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19 publications mentioning mmu-mir-329

Open access articles that are associated with the species Mus musculus and mention the gene name mir-329. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 248
Moreover, miR-329 has been found to be a suppressor of angiogenesis by targeting CD146, an endothelial biomarker which was aberrantly upregulated during pathological angiogenesis and acted as a coreceptor of vascular endothelial growth factor receptor 2 (VEGFR2) to promote disease progression [34]. [score:10]
Given that miR-329 is downregulated in GC, the introduction of this mature miRNA into the tumor tissue could serve as a therapeutic strategy by reducing the expression of target genes. [score:8]
In glioma, overexpression of miR-329 inhibited cell proliferation of glioma cells by regulating E2F1 -mediated inhibition of Akt pathway [23]. [score:8]
As shown in Figure 3C, miR-329 mimics could significantly decrease TIAM1 mRNA expression; conversely, miR-329 inhibitor significantly accelerated the TIAM1 mRNA expression (Figure 4C). [score:7]
Our data demonstrated that the downregulation of miR-329 frequently exists in GC tissue and cell lines, suggesting a tumor suppressive role of miR-329 in GC development. [score:7]
The dual-luciferase reporter assays indicated that TIAM1 was one of the functional downstream targets of miR-329, which suggested that miR-329 suppressed TIAM1 expression by interacting with the 3′UTR of TIAM1 mRNA. [score:6]
As for the mechanism, our results indicated that miR-329 directly targeted TIAM1 to inhibit cell invasiveness in GC cells. [score:6]
Moreover, miR-329 may inhibit cell proliferation in human glioma cells through regulating E2F1 -mediated suppression of Akt pathway [23]. [score:6]
Upregulation of miR-329 significantly inhibited cell proliferation, migration, and invasion in GC cell lines, indicating that repression of miR-329 might promote tumor progression in gastric carcinogenesis. [score:6]
There are no study has tested whether miR-329 could reduce tumorigenicity in a xenograft mo del, we tested the tumor-suppressive role of miR-329 in vivo through direct miRNA mimics injection and found that miR-329 significantly inhibited the growth of GC cells. [score:6]
Forced overexpression of miR-329 substantially suppressed cell proliferation, colony formation, migration, and invasion of neuroblastoma cells by regulating Lysine-specific demethylase 1 (KDM1A) [22]. [score:6]
Overexpression of miR-329 inhibited GC cell migration and invasion. [score:5]
As expected, the ectopic expression of TIAM1 rescued the miR-329 -mediated inhibition of cell proliferation and migration in HGC-27 and MGC-83 cells (Figure 5B, 5C and 5D). [score:5]
Further studies showed that overexpression of miR-329 suppressed GC cell proliferation, migration, and invasion in GC cells MGC-803 and HGC-27. [score:5]
The ectopic expression of TIAM1 rescued the miR-329 -mediated inhibition of cell proliferation in HGC-27 cells. [score:5]
We have also analyzed the correlation between miR-329 expression and the expression of TIAM1 in 20 primary GC samples. [score:5]
Exogenetic overexpression of miR-329 suppressed GC cell growth. [score:5]
Figure 2 (A) Expression levels of miR-329 in the MGC-803 cells were examined by qRT-PCR after transfection of 20 nmol/l miR-329 mimics, or scramble or control or inhibitors. [score:5]
Moreover, ectopic expression of TIAM1 significantly increased the proliferation and invasion of HGC-27 and MGC-803 cells overexpressing miR-329. [score:5]
