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20 publications mentioning dre-mir-17a-1

Open access articles that are associated with the species Danio rerio and mention the gene name mir-17a-1. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 372
Other miRNAs from this paper: dre-mir-17a-2, dre-mir-19a
Given the observation that miR-17-5p was down-regulated in TNBC cell lines and clinical tumour tissues in contrast to ETV1, we speculated that up-regulation of miR-17-5p would suppress triple -negative breast tumour cell oncogenic activity by targeting ETV1 and dysregulation of miR-17-5p would be associated with the prognosis of TNBC patients. [score:12]
To reinforce the expression of miR-17-5p in TNBC cell lines not only significantly reduced the expression of ETV1 but also inhibited cell proliferation, migration and invasion, which might suppress the development of TNBC. [score:10]
The relative expression of miR-17-5p in 105 pairs of TNBC/adjacent non-tumour tissues was divided into miR-17-5p-low expression group and -high expression group according to the relative ratio of miR-17-5p expression in tumour/adjacent non-tumour tissues < or > 0.5. [score:9]
Up-regulation of miR-17-5p could inhibit ETV1expression, and negative regulate c-Myc transcription. [score:9]
Finally, miR-17-5p could suppress TNBC development by targeting ETV1 through decreasing MMP, COX-2 and VEGF expression. [score:8]
Up-regulation of miR-17 in GIST cell lines inhibits cell proliferation by degrading ETV1 mRNA, which may suppress the tumour progression [12]. [score:8]
Furthermore, up-regulation of miR-17-5p suppresses TNBC cell growth, migration and invasion in vitro, and metastasis in vivo by targeting ETV1. [score:8]
Furthermore, up-regulation of miR-17-5p expression can effectively suppress TNBC tumourigenesis by degrading ETV1. [score:8]
Overexpression of miR-17-5p inhibits hormone -dependent breast cancer cell proliferation by targeting AIB1 or cyclin D1 [16, 25]. [score:7]
Forced expression of miR-17-5p in MDA-MB-231 or BT549 cells significantly decreased ETV1 expression and suppressed cell proliferation, migration in vitro and tumour metastasis in vivo. [score:7]
We confirmed that miR-17-5p is significantly down-regulated in TNBC cells, whereas ETV1 is significantly up-regulated [Fig. 1]. [score:7]
miR-17-5p overexpression also significantly decreased the number of migrating and invasive MDA-MB-231 and BT549 cells [Fig.   6A-H], and inhibited wound healing [Fig. 6I-L], indicating that miR-17-5p may function as a tumour suppressor in TNBC. [score:7]
Therefore, whether the joint overexpression of both miR-17-5p and COP1 or other suppressor genes is a new strategy for TNBC therapy by targeting ETV1 needs further research. [score:7]
In this study, we showed that miR-17-5p expression levels were significantly down-regulated in TNBC cell lines and clinical tumour tissues. [score:6]
Highly expressed miR-17 enhances melanoma cell motility and migration by repressing translation of the ETV1 protein, which may support the development of metastasis [9]. [score:6]
Consistent with the colony formation assays, up-regulation of miR-17-5p significantly suppressed the cells proliferation according to the CCK8 analyses after transfection for 48 h and 72 h [Fig. 5A, D]. [score:5]
It has been confirmed that miR-17-5p can function as an oncogene or tumour suppressor by targeting ETV1 in melanoma or GIST [9, 12]. [score:5]
To address this, we first utilized the Targetscan system and predicted that ETV1 is a potential target of miR-17-5p, which exhibits seed sequence complementary to miR-17-5p [Fig.   4A]. [score:5]
Our data indicate that miR-17-5p acts as a tumour suppressor in TNBC by targeting ETV1, and a low-abundance of miR-17-5p may be involved in the pathogenesis of TNBC. [score:5]
c, d, The effect of miR-17-5p on ETV1 expression in MDA-MB-231 and BT549 cells was detected by qRT-PCR and western blotting after the cells were transfected with miR-17-5p mimic or inhibitor, respectively. [score:5]
