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7 publications mentioning hsa-mir-3064

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-3064. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 301
Other miRNAs from this paper: hsa-mir-29a, hsa-mir-512-1, hsa-mir-512-2, hsa-mir-498, hsa-mir-532
Reversely, hTERT knockdown in S KOV-3 cells suppressed miR-532/miR-3064 inhibitors -induced Slug expression and increased the expression of Bax reduced by miR-532/miR-3064 inhibitors (Fig 4C, right panel). [score:12]
Lower: Western blot analysis was performed in S KOV-3 cells transfected with miR-532/miR-3064 inhibitors, together with (or without) hTERT siRNA; (B) (upper panel) and transwell invasion assay (lower panel) were performed in OC cells transfected as described above; (C) The protein expression of Slug and Bax in ES-2 (left panel) and S KOV-3 (right panel) cells transfected with miR-532/miR-3064 mimics (or miR-532/miR-3064 inhibitors) followed by hTERT overexpression (or hTERT knockdown). [score:9]
Neg mimic: negative control miRNA mimic; Neg inhibitor: negative control miRNA inhibitor; (C, D) Expression of hTERT, Slug, E-cadherin, Bax and GAPDH was determined using western blotting in ES-2 (C) or S KOV-3 (D) cells transfected with miR-532/miR-3064 mimics or miR-532/miR-3064 inhibitors, respectively; (E) The qPCR analysis of hTERT levels in OC patient samples and normal ovarian tissue samples; (F) Kaplan-Meier survival curves showing lower overall survival in patients with high (above median value) versus low (below median value) hTERT levels. [score:9]
This study shows that miR-532 and miR-3064 that were down-regulated in OC tissues, can suppress the proliferation, EMT and invasion of OC cells by directly repressing hTERT expression. [score:9]
In contrast, the silencing of miR-532/miR-3064 with miRNA inhibitors resulted in the up-regulation of Slug and down-regulation of Bax and E-cadherin (Fig 2D). [score:9]
Consistently, overexpression of miR-532 and miR-3064 downregulated the expression of Ki-67, a cell proliferation marker (Fig 5B). [score:8]
To further confirm the role of hTERT in the function of miR-532/miR-3064 in OC cells, we examined the protein expression of Slug and Bax in OC cells transfected with miR-532/miR-3064 mimics (or miR-532/miR-3064 inhibitors) followed by hTERT overexpression (or hTERT knockdown). [score:8]
Since the overexpression of hTERT induces OC cell invasion via up -regulating Slug expression [5], and the silencing of hTERT in glioma cells decreased cell proliferation by increasing the protein levels of Bax [21], we evaluated whether the modulation of hTERT levels by miR-532/miR-3064 affects the protein expressions of Slug, E-cadherin (a downstream target of Slug) and Bax in OC cells. [score:8]
These data suggest a possibility that miR-532/miR-3064 acts directly to suppress hTERT expression to suppress the EMT process and induce apoptosis in OC cells. [score:8]
We report for the first time here that miR-3064 controls the expression of hTERT, and verified its tumor suppressor functions in the suppression of OC cell proliferation and invasion. [score:7]
On the other hand, the silencing of hTERT expression by specific siRNA oligonucleotides in the presence of miR-532/miR-3064 inhibitors could suppress the proliferation and invasion of S KOV-3 cells (Fig 4A and 4B). [score:7]
Interestingly, hTERT overexpression in ES-2 cells could increase the expression of Slug reduced by miR-532/miR-3064 mimic, and can also decrease the expression of Bax elevated by miR-532/miR-3064 mimic (Fig 4C, left panel). [score:7]
Moreover, high levels of hTERT were observed in ES-2 and S KOV-3 cells expressing decreased levels of miR-532/miR-3064, while a low level of hTERT was observed in NOEC cells (Fig 1H), suggesting that miR-532/miR-3064 expression inversely correlates with hTERT expression in OC cells, and the repression of these two miRNAs might be important for OC growth and/or progression. [score:7]