As shown in Figure 1A, the expression of miR-329 was significantly down-regulated in four cell lines (MGC-803, SGC-7901, MKN-45 and HGC-27) compared with one normal gastric mucosa cell line, GES. [score:5]
We also performed western blot to detect the protein expression of TIAM1 in randomly selected xenograft mouse tumors and found that miR-329 mimics-injecting tumors expressed lower levels of TIAM1 than scramble controls (Figure 7D). [score:5]
MiR-329 can suppress neuroblastoma cell growth and motility partially by targeting KDM1A [22]. [score:4]
These findings suggest that miR-329 has an important role in inhibiting the development and progression of GC. [score:4]
The protein level of TIAM1 was analyzed in four miR-329 downregulated GC tissues. [score:4]
Migration assay analysis has shown that overexpression of miR-329 can enhance both the HGC-27 and MGC-803 cells migration; miR-329 inhibitor significantly accelerated the cell migration of MGC-803 and HGC-27 (Figure 3A and 3B). [score:4]
MiR-329 mimics/inhibitors and negative control molecules (scramble control mimic and inhibitor) were purchased from Dharmacon (Austin, TX). [score:4]
miR-329 was down-regulated in GC. [score:4]
We here performed in vitro and in vivo studies to demonstrate that miR-329 can regulate GC cell proliferation and invasion through targeting TIAM1. [score:4]
In this study we demonstrate that miR-329 was frequently downregulated in human GC cancer, and that miR-329 was significantly associated with late stage. [score:4]
miR-329 regulated cell proliferation and invasion through inhibiting TIAM1. [score:4]
On the other hand, knocking down of miR-329 by miR-329 inhibitor in HGC-27 cells increased protein levels of TIAM1 (Figure 4D). [score:4]
Figure 1 (A) qRT-PCR analysis of the expression of miR-329 in four cell lines (MGC-803, SGC-7901, MKN-45 and HGC-27) and one normal gastric mucosa cell line (GES). [score:3]
TIAM1 was inversely expressed with miR-329 in GC patients. [score:3]
Recently, several novel targets of miR-329 have been confirmed including E2F1, CD146 and KDM1A [22, 23, 34]. [score:3]
In conclusion, the identification of miR-329 as a tumor suppressive miRNA in human GC that acts by repressing TIAM1 provides additional evidence of a pivotal role for miRNAs in GC tumorigenesis and progression. [score:3]
Importantly, overexpressing miR-329 ameliorated progression of GC in an established experimental xenograft mo del. [score:3]
The expression of miR-329 in GC tissues was significant lower than in adjacent tissues (Figure 1B, p < 0.001). [score:3]
In our study, TIAM1 was identified as a target gene of miR-329 in GC. [score:3]
Recently, several studies reported that the expression of miR-329 was decreased in several different types of cancers, including glioma and neuroblastoma [22, 23]. [score:3]
These results demonstrate that TIAM1 is a functional target gene of miR-329 in GC. [score:3]
To explore the molecular mechanism underlying miR-329 function, it is important to identify its target gene. [score:3]
We discovered that miR-329 -transfected cells had much fewer growth percentages than that in the scramble mimics -transfected cells; conversely, miR-329 inhibitor significantly accelerated the cell proliferation of MGC-803 and HGC-27 (Figure 2C and 2D). [score:3]
miR-329 targets TIAM1 in GC cells. [score:3]
Moreover, the level of miR-329 was significantly lower in GC patients with late stage disease (Figure 1D). [score:3]
miR-329 inhibited the growth of HGC-27-engrafted tumors. [score:3]
MiR-329, which is located on 14q32.31, is reported to be downregulated in several cancers, including neuroblastoma and glioma multiforme [21– 23]. [score:3]