e, The effect of miR-17-5p on ETV1 expression was also observed in MCF10A cells by co-transfecting with GV141-ETV1 and miR-17-5p inhibitor. [score:5]
Kaplan–Meier curves and log-rank test showed that women in the miR-17-5p-low expression group (n = 82) had a shorter overall survival (OS) time than those in the miR-17-5p -high expression group (n = 23) (log-rank test, P < 0.001), which was consistent with ETV1 -positive tumour group [Fig. 3B, C]. [score:5]
The current study showed that miR-17-5p functions as a tumour suppressor by targeting ETV1 in TNBC progression and metastasis and is a independent favourable predictor for TNBC patients’ prognoses. [score:5]
In 79 ETV1 -positive tumours, miR-17-5p -high expression cases had significantly higher survival rates than patients with miR-17-5p-low expression (log-rank test, P < 0.001) [Fig. 3D]. [score:5]
ETV1 is a direct target of miR-17-5p. [score:4]
In this study, we found that ETV1 was a direct target of miR-17-5p. [score:4]
A systematic analysis showed that down-regulation of miR-17-5p may be a prerequisite for the onset of TNBC metastasis mediated by TGFβ [26]. [score:4]
Fig. 4ETV1 is a direct target of miR-17-5p in TNBC cells. [score:4]
These results indicate that miR-17-5p may influence the behavior of TNBC by regulating ETV1 expression. [score:4]
Furthermore, multivariate Cox regression analysis, adjusted for age and TNM stage, also confirmed that miR-17-5p and ETV1 expression statuses, and TNM stage were significantly associated with patients OS [Table  4]. [score:3]
However, rescuing the expression of ETV1 in the presence of miR-17-5p significantly recovered the cell phenotype. [score:3]
miR-17-5p degrades ETV1 expression at the protein level in melanoma cells, and at the mRNA level in GIST cells [9, 12]. [score:3]
The results showed that the miR-17-5p and ETV1 expression statuses, and patients’ age and TNM stage were significantly associated with patients OS [Table  3]. [score:3]
These findings indicate that miR-17-5p may be a therapeutic target for TNBC. [score:3]
However, the miR-17-5p inhibitor did not affect the ETV1 mRNA and protein levels in TNBC cells [Fig. 4C, D]. [score:3]
We observed that enhancement of miR-17-5p in TNBC cells significantly inhibited cell proliferation, migration and invasion. [score:3]
miR-17-5p expression in TNBC tissues and cell lines was assessed by quantitative real-time PCR (qRT-PCR). [score:3]
Fig. 1Features of miR-17-5p and ETV1 expression in TNBC cells and clinical samples. [score:3]
Luciferase reporter assay confirmed that ETV1 was a direct target of miR-17-5p. [score:3]
qRT-PCR analyses of miR-17-5p and ETV1 expression were performed on a LightCycler 480 (Roche Diagnostics, Germany) according to our previous report [13]. [score:3]
The expression levels of miR-17-5p were significantly decreased in TNBC cell lines and tumour tissues [Fig.   1A, C, and Fig.   3A]. [score:3]
However, restoration of ETV1 expression in the presence of miR-17-5p significantly recovered the proliferative and migratory capacities of the TNBC cells [Fig. 5 and Fig. 6]. [score:3]
The miR-17-5p expression levels were closely correlated with tumour size (P < 0.05) and TNM stage (P < 0.05). [score:3]
a, The relative expression of miR-17-5p in 105 pairs of TNBC/adjacent non-tumour tissues was significantly lower. [score:3]
There is an inverse correlation between the expression status of miR-17-5p and ETV1 (r = −0.28, P = 3.88 × 10 [−3]). [score:3]
Furthermore, it would be more convincing if the association between miR-17-5p and ETV1 expression could be confirmed in TNBC clinical samples with a larger cohort. [score:3]
Lower miR-17-5p expression was related to a shorter survival time of TNBC patient. [score:3]
Consequently, forced miR-17-5p expression led to a significant reduction in the number of colonies for the TNBC cells [Fig.   5B, C, E, F]. [score:3]
miR-17-5p inhibits TNBC cells proliferation, migration and invasion. [score:3]
The abundance of miR-17-5p is significantly decreased in TNBC, which is in contrast to ETV1 expression. [score:3]
