:7]
[1 to 20 of 1 sentences]
20
[+] score: 7
Moreover, we report tumor suppressor functions of miR-198, miR-135a*, miR-200c, miR-663 and miR-483-5p in myeloma, that they reduced cell viability, migration and colony formation. [score:3]
MiR-155, miR-198, miR-200c, miR-483-5p and miR-663 significantly suppressed colony formation in MM cells (Figure 3B). [score:3]
At the same time, many other miRNAs were unmasked, including miR-125a-3p, miR-155, miR-135a*, miR-198, miR-200c, miR-188-5p, miR-630, miR-663 and miR-483-5p. [score:1]
[1 to 20 of 3 sentences]
21
[+] score: 6
Other miRNAs from this paper: hsa-mir-17, hsa-mir-19a, hsa-mir-29a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-208a, hsa-mir-10a, hsa-mir-223, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, hsa-mir-126, hsa-mir-146a, hsa-mir-150, hsa-mir-155, hsa-mir-29c, hsa-mir-99b, hsa-mir-296, hsa-mir-196b, hsa-mir-515-1, hsa-mir-515-2, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-550a-1, hsa-mir-550a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-640, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-550a-3, bta-mir-29a, bta-mir-125b-1, bta-mir-126, bta-mir-10a, bta-mir-124a-1, bta-mir-17, bta-mir-29b-2, bta-mir-29c, bta-mir-150, bta-mir-122, bta-mir-125b-2, bta-mir-19a, bta-mir-99b, hsa-mir-208b, hsa-mir-548e, hsa-mir-548j, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, bta-mir-124a-2, bta-mir-124b, bta-mir-146a, bta-mir-155, bta-mir-196b, bta-mir-208a, bta-mir-208b, bta-mir-223, bta-mir-296, bta-mir-29d, bta-mir-9-1, bta-mir-9-2, bta-mir-29e, bta-mir-29b-1, hsa-mir-548q, bta-mir-2284i, bta-mir-2285a, bta-mir-2284s, bta-mir-2285d, bta-mir-2284l, bta-mir-2284j, bta-mir-2284t, bta-mir-2285b-1, bta-mir-2284d, bta-mir-2284n, bta-mir-2284g, bta-mir-2284p, bta-mir-2284u, bta-mir-2284f, bta-mir-2284a, bta-mir-2284k, bta-mir-2284c, bta-mir-2284v, bta-mir-2285c, bta-mir-2284q, bta-mir-2284m, bta-mir-2284b, bta-mir-2284r, bta-mir-2284h, bta-mir-2284o, bta-mir-2284e, hsa-mir-548s, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-548w, hsa-mir-548x, bta-mir-2284w, bta-mir-2284x, hsa-mir-548y, hsa-mir-550b-1, hsa-mir-550b-2, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-548am, hsa-mir-548an, hsa-mir-548ao, hsa-mir-548ap, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, bta-mir-2284y-1, bta-mir-2285e-1, bta-mir-2285e-2, bta-mir-2285f-1, bta-mir-2285f-2, bta-mir-2285g-1, bta-mir-2285h, bta-mir-2285i, bta-mir-2285j-1, bta-mir-2285j-2, bta-mir-2285k-1, bta-mir-2285l, hsa-mir-548ay, hsa-mir-548az, bta-mir-2285o-1, bta-mir-2285o-2, bta-mir-2285n-1, bta-mir-2285n-2, bta-mir-2285p, bta-mir-2285m-1, bta-mir-2285m-2, bta-mir-2284y-2, bta-mir-2285n-3, bta-mir-2285n-4, bta-mir-2284y-3, bta-mir-2285o-3, bta-mir-2285o-4, bta-mir-2285m-3, bta-mir-2284y-4, bta-mir-2284y-5, bta-mir-2284y-6, bta-mir-2285m-4, bta-mir-2285o-5, bta-mir-2285m-5, bta-mir-2285n-5, bta-mir-2285n-6, bta-mir-2284y-7, bta-mir-2285n-7, bta-mir-2284z-1, bta-mir-2284aa-1, bta-mir-2285k-2, bta-mir-2284z-3, bta-mir-2284aa-2, bta-mir-2284aa-3, bta-mir-2285k-3, bta-mir-2285k-4, bta-mir-2284z-4, bta-mir-2285k-5, bta-mir-2284z-5, bta-mir-2284z-6, bta-mir-2284z-7, bta-mir-2284aa-4, bta-mir-2285q, bta-mir-2285r, bta-mir-2285s, bta-mir-2285t, bta-mir-2285b-2, bta-mir-2285v, bta-mir-2284z-2, bta-mir-2285g-2, bta-mir-2285g-3, bta-mir-2285af-1, bta-mir-2285af-2, bta-mir-2285y, bta-mir-2285w, bta-mir-2285x, bta-mir-2285z, bta-mir-2285u, bta-mir-2285aa, bta-mir-2285ab, bta-mir-2284ab, bta-mir-2285ac, bta-mir-2285ad, bta-mir-2284ac, bta-mir-2285ae, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc, bta-mir-2285ag, bta-mir-2285ah, bta-mir-2285ai, bta-mir-2285aj, bta-mir-2285ak, bta-mir-2285al, bta-mir-2285am, bta-mir-2285ar, bta-mir-2285as-1, bta-mir-2285as-2, bta-mir-2285as-3, bta-mir-2285at-1, bta-mir-2285at-2, bta-mir-2285at-3, bta-mir-2285at-4, bta-mir-2285au, bta-mir-2285av, bta-mir-2285aw, bta-mir-2285ax-1, bta-mir-2285ax-2, bta-mir-2285ax-3, bta-mir-2285ay, bta-mir-2285az, bta-mir-2285an, bta-mir-2285ao-1, bta-mir-2285ao-2, bta-mir-2285ap, bta-mir-2285ao-3, bta-mir-2285aq-1, bta-mir-2285aq-2, bta-mir-2285ba-1, bta-mir-2285ba-2, bta-mir-2285bb, bta-mir-2285bc, bta-mir-2285bd, bta-mir-2285be, bta-mir-2285bf-1, bta-mir-2285bf-2, bta-mir-2285bf-3, bta-mir-2285bg, bta-mir-2285bh, bta-mir-2285bi-1, bta-mir-2285bi-2, bta-mir-2285bj-1, bta-mir-2285bj-2, bta-mir-2285bk, bta-mir-2285bl, bta-mir-2285bm, bta-mir-2285bn, bta-mir-2285bo, bta-mir-2285bp, bta-mir-2285bq, bta-mir-2285br, bta-mir-2285bs, bta-mir-2285bt, bta-mir-2285bu-1, bta-mir-2285bu-2, bta-mir-2285bv, bta-mir-2285bw, bta-mir-2285bx, bta-mir-2285by, bta-mir-2285bz, bta-mir-2285ca, bta-mir-2285cb, bta-mir-2285cc, bta-mir-2285cd, bta-mir-2285ce, bta-mir-2285cf, bta-mir-2285cg, bta-mir-2285ch, bta-mir-2285ci, bta-mir-2285cj, bta-mir-2285ck, bta-mir-2285cl, bta-mir-2285cm, bta-mir-2285cn, bta-mir-2285co, bta-mir-2285cp, bta-mir-2285cq, bta-mir-2285cr-1, bta-mir-2285cr-2, bta-mir-2285cs, bta-mir-2285ct, bta-mir-2285cu, bta-mir-2285cv-1, bta-mir-2285cv-2, bta-mir-2285cw-1, bta-mir-2285cw-2, bta-mir-2285cx, bta-mir-2285cy, bta-mir-2285cz, bta-mir-2285da, bta-mir-2285db, bta-mir-2285dc, bta-mir-2285dd, bta-mir-2285de, bta-mir-2285df, bta-mir-2285dg, bta-mir-2285dh, bta-mir-2285di, bta-mir-2285dj, bta-mir-2285dk, bta-mir-2285dl-1, bta-mir-2285dl-2, bta-mir-2285dm
miR-198 inhibits HIV-1 gene expression and replication in monocytes and its mechanism of action appears to involve repression of cyclin T1. [score:5]
The human miRNA, hsa-miR-198, for example, has a role in human immunity and has no apparent homolog in the bovine genome. [score:1]
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22
[+] score: 6
Respiratory syncytial virus altered expression of host miRNAs (let-7f, miR-198, -24, -26b, -337-3p, -520a-5p and -595) in vitro eventually affecting the anti-viral host response [14] whereas Epstein-Barr virus encoded nuclear antigen 1 (EBNA1) transcriptionally activated expression of miR-127 which affected B-cell regulators [15]. [score:6]
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23
[+] score: 5
In monocytes, miR-198 represses expression of CCNT1 [67] and although the 42 kDa CDK9 protein is generally expressed at a high level, the CDK9 T-loop is not phosphorylated [68]. [score:5]
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24
[+] score: 5
The abundance of miRNA-198 can repress the expression of cyclin T-1, and inhibit viral transcription in primary monocytes [41]. [score:5]
[1 to 20 of 1 sentences]
25
[+] score: 4
Of the 34 upregulated miRNAs examined, we identified 11 human-specific non-homologous miRNAs, including miR-1261, miR-1268, miR-1280, miR-1304, miR-1308, miR-1908, miR-198, miR-513a-5p, miR-513b, miR-548h, and miR-580 (Supplementary Table 1A). [score:4]
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[+] score: 3