Increased expression of miR-329 upon transfection in the GC cell lines (HGC-27 and MGC-803) was confirmed by qRT-PCR (Figure 2A and 2B). [score:3]
The expression of miR-329 was further examined in 40 paired GC and adjacent non-tumor gastric tissues through qRT-PCR. [score:3]
Invasion assay was then performed to evaluate the effect of miR-329 on the cell invasiveness in miR-329 overexpressing HGC-27 and MGC-803 cells and showed attenuated invasiveness of GC cells; whereas miR-329 inhibitor increased cell invasion (Figure 3C and 3D). [score:2]
The effect of miR-329 on the translation of Tiam1 mRNA into protein was assessed by luciferase reporter assay in HGC-27 cells (Figure 4B). [score:2]
To further verify the role of miR-329 in the development of GC, cell transfection was performed. [score:2]
Figure 3 (A) MGC-803 cells were transfected with 20 nmol/l miR-329 mimics, miR-329 inhibitor, or scramble or control for 24 h, and migration assay was performed. [score:2]
When tumors reached 50 mm [3], synthetic miR-329 or scrambled oligonucleotides were injected directly into the tumors. [score:2]
The protein level of TIAM1 was substantially decreased after ectopic overexpression of miR-329 in HGC-27 cell line as evidenced by western blot assays (Figure 4D). [score:2]
For the migration assays, cells were transfected with miR-329 mimics or control mimics, inhibitor or control and then added into the upper chamber of the insert (BD Bioscience, 8-μm pore size). [score:2]
Further western blot analysis in xenograft carcinoma tissues demonstrated the negative regulation of miR-329 to TIAM1 suggesting that miR-329 might be better therapeutic choices in GC. [score:2]
When tumor size reached 50 mm [3], miRNA mimics (miR-329 or scrambled control) diluted in Lipofectamine 2000 (Invitrogen) solution (100 nmol mimics in 100 μl total volume) were directly injected into the tumors, respectively. [score:2]
Consistent with the cell line data, TIAM1 were enriched in the primary GC tissues that inversely correlated to miR-329 levels. [score:1]
Correlation of miR-329 expression with patients' clinicopathological variables was evaluated by independent sample t-test (two tailed) or one-way analysis of variance, followed by Tukey post hoc test. [score:1]
Figure 4 (A) The 3′UTR of TIAM1 mRNA contains the binding sequences of miR-329. [score:1]
Figure 7 (A) Representative tumors were photographed at 15 days after the first treatment with miR-329 mimic or sramble. [score:1]
The 3′UTR of TIAM1 messenger RNA contains a complementary site for the seed region of miR-329 (Figure 4A). [score:1]
Comparison of miR-329 levels and levels corresponding to TIAM1 in GC exhibited significantly inverse correlation between TIAM1 and miR-329 (r2 = 0.329, P = 0.0081) (Figure 6D). [score:1]
The protein level of TIAM1 was reduced when miR-329 mimics were transfected with pcDNA3-TIAM1 after 48 h in both HGC-27 and MGC-83 cells (Figure 5A). [score:1]
The statistical analysis of miR-329 expression between GC tissues and control tissues was evaluated by independent sample t-test (two tailed). [score:1]
In this study, we aimed to determine the expression and function of miR-329 in GC and investigate the molecular mechanism of miR-329 in GC cells. [score:1]
Figure 5 (A) miR-329 decreased TIAM1 protein levels in both the MGC-803 and HGC-27 cells. [score:1]
In agreement with the tumor growth curve, the volumes and weights of tumors treated by miR-329 mimics were significantly lower than scrambled mimics -injected tumors (Figure 7B and 7C). [score:1]
However, the function and molecular mechanism of miR-329 in human GC are elusive. [score:1]