miR-17-5p ETV1 Triple -negative breast cancer Triple -negative breast cancer (TNBC) is a challenging disease with the worst outcome among all breast cancer subtypes worldwide [1]. [score:3]
The Fisher’s exact test was used to analyse the relationship between miR-17-5p and ETV1 expression and clinicopathological features. [score:3]
Moreover, rescue of ETV1 expression in the presence of miR-17-5p significantly restore the cell phenotype. [score:3]
Whether miR-17-5p contributes to triple -negative breast tumour cell function via ETV1 targeting has not yet been reported. [score:3]
c, Significant difference in OS was observed between miR-17-5p -high (n = 23) and -low (n = 82) expression group (P < 0.001). [score:3]
High miR-17-5p expression was associated with a significantly favourable prognosis, in either the ETV1 -positive or ETV1 -negative groups (log-rank test, P < 0.001; P < 0.001). [score:3]
The results support that miR-17-5p may function as a tumour suppressor in TNBC, which is consistent with the literature [26]. [score:3]
Restoration of ETV1 expression in the presence of miR-17-5p significantly rescued the colony potential of the cells. [score:3]
After 2 days, metastases were detected in 61 of 65 embryos injected with control cells, whereas metastases were only observed in 9 of 64 embryos injected with MDA-MB-231 cells overexpressing miR-17-5p [Fig.   7A]. [score:3]
To confirm the same modulatory mode between miR-17-5p and ETV1 existing in CSC from TNBC cells would be essential for achieving long term therapeutic success for TNBC patients by targeting these rare cells. [score:3]
miR-17-5p expression patterns vary with tumour types [12, 16, 17]. [score:3]
We speculate that it may be because of the lower level of miR-17-5p in TNBC cells, which would not respond to further inhibition of miR-17-5p. [score:3]
For the restoration of ETV1 expression, GV141-ETV1 was transfected into the cells in the presence of miR-17-5p with Lipofectamine RNAiMAX (Invitrogen, USA) according to the manufacturer’s protocol. [score:3]
Positive expression of miR-17-5p in TNBC (d, e) and non-tumour tissues (b) was also presented. [score:3]
a, b, QRT-PCR analyses of miR-17-5p and ETV1 expression levels in TNBC cells. [score:3]
In the present study, an inverse expression pattern of miR-17-5p and ETV1 in TNBC cell lines and tumour tissues was detected. [score:3]
To validate whether the expression statuses of miR-17-5p or ETV1 are independent prognostic predictors of OS for TNBC patients, we performed univariate and multivariate Cox regression analyses respectively. [score:3]
Expression status of miR-17-5p is inversely related to ETV1 and is proportional to the prognoses of TNBC patients. [score:3]
However, additional evidences are required to validate the detailed mechanisms of miR-17-5p in TNBC tumourigenesis and as a potential therapeutic target. [score:3]
Based on Targetscan prediction, we found that ETV1 transcription may be controlled by miR-17-5p [10]. [score:3]
In addition, we co -transfected MCF10A cells with GV141-ETV1 (15 μg/μl) and miR-17-5p inhibitor (100 nmol/L). [score:3]
a, Target sequences of miR-17-5p in ETV1 3′-UTR and mutant sites in 3′-UTR. [score:3]
The miR-17-5p mimic, inhibitor and negative control oligos were purchased from RiboBio (China) and transfected into cells using Lipofectamine RNAiMAX (Invitrogen, USA) according to the manufacturer’s instructions. [score:3]
Moreover, the inhibitory effect of miR-17-5p on the luciferase activity was abrogated when we mutated the miR-17-5p binding site in the 3’UTR of ETV1 mRNA [Fig. 4B]. [score:3]
Restoration of ETV1 expression in the presence of miR-17-5p significantly recovered the cells migratory and invasive capabilities observed with Transwell (a- h) and wound closure (i- l) assays. [score:2]
Original magnification: 100 × To verify that the direct interaction between miR-17-5p and ETV1 changes the functional phenotype of TNBC cells, we treated MDA-MB-231 and BT549 cells as described above. [score:2]