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-98, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-107, hsa-mir-16-2, hsa-mir-148a, hsa-mir-30d, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-205, hsa-mir-210, hsa-mir-181a-1, hsa-mir-222, hsa-mir-224, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-27b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-132, hsa-mir-137, hsa-mir-140, hsa-mir-141, hsa-mir-142, hsa-mir-143, hsa-mir-144, hsa-mir-153-1, hsa-mir-153-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-134, hsa-mir-136, hsa-mir-146a, hsa-mir-150, hsa-mir-184, hsa-mir-185, hsa-mir-186, hsa-mir-206, hsa-mir-320a, hsa-mir-200c, hsa-mir-128-2, hsa-mir-200a, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-299, hsa-mir-26a-2, hsa-mir-373, hsa-mir-376a-1, hsa-mir-342, hsa-mir-133b, hsa-mir-424, hsa-mir-429, hsa-mir-433, hsa-mir-451a, hsa-mir-146b, hsa-mir-494, hsa-mir-193b, hsa-mir-455, hsa-mir-376a-2, hsa-mir-33b, hsa-mir-644a, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-301b, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-320e, hsa-mir-3613, hsa-mir-4668, hsa-mir-4674, hsa-mir-6722
Several research groups demonstrated that miRNA-548d, miRNA-224, miRNA-373, miRNA-198, miRNA-106a, miRNA-26b, and miRNA-301b show altered expression in PD patients (Alvarez-Erviti et al., 2013; Burgos et al., 2014; Cardo et al., 2014). [score:3]
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[+] score: 3
Specifically we can map hsa-miR-122, hsa-miR-495, hsa-miR-34b, hsa-miR-198, hsa-miR -202, hsa-miR-510 and hsa-miR-658 to expression derived from diverse tissues of origin (Table S3), supporting the hypothesis that non-hematopoietically derived miRNAs can enter and persist in circulation. [score:3]
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28
[+] score: 3
Other miRNAs from this paper: hsa-mir-130b
Considering REs where both ΔN-P63α/P53 and TA-P63β/P53 ratios were above the 1.5 threshold (P48, PERP and mir-198), we noticed an enrichment of CAAG sequences at core motif (3/5, 60%). [score:1]
However, a group of five canonical REs (without spacer) was identified (P48, PERP, COL18A1, H2, miR-198) that exhibited comparable or even higher responsiveness to ΔN-P63α or TA-P63β than to P53 (Table S5). [score:1]
In the case of the miR-198 RE, two single nucleotide changes from CAAG to CATG in both core motifs led to ~30 fold increase in responsiveness to P53 but only to a 2.5 fold increase to TA-P63β (Tables S2, S4 and S5). [score:1]
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29
[+] score: 3
Other polymorphisms have been associated with neurological disease, such as in the noncoding genes of miR-198 and miR-206 associated with schizophrenia [156], as well as in the binding site of miR-189 in Slit and Trk-like 1 (SLITRK1) mRNA associated with Tourette syndrome [157]. [score:3]
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30
[+] score: 3
Sundaram GM Common JE Gopal FE Srikanta S Lakshman K Lunny DP 'See-saw' expression of microRNA-198 and FSTL1 from a single transcript in wound healingNature. [score:3]
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[+] score: 3
Among the 65 differentially expressed microRNAs, 13 intronic ones were observed that are highly or moderately correlated with their host genes, such as mir-555/ASH1L, mir-22/C17orf93, mir-198/FSTL1, mir-561/GULP1 and mir-564/KIF15, 18 poorly correlated and four negatively correlated with their host genes (Table S3). [score:3]
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[+] score: 2
When combined with the detection of CEA and CYFRA 21-1, miR-198 quantification even improved the sensitivity and specificity for the diagnosis of lung cancer [179]. [score:1]