Moreover, our investigation for the expression of TIAM1 and miR-329 in 20 GC patients indicated that there was an inverse correlation between miR-329 and TIAM1 levels. [score:1]
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[+] score: 35
Candidate target genes regulated by the upregulated miRNAs (mmu-miR-199a-5p, mmu-miR-329-3p, mmu-miR-136-5p and mmu-miR-16-1-3p). [score:7]
Of these miRNAs, four were upregulated (mmu-miR-199a-5p, mmu-miR-329-3p, mmu-miR-136-5p, and mmu-miR-16-1-3p), and one was downregulated (mmu-miR-212-3p). [score:7]
Among the upregulated miRNAs, 292, 178, 164, and 243 candidate target genes were predicted for mmu-miR-199a-5p, mmu-miR-329-3p, mmu-miR-136-5p, and mmu-miR-16-1-3p, respectively (S2 Table). [score:6]
In humans, miR-329 may inhibit cell proliferation in human glioma cells by regulating E2F1 -mediated suppression of the Akt pathway [32]. [score:6]
Of the five differentially expressed miRNAs, four miRNAs, namely, mmu-miR-199a-5p, mmu-miR-329-3p, mmu-miR-136-5p, and mmu-miR-16-1-3p, were significantly upregulated in the vitrified blastocysts. [score:6]
In this study, 5 of the 760 identified miRNAs, namely, mmu-miR-199a-5p, mmu-miR-329-3p, mmu-miR-136-5p, mmu-miR-16-1-3p, and mmu-miR-212-3p, showed significantly different expression between the vitrified and fresh mouse blastocysts. [score:3]
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[+] score: 13
org) was used to visualize the correlations of graphically depicting the regulation of the mRNA targets of the most interesting up-regulated mmu-miR-669c, mmu-miR-329, and down-regulated mmu-miR-688, mmu-miR-30c-1 [*], mmu-miR-201, mmu-miR-761, mmu-miR-715 microRNAs in Tff2- KO mice in a convenient way. [score:10]
Similarly, mmu-miR-329 (targeting Axin1 and Dvl2) is participating in basal cell carcinoma. [score:3]
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[+] score: 8
In addition, using bioinformatic analysis Lin, et al. find that oxygen-glucose deprivation/reoxygenation (OGD/R) alteres the expression of circular RNA, and that the upregulated expression of mmu-circRNA-015947 interacts with miRNAs (mmu-miR-188-3p, mmu-miR-329-5p, mmu-miR-3057-3p, mmu-miR-5098, and mmu-miR-683) [22]. [score:8]
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[+] score: 8
We randomly picked 9 miRNAs (miR-337, miR-540-3p, miR-127, miR-434-5p, miR-329, miR-543-3p, miR-376a, miR-300, and miR-381) expressed from the Dlk1-Dio3 locus and validated their expression by qRT-PCR. [score:5]
108 ± 4.23, P = 0.091), whereas overexpression of the remaining 7 miRNAs (miR-127, miR-300, miR-329, miR-337-3p, miR-376a, miR-379, and miR-381) showed no significant effect on myotube diameter (Figure 2D). [score:3]
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[+] score: 5
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-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-22, hsa-mir-28, hsa-mir-29b-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-145a, mmu-mir-150, mmu-mir-10b, mmu-mir-195a, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-206, mmu-mir-143, hsa-mir-10a, hsa-mir-10b, hsa-mir-199a-2, hsa-mir-217, hsa-mir-218-1, hsa-mir-223, hsa-mir-200b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-150, hsa-mir-195, hsa-mir-206, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-21a, mmu-mir-22, mmu-mir-29c, rno-let-7d, rno-mir-329, rno-mir-331, mmu-mir-331, rno-mir-148b, mmu-mir-148b, rno-mir-135b, mmu-mir-135b, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-10a, mmu-mir-17, mmu-mir-28a, mmu-mir-200c, mmu-mir-218-1, mmu-mir-223, mmu-mir-199a