Furthermore, the western blotting analysis demonstrated that the transfection with miR-532/miR-3064 mimics reduced hTERT expression (Fig 2C), while the knockdown of miR-532/miR-3064 using miRNA inhibitors increased the levels of hTERT protein (Fig 2D). [score:6]
When hTERT levels were down-regulated by the transfection of miR-532/miR-3064 mimics, Slug levels were decreased, and Bax and E-cadherin expression was induced (Fig 2C). [score:6]
To ascertain whether hTERT is directly targeted by miR-532/miR-3064, we performed gain-of-function experiments using ES-2 cells that express relatively low levels of miR-532/miR-3064. [score:6]
Together, these data suggest that miR-532/miR-3064 acts directly to suppress hTERT expression in OC cells. [score:6]
In S KOV-3 cells, the down-regulation of miR-532/miR-3064 by miRNA inhibitors led to a scattered morphology consistent with EMT (Fig 3B). [score:6]
In conclusion, our data suggest that hTERT overexpression might be caused by the loss of miR-532/miR-3064 (two direct suppressors of hTERT), and has a key role in enhancing OC cell proliferation and invasion. [score:6]
Our in vivo experiments revealed that reduced levels of miR-532/miR-3064 correlate with hTERT up-regulation in OC tissues, and associate with worse OC patient survival, indicating that these two miRNAs could be causal factors in the overexpression of hTERT in OC. [score:6]
We found that the expression of miR-532/miR-3064 was significantly down-regulated in OC tissues compared with normal specimens (Fig 1B and 1C). [score:5]
Collectively, these results support that hTERT inhibition is a key contributor of miR-532/miR-3064's tumor suppressive roles in OC cells. [score:5]
To examine whether these interactions between miR-532/miR-3064 and hTERT 3'-UTR are direct, mutations targeting the predicted -binding sites of miR-532 or miR-3064 within the hTERT 3'-UTR were generated. [score:5]
Conversely, the transfection of inhibitors for miR-532 or miR-3064 to another OC cell line S KOV-3 expressing relatively high levels of miR-532/miR-3064 enhanced the luciferase activity of the WT hTERT 3'-UTR (Fig 2B). [score:5]
0173912.g001 Fig 1. (A) A schematic diagram explains base pairing between miR-532/3064 with the 3'-UTR sequences of hTERT; (B, C) qPCR analysis of miR-532 (B)/miR-3064 (C) levels in 60 OC patient samples and 20 normal ovarian tissue samples; (D, E) Endogenous expression of miR-532 (D)/miR-3064 (E) was determined using qPCRs in OC cell lines (S KOV-3 and ES-2) and normal ovarian epithelial NOEC cells; (F, G) OC patients were categorized into two groups with high (above median, n = 30) or low (below median, n = 30) miRNA expression. [score:5]
Using target prediction programs (TargetScan and DIANA-MicroT-CDS), we found that hTERT contains seed sequences for two putative miRNAs (miR-532 and miR-3064) in its 3'-UTR. [score:5]
60 OC patients were divided into two groups with higher (n = 30) or lower (n = 30) expression of miR-532 or miR-3064, using the median expression values of miR-532 or miR-3064 in OC samples. [score:5]
miR-532/miR-3064 overexpression inhibits, whereas miR-532/miR-3064 silencing promotes proliferation and invasion in OC cells. [score:5]
Kaplan-Meier survival curves for OC patients were plotted based on high or low miR-532 (F)/miR-3064 (G) expression; (H) Western blot analysis for the expression of hTERT or GAPDH in S KOV-3, ES-2 and NOEC cells. [score:5]
The forced expression of the hTERT cDNA vector lacking the 3'-UTR sequence could recover hTERT protein expression in ES-2 cells transfected with miR-532/miR-3064 mimics (Fig 4A). [score:5]