Our results suggest that there might exist a signaling pathway, c-Myc/p53—miR-17-5p—ETV1—MMP, COX-2 and VEGF [Fig. 7B], playing a role in TNBC development [3, 6, 29]. [score:2]
As predicted, enhancement of miR-17-5p significantly suppressed the proliferative and migratory capacities of the treated TNBC cells compared to control cells. [score:2]
MDA-MB-231 and BT549 cells were transfected with with LV-miR-17-5p or LV-NC. [score:1]
MDA-MB-231 cells were transfected with miR-17-5p mimic (50 nmol/L) or negative control oligos (50 nmol/L). [score:1]
Briefly, negative control oligos or miR-17-5p mimic transfected MDA-MB-231 cells were labelled with the fluorescent dye CM-Dil (Life Technologies, USA). [score:1]
miR-17-5p decreased the number of migrating and invasive MDA-MB-231 and BT549 cells. [score:1]
miR-17-5p is a independent favourable predictor for the prognoses of TNBC patients in contrast to ETV1. [score:1]
As shown in Fig. 4C-E, miR-17-5p significantly decreased both the ETV1 mRNA and protein levels, consistent with the report [12]. [score:1]
In this study, we investigated the expression status of both miR-17-5p and ETV1 and their association in TNBC. [score:1]
, China) (LV-miR-17-5p). [score:1]
We performed in situ hybridization (ISH) and immunohistochemistry (IHC) to detect the location of miR-17-5p and ETV1 in TNBC patient samples, respectively. [score:1]
The abundance of miR-17-5p was significantly decreased in TNBC cell lines and clinical TNBC tissues. [score:1]
These data suggest that miR-17-5p and ETV1 are independent prognostic predictors of OS for TNBC patient. [score:1]
To investigate the modulatory mode of miR-17-5p on ETV1 in TNBC cells, we treated MDA-MB-231 and BT549 cells with miR-17-5p mimic (50 nmol/L) or inhibitor (100 nmol/L), respectively. [score:1]
The mutual phenomenon is the relatively low abundance of COP1 and miR-17-5p in TNBC, which might be the source of TNBC occurrence. [score:1]
miR-17-5p was cloned into the GV248 vector containing GFP and was packaged into a lentivirus by Genechem (Genechem Co. [score:1]
The localization of miR-17-5p and ETV1 was observed by in situ hybridization (ISH) and immunohistochemistry (IHC), respectively. [score:1]
However, the miR-17 level is significantly lower in GIST. [score:1]
MDA-MB-231 and BT549 cells were infected with 1 × 10 [8] TU/ml LV-miR-17-5p or LV-NC in enhanced infection solution containing 5 μg/μl polybrene (Genechem Co. [score:1]
d, In 79 cases of ETV1 -positive TNBCs, miR-17-5p -high cases had significant higher survival rate than those of miR-17-5p-low group (P < 0.001). [score:1]
ETV1 is involved in miR-17-5p -induced anti-proliferative and anti-migratory effects on TNBC cells. [score:1]
We hypothesize that miR-17-5p decrease in TNBC might be associated with c-Myc or p53 abnormal activity [29, 30]. [score:1]
b, c, e, f, miR-17-5p led to a significant reduction of colony numbers in TNBC cells. [score:1]
Both univariate and multivariate analyses showed that miR-17-5p and ETV1 were independent risk factors in the prognosis of TNBC patient. [score:1]
The abundance and function of miR-17-5p vary with tumour type, even if observed in same tumour type. [score:1]
Fragments of the ETV1 mRNA 3′-UTRs containing the putative or mutated miRNA binding sites for miR-17-5p were cloned into the GV306 luciferase reporter vector (GeneChem, China). [score:1]
b, miR-17-5p transcription might be activated by c-Myc, and repressed by p53. [score:1]
The results indicate that miR-17-5p is a favourable prognostic factor, while ETV1 is a poor prognostic factor for the patient. [score:1]
miR-17-5p enhancement is a independent favourable prognostic factor for TNBC patients in contrast to ETV1. [score:1]
To further observe the potential functional link between miR-17-5p and ETV1 in vivo, we utilized a metastatic zebrafish mo del. [score:1]
a, c, Negative control of miR-17-5p in TNBC and adjacent non-tumour tissues. [score:1]
MDA-MB-231 and BT549 cells were transfected with LV-miR-17-5p or LV-NC. [score:1]
In situ observation of miR-17-5p was performed using 4-μm sections of samples with a digoxigenin -labelled oligonucleotide miR-17-5p detection probe (Exiqon, USA), as previously described [13]. [score:1]