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, mmu-mir-217, hsa-mir-29c, hsa-mir-200a, hsa-mir-365a, mmu-mir-365-1, hsa-mir-365b, hsa-mir-135b, hsa-mir-148b, hsa-mir-331, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-10a, rno-mir-10b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-22, rno-mir-28, rno-mir-29b-1, rno-mir-29c-1, rno-mir-124-3, rno-mir-124-1, rno-mir-124-2, rno-mir-133a, rno-mir-143, rno-mir-145, rno-mir-150, rno-mir-195, rno-mir-199a, rno-mir-200c, rno-mir-200a, rno-mir-200b, rno-mir-206, rno-mir-217, rno-mir-223, dre-mir-7b, dre-mir-10a, dre-mir-10b-1, dre-mir-217, dre-mir-223, hsa-mir-429, mmu-mir-429, rno-mir-429, mmu-mir-365-2, rno-mir-365, dre-mir-429a, hsa-mir-329-1, hsa-mir-329-2, hsa-mir-451a, mmu-mir-451a, rno-mir-451, dre-mir-451, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-1-2, dre-mir-1-1, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-10b-2, dre-mir-16a, dre-mir-16b, dre-mir-16c, dre-mir-17a-1, dre-mir-17a-2, dre-mir-21-1, dre-mir-21-2, dre-mir-22a, dre-mir-22b, dre-mir-29b-1, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-143, dre-mir-145, dre-mir-150, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-206-1, dre-mir-206-2, dre-mir-365-1, dre-mir-365-2, dre-mir-365-3, dre-let-7j, dre-mir-135b, rno-mir-1, rno-mir-133b, rno-mir-17-2, mmu-mir-1b, dre-mir-429b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, rno-mir-133c, mmu-mir-28c, mmu-mir-28b, hsa-mir-451b, mmu-mir-195b, mmu-mir-133c, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-451b, mmu-let-7k, rno-let-7g, rno-mir-29c-2, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
Brain stem let-7c-1, miR-17, miR-135b, miR-150, miR-199a, miR-218-1, miR-223, miR-329. [score:1]
Hypothalamus miR-17, miR-29c, miR-124a-1, miR-128a, miR-150, miR-199a, miR-217, miR-223, miR-329, miR-429. [score:1]
Spinal cord miR-28, miR-217, miR-218-1, miR-329, miR-331. [score:1]
Olfactory bulb let-7b, let-7c-1, let-7c-2, miR-10a, miR-16, miR-17, miR-21, miR-22, miR-28, miR-29c, miR-124a-1, miR-124a-3, miR-128a, miR-135b, miR-143, miR-148b, miR-150, miR-199a, miR-206, miR-217, miR-223, miR-29b-1, miR-329, miR-331, miR-429, miR-451. [score:1]
Cortex let-7c-1, miR-10a, miR-21, miR-124a-1, miR-128a, miR-135b, miR-150, miR-199a, miR-217, miR-329, miR-451. [score:1]
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[+] score: 5
The array uncovered the induction of 117 miRNAs with the signal intensity ≥500 (the fluorescence amount of each miRNA probe is measured by a photo multiplier tube or charge-coupled device and signal scaled across the range of detection for the platform) in GA muscle (Table 1, Fig. 1A and 1B), including the highly downregulated miRNAs (≥1.5-fold) miR-194-5p, miR-101b-3p, miR-148a-3p, miR-199b-5p, miR-335-5p, miR-127-3p, miR-379-5p, miR-541-5p, miR-382-5p, miR-329-3p, miR-299-5p and miR-434-3p, and the highly up-regulated miRNAs (≥1.5 fold), miR-146b-5p and miR-146a-5p (Fig. 1C). [score:5]
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[+] score: 5
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-17, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-32, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-137, mmu-mir-140, mmu-mir-150, mmu-mir-155, mmu-mir-24-1, mmu-mir-193a, mmu-mir-194-1, mmu-mir-204, mmu-mir-205, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-204, hsa-mir-205, hsa-mir-222, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-137, hsa-mir-140, hsa-mir-143, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-150, hsa-mir-193a, hsa-mir-194-1, 