In pleural effusion from patients with lung cancer, the level of miR-198 was also decreased. [score:1]
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[+] score: 2
Starting from CON E, CON C or miR-198 REs, 1 or 2 nt changes (underlined) were introduced in the core (CWWG, depicted in grey) or the core-flanking R and Y positions. [score:1]
The enhanced relative transactivation by p73 S139F was reduced when changes were introduced resulting in the AT motif in either one (ConQ, miR-198 SNP) or both core sites (ConG) (Figure 5). [score:1]
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Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-96, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, hsa-mir-16-2, hsa-mir-196a-1, hsa-mir-129-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-196a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-204, hsa-mir-210, hsa-mir-211, hsa-mir-212, hsa-mir-181a-1, hsa-mir-214, hsa-mir-215, hsa-mir-216a, hsa-mir-217, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-224, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-130a, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-137, hsa-mir-138-2, hsa-mir-140, hsa-mir-141, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-129-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-150, hsa-mir-184, hsa-mir-185, hsa-mir-195, hsa-mir-206, hsa-mir-320a, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-101-2, hsa-mir-219a-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-99b, hsa-mir-296, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-365a, hsa-mir-365b, hsa-mir-375, hsa-mir-376a-1, hsa-mir-378a, hsa-mir-382, hsa-mir-383, hsa-mir-151a, hsa-mir-148b, hsa-mir-338, hsa-mir-133b, hsa-mir-325, hsa-mir-196b, hsa-mir-424, hsa-mir-20b, hsa-mir-429, hsa-mir-451a, hsa-mir-409, hsa-mir-412, hsa-mir-376b, hsa-mir-483, hsa-mir-146b, hsa-mir-202, hsa-mir-181d, hsa-mir-499a, hsa-mir-376a-2, hsa-mir-92b, hsa-mir-33b, hsa-mir-151b, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-301b, hsa-mir-216b, hsa-mir-103b-1, hsa-mir-103b-2, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-378b, hsa-mir-320e, hsa-mir-378c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-219b, hsa-mir-203b, hsa-mir-451b, hsa-mir-499b, hsa-mir-378j
The binding of KH-type splicing regulatory protein to primary transcripts is essential for the processing of mir-198 (Sundaram et al. 2013). [score:2]
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[+] score: 2
Other miRNAs from this paper: hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-324
MiR-198 enhances temozolomide sensitivity in glioblastoma by targeting MGMT. [score:2]
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[+] score: 1
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-16-1, hsa-mir-17, hsa-mir-19a, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-96, hsa-mir-100, hsa-mir-106a, hsa-mir-107, hsa-mir-192, hsa-mir-129-1, hsa-mir-148a, hsa-mir-139, hsa-mir-10b, hsa-mir-34a, hsa-mir-182, hsa-mir-203a, hsa-mir-205, hsa-mir-210, hsa-mir-212, hsa-mir-214, hsa-mir-215, hsa-mir-216a, hsa-mir-217, hsa-mir-221, hsa-mir-223, hsa-mir-200b, hsa-let-7g, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-130a, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-141, hsa-mir-142, hsa-mir-143, hsa-mir-144, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-129-2, hsa-mir-134, hsa-mir-146a, hsa-mir-149, hsa-mir-150, hsa-mir-154, hsa-mir-320a, hsa-mir-155, hsa-mir-128-2, hsa-mir-200a, hsa-mir-302a, hsa-mir-34b, hsa-mir-34c, hsa-mir-99b, hsa-mir-26a-2, hsa-mir-302c, hsa-mir-367, hsa-mir-370