b, Relative luciferase activity of ETV1 3′-UTR and mutant in the miR-17-5p mimic -transfected 293 T cells. [score:1]
To investigate the effect of miR-17-5p on ETV1 protein expression, western blotting was conducted. [score:1]
c, d, The expression levels of miR-17-5p and ETV1 in clinical TNBC samples evaluated by qRT-PCR. [score:1]
In addition to miR-17-5p, other members of the miR-17-92 cluster, such as miR-19a/b, etc. [score:1]
The constructs were then co -transfected with miR-17-5p mimic or negative control oligos into 293 T cells using Lipofectamine 2000 (Invitrogen, USA) according to the manufacturer’s instructions. [score:1]
The ETV1 mRNA and protein levels were significantly increased in TNBC cell lines and tissues [Fig. 1B, D and Additional file 3: Fig. S1], which was inversely correlated with miR-17-5p (r = −0.28, P = 3.88 × 10 [−3]) [Table  1]. [score:1]
miR-17-5p has been linked to tumourigenesis in a broad range of cancers, including hepatocellular carcinoma [19], gastric cancer [20], ovarian cancer [21], prostate cancer [22], and breast cancer [23, 24]. [score:1]
miR-17-5p probe sequence was (5′-3′) CTACCTGCACTGTAAGCACTTTG. [score:1]
miR-17-5p belongs to the miR-17-92 cluster, which plays a critical role in tumourigenesis [11]. [score:1]
miR-17-5p is a independent favourable prognostic factor for TNBC patient. [score:1]
Women with ETV1 -negative/miR-17-5p -high tumours had the best survival relative to women with other subtypes (log-rank test, P < 0.001) [Fig. 3E]. [score:1]
The level of miR-17-5p was normalized to U6, and the level of ETV1 was normalized to GAPDH. [score:1]
a, Control oligos (50 nmol/L) or miR-17-5p mimic (50 nmol/L) transfected MDA-MB-231 cells were labelled with fluorescent dye CM-Dil and then microinjected into the perivitelline spaces of 48-hpf zebrafish embryos. [score:1]
To examine the biological effects of miR-17-5p on TNBC cells and to achieve a higher abundance of miR-17-5p, we transfected MDA-MB-231 and BT549 cells with LV-miR-17-5p or LV-NC. [score:1]
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2
[+] score: 26
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-17, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, mmu-let-7g, mmu-let-7i, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-134, mmu-mir-137, mmu-mir-138-2, mmu-mir-145a, mmu-mir-24-1, hsa-mir-192, mmu-mir-194-1, mmu-mir-200b, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-215, hsa-mir-221, hsa-mir-200b, mmu-mir-296, mmu-let-7d, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-137, hsa-mir-138-2, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-134, hsa-mir-138-1, hsa-mir-194-1, mmu-mir-192, 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-24-2, mmu-mir-346, hsa-mir-200c, mmu-mir-17, mmu-mir-25, mmu-mir-200c, mmu-mir-221, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-200a, hsa-mir-296, hsa-mir-369, hsa-mir-346, mmu-mir-215, gga-let-7i, gga-let-7a-3, gga-let-7b, gga-let-7c, gga-mir-221, gga-mir-17, gga-mir-138-1, gga-mir-124a, gga-mir-194, gga-mir-215, gga-mir-137, gga-mir-7-2, gga-mir-138-2, gga-let-7g, gga-let-7d, gga-let-7f, gga-let-7a-1, gga-mir-200a, gga-mir-200b, gga-mir-124b, gga-let-7a-2, gga-let-7j, gga-let-7k, gga-mir-7-3, gga-mir-7-1, gga-mir-24, gga-mir-7b, gga-mir-9-2, dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-192, dre-mir-221, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, 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-7a-3, 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-17a-2, dre-mir-24-4, dre-mir-24-2, dre-mir-24-3, dre-mir-24-1, dre-mir-25, dre-mir-92b, 