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-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-34a, rno-mir-322-1, mmu-mir-322, rno-let-7d, rno-mir-329, rno-mir-140, rno-mir-350-1, mmu-mir-350, hsa-mir-200c, hsa-mir-155, mmu-mir-17, mmu-mir-25, mmu-mir-32, mmu-mir-200c, mmu-mir-33, mmu-mir-222, mmu-mir-135a-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-375, mmu-mir-375, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-17-1, rno-mir-19b-1, rno-mir-19b-2, rno-mir-23a, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-27b, rno-mir-29a, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-32, rno-mir-33, rno-mir-34a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-106b, rno-mir-126a, rno-mir-135a, rno-mir-137, rno-mir-143, rno-mir-150, rno-mir-193a, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-204, rno-mir-205, rno-mir-222, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, mmu-mir-410, hsa-mir-329-1, hsa-mir-329-2, mmu-mir-470, hsa-mir-410, hsa-mir-486-1, hsa-mir-499a, rno-mir-133b, mmu-mir-486a, hsa-mir-33b, rno-mir-499, mmu-mir-499, mmu-mir-467d, hsa-mir-891a, hsa-mir-892a, hsa-mir-890, hsa-mir-891b, hsa-mir-888, hsa-mir-892b, rno-mir-17-2, rno-mir-375, rno-mir-410, mmu-mir-486b, rno-mir-31b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-126b, rno-mir-9b-2, hsa-mir-499b, mmu-let-7j, mmu-mir-30f, mmu-let-7k, hsa-mir-486-2, mmu-mir-126b, rno-mir-155, rno-let-7g, rno-mir-15a, rno-mir-196b-2, rno-mir-322-2, rno-mir-350-2, rno-mir-486, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Among a myriad of alternative interesting expression profiles, miR-329 and miR-350 displayed a biphasic pattern of expression in the mouse epididymis (being present in the caput and cauda, but absent in the corpus), but were entirely absent in the rat epididymis and present in all regions of the human epididymis (S4 Table). [score:5]
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[+] score: 4
Impressively, of the 17 upregulated miRNAs in MRL- lpr mice, 11 miRNAs (miR-154, miR-127, miR-379, miR-382, miR-433, miR-300, miR-376b, miR-394, miR-299, miR-495, and miR-329) are located at a genomic imprinted DLK1-Dio3 region. [score:4]
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Further, three other up-regulated miRNAs (mmu-miR-210-5p, mmu-miR-329-5p, and mmu-let-7b-3p) are proposed to be involved in the Bone morphogenic protein (BMP) signaling pathway. [score:4]
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[+] score: 4
As observed in Figure 7, 12 miRNAs were up-regulated by UniPR1331 administration resulting in the reduction of a series of gene products including VEGF-A (miR-329, miR-263 and mir-34b), WNT5A (miR-183, miR-487b), Twist1 (miR-183 and miR-329) and ANGPT4. [score:4]
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[+] score: 3
Target sites of two miRNA families, miR-488 and miR-329, are also very well conserved across both species. [score:3]
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Inhibition of 14q32 microRNAs miR-329, miR-487b, miR-494 and miR-495 increases neovascularization and blood flow recovery after ischemia. [score:3]
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Welten S. M. Bastiaansen A. J. de Jong R. C. de Vries M. R. Peters E. A. Boonstra M. C. Sheikh S. P. La Monica N. Kandimalla E. R. Quax P. H. Inhibition of 14q32 microRNAs miR-329, miR-487b, miR-494, and miR-495 increases neovascularization and blood flow recovery after ischemia Circ. [score:3]
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Welten SM Inhibition of 14q32 MicroRNAs miR-329, miR-487b, miR-494, and miR-495 increases neovascularization and blood flow recovery after ischemiaCirc. [score:3]