0173912.g003 Fig 3. (A, B) Cell morphology of OC cells transfected with either miR-532/miR-3064 mimics (A) or miR-532/miR-3064 inhibitors (B); (C, D) Representative images of invaded ES-2 (C) and S KOV-3 (D) cells transfected as indicated; (E, F) (E) and transwell invasion assay (F) with OC cells transfected with miR-532/miR-3064 mimics or miR-532/miR-3064 inhibitors. [score:4]
Our luciferase assays suggested that, the overexpression of either miR-532 or miR-3064 mimic markedly suppressed the luciferase activity of the wild-type (WT) version of hTERT 3'-UTR in ES-2 cells (Fig 2A). [score:4]
Consistent with our findings, miR-3064 was shown to be down-regulated in colon cancer tissue relative to normal tissue [27]. [score:4]
Our in vitro results further show that the direct inhibition of hTERT achieved by transient transfection of miR-532/miR-3064 mimics can repress OC cell proliferation and invasion. [score:4]
To understand the potential roles of miR-532/miR-3064 in regulating OC cell proliferation and invasion, we performed cell proliferation assay and in vitro cell invasion assay, and found that the ectopic expression of miR-532/miR-3064 strongly suppresses the proliferative and invasive capacity of OC cells (Fig 3C, 3E and 3F). [score:4]
However, the transfection with mimics or inhibitors for miR-532/miR-3064 did not significantly influence the luciferase activity of the mutated version of hTERT 3'-UTR in OC cells (Fig 2A and 2B). [score:3]
We screened OC patient clinical tissues (n = 60) and normal ovarian epithelial tissues (n = 20) for the endogenous expression of miR-532 and miR-3064 using qPCR. [score:3]
Re -expression of miR-532 or miR-3064 might be a possible strategy for the treatment of OC. [score:3]
Kaplan-Meier analysis demonstrated that reduced expression of either miR-532 or miR-3064 was significantly associated with poorer prognosis in patients with OC (Fig 1F and 1G). [score:3]
Low expression of miR-532/miR-3064 is associated with poor survival of patients with OC. [score:3]
ES-2 cells overexpressing miR-532 or miR-3064 exhibited attenuated tumorigenic ability 26 days after implantation (Fig 5A). [score:3]
We further analyzed the expression of miR-532/miR-3064 in OC cell lines and normal ovarian epithelial NOEC cells. [score:3]
Identification of hTERT as a target for miR-532 and miR-3064 in OC cells. [score:3]
In an OC xenograft mo del, overexpressing miR-532/miR-3064 significantly decreased tumor growth of OC cells in vivo. [score:3]
Transient overexpression of miR-532 and miR-3064 resulted in significant repression of hTERT mRNA in human OC cell lines (ES-2 and S KOV-3) (data not shown). [score:3]
These data suggest that increasing miR-532 and miR-3064 levels can suppress the growth of OC cells in vivo. [score:3]
hTERT is a critical mediator of miR-532/miR-3064's tumor suppressive effects in OC cells. [score:3]
Therefore, we selected miR-532 and miR-3064 as our experimental targets. [score:3]
Furthermore, we analyzed whether miR-532/miR-3064 expression levels correlate with human OC patient survival. [score:3]
Using qPCR analysis, we detected an inverse relationship between the expression of miR-532/miR-3064 and hTERT mRNA levels in OC tissues (Fig 1B and 1C; Fig 2E). [score:3]
Lentiviral vectors (pEZX-MR03) for overexpression of miR-532/miR-3064 and the negative control lentiviral vector were purchased from Applied Biological Materials Inc. [score:3]
miR-532 and miR-3064 inhibits OC growth in a mouse mo del. [score:3]
Importantly, “rescuing” hTERT expression in the presence of miR-532/miR-3064 mimics enhances the proliferation and invasion of ES-2 cells (Fig 4B). [score:3]
Lentiviral overexpression of miR-532 and miR-3064. [score:3]
0173912.g005 Fig 5miR-532 and miR-3064 inhibit OC growth in vivo. [score:3]
miR-532 and miR-3064 inhibit OC growth in vivo. [score:3]
Our analysis revealed lower levels of both miR-532 and miR-3064 in ES-2 and S KOV-3 cells than that in NOEC cells (Fig 1D and 1E), indicating that these two miRNAs are potential tumor suppressors in OC. [score:3]