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-137-1, dre-mir-137-2, dre-mir-138-1, dre-mir-145, dre-mir-194a, dre-mir-194b, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-430c-2, dre-mir-430c-3, dre-mir-430c-4, dre-mir-430c-5, dre-mir-430c-6, dre-mir-430c-7, dre-mir-430c-8, dre-mir-430c-9, dre-mir-430c-10, dre-mir-430c-11, dre-mir-430c-12, dre-mir-430c-13, dre-mir-430c-14, dre-mir-430c-15, dre-mir-430c-16, dre-mir-430c-17, dre-mir-430c-18, dre-mir-430a-2, dre-mir-430a-3, dre-mir-430a-4, dre-mir-430a-5, dre-mir-430a-6, dre-mir-430a-7, dre-mir-430a-8, dre-mir-430a-9, dre-mir-430a-10, dre-mir-430a-11, dre-mir-430a-12, dre-mir-430a-13, dre-mir-430a-14, dre-mir-430a-15, dre-mir-430a-16, dre-mir-430a-17, dre-mir-430a-18, dre-mir-430i-1, dre-mir-430i-2, dre-mir-430i-3, dre-mir-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, mmu-mir-470, hsa-mir-485, hsa-mir-496, dre-let-7j, mmu-mir-485, mmu-mir-543, mmu-mir-369, hsa-mir-92b, gga-mir-9-1, hsa-mir-671, mmu-mir-671, mmu-mir-496a, mmu-mir-92b, hsa-mir-543, gga-mir-124a-2, mmu-mir-145b, mmu-let-7j, mmu-mir-496b, mmu-let-7k, gga-mir-124c, gga-mir-9-3, gga-mir-145, dre-mir-138-2, dre-mir-24b, gga-mir-9-4, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3, gga-mir-9b-1, gga-let-7l-1, gga-let-7l-2, gga-mir-9b-2
MicroRNA-17-92a upregulation by estrogen leads to Bim targeting and inhibition of osteoblast apoptosis. [score:7]
Mdm2 is negatively regulated by several miRNAs including miR-192 (Pichiorri et al., 2010), miR-194 (Pichiorri et al., 2010), miR-215 (Pichiorri et al., 2010), miR-221 (Kim et al., 2010), and miR-17 (Li and Yang, 2012) in different cellular contexts; however, whether these or other miRNAs regulate Mdm2 expression during the CNS development must be determined. [score:6]
Stress response of glioblastoma cells mediated by miR-17-5p targeting PTEN and the passenger strand miR-17-3p targeting. [score:5]
Although from the beginning of the spinal cord development the p2 progenitors express the pMN marker, Olig2, it is repressed by miR-17-3p through development progression, thus ensuring the proper specification of the pMN/p2 boundary and the production of V2 interneurons (Chen et al., 2011a). [score:5]
In this sense, mice lacking the miR-17/92 cluster present a dorsal shift in pMN/p2 boundary and incorrect production of V2 interneurons (Chen et al., 2011a). [score:1]
Mir-17-3p controls spinal neural progenitor patterning by regulating Olig2/Irx3 cross-repressive loop. [score:1]
Therefore, Olig2 repression mediated by miR-17-3p is crucial for the correct patterning of ventral spinal NPs domains and thus, it is possible that other miRNAs also participate in NPs specifications in different CNS regions. [score:1]
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3
[+] score: 12
Other miRNAs from this paper: dre-mir-10a, dre-mir-10b-1, dre-mir-183, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, 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-mir-1-2, 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-10c, dre-mir-10d, dre-mir-15a-1, dre-mir-15a-2, dre-mir-17a-2, dre-mir-20a, dre-mir-29b-1, dre-mir-29b-2, dre-mir-29a, dre-mir-92a-1, dre-mir-92a-2, dre-mir-92b, dre-mir-101a, dre-mir-101b, 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-145, dre-mir-430c-2, dre-mir-430c-3, dre-mir-430c-4, dre-mir-430c-5, dre-mir-430c-6, dre-mir-430c-7, dre-mir-430c-8, dre-mir-430c-9, dre-mir-430c-10, dre-mir-430c-11, dre-mir-430c-12, dre-mir-430c-13, dre-mir-430c-14, dre-mir-430c-15, dre-mir-430c-16, dre-mir-430c-17, dre-mir-430c-18, dre-mir-430a-2, dre-mir-430a-3, dre-mir-430a-4, dre-mir-430a-5, dre-mir-430a-6, dre-mir-430a-7, dre-mir-430a-8, dre-mir-430a-9, dre-mir-430a-10, dre-mir-430a-11, dre-mir-430a-12, dre-mir-430a-13, dre-mir-430a-14, dre-mir-430a-15, dre-mir-430a-16, dre-mir-430a-17, dre-mir-430a-18, dre-mir-430i-1, dre-mir-430i-2, dre-mir-430i-3, dre-mir-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, dre-mir-499, ola-mir-430a-1, ola-mir-430c-1, ola-mir-430b-1, ola-mir-430c-2, ola-mir-430c-3, ola-mir-430d-1, ola-mir-430a-2, ola-mir-430c-4, ola-mir-430d-2, ola-mir-430a-3, ola-mir-430a-4, ola-mir-430c-5, ola-mir-430d-3, ola-mir-430b-2, ola-mir-430c-6, ola-mir-430c-7, ola-mir-20a-1, ola-mir-92a-2, ola-mir-9a-2, ola-mir-101a, ola-mir-9b-1, ola-mir-499, ola-let-7a-1, ola-mir-9a-3, ola-mir-183-1, ola-let-7a-2, ola-mir-29b-1, ola-mir-29a, ola-mir-124-1, ola-mir-124-2, ola-mir-9a-4, ola-mir-101b, ola-let-7a-4, ola-mir-10d, ola-mir-9a-1, ola-mir-92b, ola-mir-9b-2, ola-mir-1-2, ola-mir-124-3, ola-mir-15a, ola-mir-10b, ola-mir-92a-1, ola-mir-20a-2, ola-mir-17, ola-mir-29b-2, ola-mir-29c, ola-mir-183-2, ola-let-7a-3, ola-mir-9a-5, ola-mir-145, dre-mir-29b3