, hsa-mir-375, hsa-mir-376a-1, hsa-mir-378a, hsa-mir-379, hsa-mir-328, hsa-mir-151a, hsa-mir-135b, hsa-mir-335, hsa-mir-133b, hsa-mir-449a, hsa-mir-451a, hsa-mir-410, hsa-mir-486-1, hsa-mir-146b, hsa-mir-520f, hsa-mir-518d, hsa-mir-517c, hsa-mir-376a-2, hsa-mir-92b, hsa-mir-584, hsa-mir-602, hsa-mir-629, hsa-mir-638, hsa-mir-449b, hsa-mir-449c, hsa-mir-378d-2, hsa-mir-298, hsa-mir-1246, hsa-mir-1908, hsa-mir-718, hsa-mir-2861, hsa-mir-378b, hsa-mir-378c, hsa-mir-4306, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-3976, hsa-mir-4644, hsa-mir-203b, hsa-mir-451b, hsa-mir-4728, hsa-mir-4734, hsa-mir-378j, hsa-mir-6165, hsa-mir-486-2
Singh et al. (2014)MiR-198, MiR-26a, MiR-34a, MiR-49a, let-7a, MiR-328, MiR-130a, MiR-149, MiR-602, MiR-92b The human breast cancer cell lines, culture supernatants from MCF7, and MDA-MB231 cells qRT-PCR analysis, and Western blotting The extracellular vesicles carry oncogenic proteins and miRNAs, which may further be applicable for early detection of breast malignancy as well as delineating the possible role of extracellular vesicles in tumorigenesis and metastasis. [score:1]
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This screen identified 10 microRNAs (miR-21, miR-19a, miR-17-5p, miR-26a, miR-26b, miR-107, miR-106b, miR-27a, miR-103, miR-25) that increased more than 50 % TFK-1 growth and 11 microRNAs (miR-513, miR-200b, miR-198, miR-200c, miR-520e, miR-429, miR-124a, miR-101, miR-29b, miR-494, miR-410) that decreased >50 % cell growth (Fig.   1c). [score:1]
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[+] score: 1
Other miRNAs from this paper: hsa-mir-302b, hsa-mir-302c, hsa-mir-527
In some cases, we were able to discriminate the promoters engaged exclusively in miRNA transcription from those of host genes, since mapping on opposite strands (i. e., MIR198, located in the 3’ UTR of the FLST1 gene) or into intergenic regions (MIR302B, MIR302C and MIR527). [score:1]
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Interestingly, Hansen et al. [13] also identified ATF2 in their network of schizophrenia-related genes although they started out from two other microRNAs, mir-206 and mir-198, in which they found SNPs in the studied schizophrenia patient cohort. [score:1]
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Based on these data and the previous reports about the candidate miRNAs’ function, six cancer-related or tumor-suppressing miRNAs were chosen for further investigation, including miR-198, miR-126, miR-133a, miR-137, miR-22, and miR-372 [18– 23]. [score:1]
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For example, rs2999200 was found to be significantly associated with miR-198, miR-509-3-5p and miR-519e* (p = 8.8x10 [-13], p = 6.9x10 [-11] and p = 4.3x10 [-13], respectively). [score:1]
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Some notable examples include miR-130a, miR-132, miR-155, miR-198, miR-21, miR-31 and miR-378a 13, 23, 24, 26, 28– 30. miR-155 acts as an important player in controlling the inflammatory response during skin repair; genetic deletion of miR-155 in mice leads to accelerated healing associated with elevated numbers of macrophages and increased type-1 collagen deposition in wounded tissue [30]. [score:1]
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Similarly, miR-198 has a site in the coding region, as well as conserved sites in the UTR region, of a sodium and chloride GABA transporter (Ensembl ID ENSG00000157103). [score:1]
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