To test the possibility that miR-532/miR-3064 suppresses OC cell proliferation and invasion, we transiently transfected ES-2 cells with miR-532/miR-3064 mimics and observed that elevating miR-532/miR-3064 levels induced a cellular phenotypic change from a fibroblastic mesenchymal morphology to a more rounded epithelial-like morphology (Fig 3A). [score:3]
0173912.g002 Fig 2. (A, B) Luciferase assay was performed in OC cells that were co -transfected with reporter vectors carrying either the wild-type (WT) version or the mutated (MUT) version of hTERT 3'-UTR, along with either miR-532/miR-3064 mimics (A) or miR-532/miR-3064 inhibitors (B). [score:2]
More importantly, lower levels of miR-532/miR-3064 were significantly associated with advanced tumor stage, higher tumor grade and higher incidence of lymph node metastasis (S1 Table). [score:1]
ES-2 cells were infected with lentivirus and selected using 1 μg/ml puromycin for 4 weeks, to establish stable miR-532, miR-3064 or negative control (Neg) transfectants. [score:1]
In contrast, the silencing of miR-532 or miR-3064 stimulates OC cell proliferation and invasion (Fig 3D, 3E and 3F). [score:1]
0173912.g004 Fig 4. (A) Upper: western blot analysis of hTERT and GAPDH levels in ES-2 cells after transfection with miR-532/miR-3064 mimics, along with (or without) hTERT cDNA vector (ORF) lacking the 3'-UTR region. [score:1]
Association between miR-532/miR-3064 expression and clinicopathological characteristics of epithelial ovarian cancer. [score:1]
Given the oncogenic roles of hTERT in promoting OC cell proliferation and invasion [5, 6], we next determined whether hTERT serves as a critical mediator of miR-532/miR-3064's roles in cellular proliferation and invasiveness. [score:1]
To delineate the clinical significance of miR-532 or miR-3064, we determined the correlations between the levels of miR-532/miR-3064 and clinicopathological factors. [score:1]
To evaluate the effects of miR-532 and miR-3064 on tumor growth in vivo, we manipulated the expression levels of miR-532 and miR-3064 in ES-2 cells, and then injected ES-2 cells into the flanks of nude mice to establish subcutaneous OC xenografts. [score:1]
Until now, little has been known about the role of miR-3064 in human tumors. [score:1]
Predicted miR-532- or miR-3064 -binding sites were mutated by RiboBio Co. [score:1]
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[+] score: 10
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-17, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, mmu-mir-23b, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-127, mmu-mir-128-1, mmu-mir-132, mmu-mir-133a-1, mmu-mir-188, mmu-mir-194-1, mmu-mir-195a, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-205, mmu-mir-206, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-122, mmu-mir-30e, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-205, hsa-mir-211, hsa-mir-212, hsa-mir-214, hsa-mir-217, hsa-mir-200b, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-128-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-127, hsa-mir-138-1, hsa-mir-188, hsa-mir-194-1, hsa-mir-195, hsa-mir-206, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-23a, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-31, mmu-mir-351, hsa-mir-200c, mmu-mir-17, mmu-mir-19a, mmu-mir-100, mmu-mir-200c, mmu-mir-212, mmu-mir-214, mmu-mir-26a-2, mmu-mir-211, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-19b-1, mmu-mir-138-1, mmu-mir-128-2, hsa-mir-128-2, mmu-mir-217, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, mmu-mir-379, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-412, mmu-mir-431, hsa-mir-431, hsa-mir-451a, mmu-mir-451a, mmu-mir-467a-1, hsa-mir-412, hsa-mir-485, hsa-mir-487a, hsa-mir-491, hsa-mir-503, hsa-mir-504, mmu-mir-485, hsa-mir-487b, mmu-mir-487b, mmu-mir-503, hsa-mir-556, hsa-mir-584, mmu-mir-665, mmu-mir-669