Before a sequence of the N. furzeri genome assembly became available [50], we could show by use of the Danio rerio reference from miRBase that aging in the N. furzeri brain displays evolutionary conserved miRNA regulation, converging in a regulatory network centred on the antagonistic actions of the oncogenic MYC and tumor-suppressor TP53 [2], and the expression of miR-15a and the miR-17/92 cluster is mainly localized in neurogenetic regions of the adult brain [10]. [score:7]
Furthermore, up to two smaller and lesser conserved clusters, containing at least two miRNAs of the miR-17 or miR-92 family, were identified per fish species, similar to what is known for mammals. [score:1]
b Structure comparison of the miR-17/92 cluster. [score:1]
For detailed lists of miRNA family assignments, see Supplement Table 4 The age -dependent expression of the following miRNAs was previously demonstrated by qPCR: tni-miR-15a, tni-miR-101a, tni-miR-101b, dre-miR-145, hsa-miR 29c-1 (100% identical to dre-miR-29a), hsa-let-7a-5p, hsa-miR-124a-1, hsa-miR-1-2, olamiR-21, ola-miR-183-5p and, from cluster dre-miR-17a/18a/19a, and dre-miR-20a (the used primers were Qiagen miScript primer). [score:1]
For detailed lists of miRNA family assignments, see Supplement Table 4 The age -dependent expression of the following miRNAs was previously demonstrated by qPCR: tni-miR-15a, tni-miR-101a, tni-miR-101b, dre-miR-145, hsa-miR 29c-1 (100% identical to dre-miR-29a), hsa-let-7a-5p, hsa-miR-124a-1, hsa-miR-1-2, olamiR-21, ola-miR-183-5p and, from cluster dre-miR-17a/18a/19a, and dre-miR-20a (the used primers were Qiagen miScript primer). [score:1]
Two highly conserved clusters could be identified for each species, as well as some smaller less conserved clusters, containing at least two miRNAs of the miR-17/92 cluster. [score:1]
[1 to 20 of 6 sentences]
4
[+] score: 10
In summary, miR-140 regulates the migration of neural crest cells, miR-200b regulates palatal fusion and the miR-17-92b cluster regulates palatal shelf growth. [score:4]
Targeted deletion reveals essential and overlapping functions of the miR-17 through 92 family of miRNA clusters. [score:3]
Germline deletion of the miR-17 approximately 92 cluster causes skeletal and growth defects in humans. [score:1]
It contains 6 miRNAs (miR-17, miR-18a, miR-19a, miR-20a, miR-19b-1, and miR-92a-1), with highly conserved sequences and organization. [score:1]
The miR-17~92 cluster collaborates with the Sonic Hedgehog pathway in medulloblastoma. [score:1]
[1 to 20 of 5 sentences]
5
[+] score: 9
For instance, miR-92a (miR-17∼92 cluster) is expressed in vascular endothelial cells and suppresses the function of pro-angiogenic proteins by inhibiting translation of their mRNAs [27]. [score:9]
[1 to 20 of 1 sentences]
6
[+] score: 9
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-21, hsa-mir-29a, hsa-mir-96, mmu-let-7g, mmu-let-7i, mmu-mir-124-3, mmu-mir-140, mmu-mir-181a-2, mmu-mir-182, mmu-mir-183, mmu-mir-194-1, mmu-mir-200b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-181a-1, hsa-mir-200b, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-140, hsa-mir-194-1, 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-21a, mmu-mir-29a, mmu-mir-96, mmu-mir-34a, mmu-mir-135b, hsa-mir-200c, hsa-mir-181b-2, mmu-mir-17, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-376c, hsa-mir-376a-1, mmu-mir-376a, hsa-mir-135b, mmu-mir-181b-2, mmu-mir-376b, dre-mir-34a, dre-mir-181b-1, dre-mir-181b-2, dre-mir-182, dre-mir-183, dre-mir-181a-1, 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-15a-1, dre-mir-15a-2, dre-mir-17a-2, dre-mir-21-1, dre-mir-21-2, dre-mir-29a, dre-mir-96, 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-140, dre-mir-181c, dre-mir-194a, dre-mir-194b, dre-mir-200b, dre-mir-200c, hsa-mir-376b, hsa-mir-181d, hsa-mir-507, dre-let-7j, dre-mir-135b, dre-mir-181a-2, hsa-mir-376a-2, mmu-mir-376c, dre-mir-34b, dre-mir-34c, mmu-mir-181d, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, dre-mir-181a-4, dre-mir-181a-3, dre-mir-181a-5, dre-mir-181b-3, dre-mir-181d, mmu-mir-124b