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[+] score: 2
miR-329 is also reported to regulate dendritic outgrowth in an activity dependent manner [39]. [score:2]
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For example, mir-329 appears to have diverged between human and mouse: at the syntenic location in human we find two identical copies of a miRNA distantly-related to mmu-mir-329 (HP-33 and HP-34). [score:1]
Furthermore, this cluster has a complex composition, containing other related sequences {hsa-mir-323, HP-33, HP-34, HP-35, HN-6} whereas the corresponding mouse cluster {mmu-mir-323, mmu-mir-329, MP-35, MN-7, MP-37} additionally contains a rodent-specific sequence, MN-7, which is not related to the other sequences in the cluster. [score:1]
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Other miRNAs from this paper: mmu-mir-1a-1, mmu-mir-127, mmu-mir-134, mmu-mir-136, mmu-mir-154, mmu-mir-181a-2, mmu-mir-143, mmu-mir-196a-1, mmu-mir-196a-2, mmu-mir-21a, rno-mir-329, mmu-mir-1a-2, mmu-mir-181a-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-375, mmu-mir-379, mmu-mir-181b-2, rno-mir-21, rno-mir-127, rno-mir-134, rno-mir-136, rno-mir-143, rno-mir-154, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-196a, rno-mir-181a-1, mmu-mir-196b, rno-mir-196b-1, mmu-mir-412, mmu-mir-370, oar-mir-431, oar-mir-127, oar-mir-432, oar-mir-136, mmu-mir-431, mmu-mir-433, rno-mir-431, rno-mir-433, ssc-mir-181b-2, ssc-mir-181c, ssc-mir-136, ssc-mir-196a-2, ssc-mir-21, rno-mir-370, rno-mir-412, rno-mir-1, mmu-mir-485, mmu-mir-541, rno-mir-541, rno-mir-493, rno-mir-379, rno-mir-485, mmu-mir-668, bta-mir-21, bta-mir-181a-2, bta-mir-127, bta-mir-181b-2, bta-mir-181c, mmu-mir-181d, mmu-mir-493, rno-mir-181d, rno-mir-196c, rno-mir-375, mmu-mir-1b, bta-mir-1-2, bta-mir-1-1, bta-mir-134, bta-mir-136, bta-mir-143, bta-mir-154a, bta-mir-181d, bta-mir-196a-2, bta-mir-196a-1, bta-mir-196b, bta-mir-329a, bta-mir-329b, bta-mir-370, bta-mir-375, bta-mir-379, bta-mir-412, bta-mir-431, bta-mir-432, bta-mir-433, bta-mir-485, bta-mir-493, bta-mir-541, bta-mir-181a-1, bta-mir-181b-1, ssc-mir-1, ssc-mir-181a-1, mmu-mir-432, rno-mir-668, ssc-mir-143, ssc-mir-181a-2, ssc-mir-181b-1, ssc-mir-181d, ssc-mir-196b-1, ssc-mir-127, ssc-mir-432, oar-mir-21, oar-mir-181a-1, oar-mir-493, oar-mir-433, oar-mir-370, oar-mir-379, oar-mir-329b, oar-mir-329a, oar-mir-134, oar-mir-668, oar-mir-485, oar-mir-154a, oar-mir-154b, oar-mir-541, oar-mir-412, mmu-mir-21b, mmu-mir-21c, ssc-mir-196a-1, ssc-mir-196b-2, ssc-mir-370, ssc-mir-493, bta-mir-154c, bta-mir-154b, oar-mir-143, oar-mir-181a-2, chi-mir-1, chi-mir-127, chi-mir-134, chi-mir-136, chi-mir-143, chi-mir-154a, chi-mir-154b, chi-mir-181b, chi-mir-181c, chi-mir-181d, chi-mir-196a, chi-mir-196b, chi-mir-21, chi-mir-329a, chi-mir-329b, chi-mir-379, chi-mir-412, chi-mir-432, chi-mir-433, chi-mir-485, chi-mir-493, rno-mir-196b-2, bta-mir-668, ssc-mir-375
The largest miRNA family was the miR-154 family with 18 family members, next was the miR-379 family with six family members, then the miR-368 family with five family members, and finally the miR-329 family with four family members; other families had only one family member). [score:1]
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The well-studied miRNAs within this group included let-7 family (let-7c/d/f/k), miR-212 cluster (miR-212-3p and miR-132-3p/5p), miR-23a/b, miR-9-3p/5p, miR-411 clusters (miR-299a and miR-329) and miR-466 clusters (miR-466m-5p and miR-669f-5p) (Figure 2 and Table 1). [score:1]
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