a-1, mmu-mir-674, mmu-mir-690, mmu-mir-669a-2, mmu-mir-669a-3, mmu-mir-669c, mmu-mir-696, mmu-mir-491, mmu-mir-504, hsa-mir-665, mmu-mir-467e, mmu-mir-669k, mmu-mir-669f, hsa-mir-664a, mmu-mir-1896, mmu-mir-1894, mmu-mir-1943, mmu-mir-1983, mmu-mir-1839, mmu-mir-3064, mmu-mir-3072, mmu-mir-467a-2, mmu-mir-669a-4, mmu-mir-669a-5, mmu-mir-467a-3, mmu-mir-669a-6, mmu-mir-467a-4, mmu-mir-669a-7, mmu-mir-467a-5, mmu-mir-467a-6, mmu-mir-669a-8, mmu-mir-669a-9, mmu-mir-467a-7, mmu-mir-467a-8, mmu-mir-669a-10, mmu-mir-467a-9, mmu-mir-669a-11, mmu-mir-467a-10, mmu-mir-669a-12, mmu-mir-3473a, hsa-mir-23c, hsa-mir-4436a, hsa-mir-4454, mmu-mir-3473b, hsa-mir-4681, hsa-mir-4436b-1, hsa-mir-4790, hsa-mir-4804, hsa-mir-548ap, mmu-mir-3473c, mmu-mir-5110, mmu-mir-3473d, mmu-mir-5128, hsa-mir-4436b-2, mmu-mir-195b, mmu-mir-133c, mmu-mir-30f, mmu-mir-3473e, hsa-mir-6825, hsa-mir-6888, mmu-mir-6967-1, mmu-mir-3473f, mmu-mir-3473g, mmu-mir-6967-2, mmu-mir-3473h
Out of these 25 miRNAs, 18 miRNAs were differentially expressed in a consistent manner between the 2 groups (Figure 4A, highlighted); 8 miRNAs were downregulated in both groups (miR-16, miR-200, miR-205, miR-3064, miR-379, miR-431, miR-485 and miR-491) and 10 miRNAs were upregulated in both groups (miR-194, miR-1894, miR-211, miR-3072, miR- 3077, miR-4436, miR-5128, miR-669a, miR-669c and miR-6967). [score:9]
WT) Musmusculus mmu-miR-205_st 0.0031763 –11.649 Musmusculus mmu-miR-200c_st 0.0246158 –3.802 Musmusculus mmu-miR-184_st 0.0170031 –3.06739 Musmusculus mmu-miR-431_st 0.00570439 –2.43854 Musmusculus mmu-miR-669e_st 0.00155807 –2.42538 Musmusculus mmu-miR-3470a_st 0.00672318 –1.97946 Musmusculus mmu-miR-491_st 0.00328488 –1.94599 Musmusculus mmu-miR-3064-5p_st 0.0276855 –1.77619 Musmusculus mmu-miR-466f_st 0.00409442 –1.75841 Musmusculus mmu-miR-2182_st 0.00532508 –1.70938 Musmusculus mmu-miR-341_st 0.0497367 –1.70718 Musmusculus mmu-miR-665-star_st 0.00544338 –1.69474 Musmusculus mmu-miR-1943-star_st 0.0157678 –1.64527 Musmusculus mmu-miR-486_st 0.0396356 –1.63793 Musmusculus mmu-miR-467a-star_st 0.00240509 –1.60868 Musmusculus mmu-miR-669f-5p_st 0.0107809 –1. [score:1]
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[+] score: 8
Different results were obtained with 5′- and 3′-tailed mirtrons, where disruption of the splicing sites did not inhibit the accumulation of hsa-miR-3064-5p, hsa-miR-6515-5p, hsa-miR-3940-5p, and hsa-miR-6850-5p (Fig.   1). [score:3]
Despite successful experimental validation of mirtronic miRNAs derived from conventional mirtrons, analysis of the annotated 5′-tailed mirtrons containing hsa-miR-3064-5p and hsa-miR-6515-5p or 3′-tailed mirtrons with hsa-miR-3940-5p and hsa-miR-6850-5p revealed no splicing requirement for the biogenesis of the intron-derived miRNAs. [score:1]
Introns containing validated mirtronic miRNA hsa-mir-1226-3p or predicted miRNAs hsa-mir-1227-3p, hsa-mir-1229-3p, hsa-mir-1236-3p, and hsa-mir-1238-3p processed from conventional; hsa-miR-3064-5p and hsa-miR-6515-5p from 5′-tailed; and hsa-miR-3940-5p and hsa-miR-6850-5p from 3′-tailed mirtrons are depicted as red lines. [score:1]
Putative human conventional mirtron-derived hsa-miR-1227-3p, hsa-miR-1229-3p, hsa-miR-1236-3p, and hsa-miR-1238-3p [15] and 3′-tailed mirtron-derived hsa-miR-3940-5p and hsa-miR-6850-5p were identified in short 69–102 nucleotide introns, whereas hsa-miR-3064-5p and hsa-miR-6515-5p were processed from both long (1236 nt) and short (88 nt) 5′-tailed mirtrons [12]. [score:1]
Schemes represent protein-coding genes, harboring reside-verified mirtronic miRNA hsa-miR-1226-3p, putative conventional mirtronic miRNAs hsa-miR-1227-3p, hsa-miR-1229-3p, and hsa-miR-1238-3p, mirtronic miRNAs, located in 5′-tailed mirtrons hsa-miR-3064-5p and hsa-miR-6515-5p and mirtronic miRNAs, located in 3′-tailed mirtrons hsa-miR-3940-5p and hsa-miR-6850-5p. [score:1]
Full sequence of mirtrons (except of hsa-miR-3064) is written above each scheme, where sequence of more abundant miRNA of the hairpin is marked in red, less abundant in blue, and tail is marked in green. [score:1]
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[+] score: 4
Specifically, miR-1182, miR-1207-5p, miR-1266, miR-532 and miR-3064, which bind within the h TERT 3’UTR, are downregulated and associated with a poor clinical outcome in bladder, gastric and ovarian cancer [169– 171]. [score:4]
[1 to 20 of 1 sentences]
[+] score: 3
01 Stress response, cell proliferation miR-542 ↓2.60 NA miR-574 ↑2.09 Inflammation (Tlr9 activation), cell proliferation, apoptosis miR-669j ↑3.12 NA miR-672 ↑2.40 NA miR-674 ↑2.19 NA miR-744 ↑4.35Oncogene (Tgf) suppression miR-873 ↑2.53 ↑3.22 NA miR-1930 ↑3.31 NA miR-1934 ↑2.17 ↑3.27 NA miR-1942 ↑2.49 NA miR-3064 ↑2.50 NA miR-3065 ↑3.20 NA miR-3069 ↑2.98 NA miR-3071 ↑3.51 NA miR-3073 ↓2.78 NA miR-3092 ↑3.48 NA miR-3093 ↑3.28 NA miR-3109 ↓2.07 NAAll reported variations were statistically significant (P < 0.05). [score:3]
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[+] score: 2
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-15a, hsa-mir-18a, hsa-mir-33a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, mmu-mir-27b, mmu-mir-126a, mmu-mir-128-1, mmu-mir-140, mmu-mir-146a, mmu-mir-152, mmu-mir-155, mmu-mir-191, hsa-mir-10a, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, mmu-mir-297a-1, mmu-mir-297a-2, hsa-mir-27b, hsa-mir-128-1, hsa-mir-140, hsa-mir-152, hsa-mir-191, hsa-mir-126, hsa-mir-146a, mmu-let-7a-1, mmu-let-7a-2, mmu-mir-15a, mmu-mir-18a, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-342, hsa-mir-155, mmu-mir-107, mmu-mir-10a, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-33, mmu-mir-211, hsa-mir-374a, hsa-mir-342, gga-mir-33-1, gga-let-7a-3, gga-mir-155, gga-mir-18a, gga-mir-15a, gga-mir-218-1, gga-mir-103-2, gga-mir-107, gga-mir-128-1, gga-mir-140, gga-let-7a-1, gga-mir-146a, gga-mir-103-1, gga-mir-218-2, gga-mir-126, gga-let-7a-2, gga-mir-27b, mmu-mir-466a, mmu-mir-467a-1, hsa-mir-499a, hsa-mir-545, hsa-mir-593, hsa-mir-600, hsa-mir-33b, gga-mir-499, gga-mir-211, gga-mir-466, mmu-mir-675, mmu-mir-677, mmu-mir-467b, mmu-mir-297b, mmu-mir-499, mmu-mir-717, hsa-mir-675, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-297c, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-467c, mmu-mir-467d, mmu-mir-466d, hsa-mir-297, mmu-mir-467e, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-467f, mmu-mir-466j, mmu-mir-467g, mmu-mir-467h, hsa-mir-664a, hsa-mir-1306, hsa-mir-1307, gga-mir-1306, hsa-mir-103b-1, hsa-mir-103b-2, gga-mir-10a, mmu-mir-1306, mmu-mir-3064, mmu-mir-466m, mmu-mir-466o, mmu-mir-467a-2, mmu-mir-467a-3, mmu-mir-466c-2, mmu-mir-467a-4, mmu-mir-466b-4, mmu-mir-467a-5, mmu-mir-466b-5, mmu-mir-467a-6, mmu-mir-466b-6, mmu-mir-467a-7, mmu-mir-466b-7, mmu-mir-467a-8, mmu-mir-467a-9, mmu-mir-467a-10, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, hsa-mir-466, hsa-mir-3173, hsa-mir-3618, hsa-mir-499b, mmu-mir-466q, hsa-mir-664b, gga-mir-3064, mmu-mir-126b, gga-mir-33-2, mmu-mir-3618, mmu-mir-466c-3, gga-mir-191
Using this approach, we proposed a novel miRNA gene in chicken (mir-3064) based on its pre-miRNA region that was found conserved in human and mouse (Figure S5). [score:1]
A) Human (hsa-mir-3064) and mouse (mmu-mir-3064) miRNA genes matching the sequence in chicken. [score:1]
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[+] score: 1
Note that there is not evidence for small RNA generation across most of the aligned species, and only in a small number of the species exhibit a classic "saddle-shaped" evolutionary profile in which the hairpin loop clearly evolves more quickly than does the hairpin arms (e. g. as is seen for mir-1224, mir-3064, and mir-877). [score:1]
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