Specific examples of predicted miRNA-target pairs were IGF-1, PIK3R1, and PTPN11, which were downregulated, with upregulation of miR-29a, miR-17, and miR-200c, respectively. [score:9]
[1 to 20 of 1 sentences]
7
[+] 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-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-20a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-92a-1, hsa-mir-92a-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-15b, mmu-mir-23b, mmu-mir-27b, mmu-mir-130a, mmu-mir-133a-1, mmu-mir-140, mmu-mir-24-1, hsa-mir-196a-1, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-206, hsa-mir-30c-2, hsa-mir-196a-2, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-200b, mmu-mir-301a, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-23b, hsa-mir-27b, hsa-mir-130a, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-140, hsa-mir-206, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-196a-1, mmu-mir-196a-2, 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-18a, mmu-mir-20a, mmu-mir-24-2, mmu-mir-27a, mmu-mir-92a-2, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-17, mmu-mir-19a, mmu-mir-200c, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-19b-1, mmu-mir-92a-1, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-301a, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, hsa-mir-196b, mmu-mir-196b, dre-mir-196a-1, dre-mir-199-1, dre-mir-199-2, dre-mir-199-3, hsa-mir-18b, 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-15a-1, dre-mir-15a-2, dre-mir-15b, dre-mir-17a-2, dre-mir-18a, dre-mir-18b, dre-mir-18c, dre-mir-19a, dre-mir-20a, dre-mir-23b, dre-mir-24-4, dre-mir-24-2, dre-mir-24-3, dre-mir-24-1, dre-mir-27a, dre-mir-27b, dre-mir-27c, dre-mir-27d, dre-mir-27e, dre-mir-30c, dre-mir-92a-1, dre-mir-92a-2, dre-mir-92b, dre-mir-130a, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-140, dre-mir-196a-2, dre-mir-196b, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-206-1, dre-mir-206-2, dre-mir-301a, dre-let-7j, hsa-mir-92b, mmu-mir-666, mmu-mir-18b, mmu-mir-92b, mmu-mir-1b, dre-mir-196c, dre-mir-196d, mmu-mir-3074-1, mmu-mir-3074-2, hsa-mir-3074, mmu-mir-133c, mmu-let-7j, mmu-let-7k, dre-mir-24b
Targeted knockouts of Mir17 and Mir92 in mice results in hypoplasia of most skull bones, including reduced ossification and cleft palate, similar to human patients (Ventura et al., 2008; de Pontual et al., 2011; Li et al., 2012; Wang et al., 2013). [score:3]
Another miRNA family involved in craniofacial development is the MIR17 and MIR92 family, which has been linked to Feingold syndrome in human patients (Kannu et al., 2013; Tassano et al., 2013). [score:2]
Germline deletion of the miR-17 approximately 92 cluster causes skeletal and growth defects in humans. [score:1]
Similarly, Mir92a which is in the Mirc1 cluster on mouse chromosome 14 containing Mir17, Mir18, Mir19a, Mir20a, Mir19b-1, and Mir92a-1, is required to promote proliferation of orofacial development (Ning et al., 2013). [score:1]
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8
[+] score: 6
Other miRNAs from this paper: dre-mir-17a-2, ola-mir-17
Furthermore, ERα inhibits the expression of p21 by up -regulating miR-17 (Liao et al., 2014). [score:6]
[1 to 20 of 1 sentences]
9
[+] score: 5
There are six members of the miR-17-92 group, which includes miR-17, miR-18a, miR-19a, miR-20a, miR-19b-1 and miR-92a-1. In the present study, miR-17 and miR-92 were in Cluster 2 (increased with age), which suggests a potential role of these miRNA in the inhibition of cardiomyocyte proliferation in late gestation, however, miR-20a and miR-19b were in Cluster 6 (peaked before birth, but then decreased into postnatal life) and the expression of miR-18a and 19a did not change with age. [score:5]
[1 to 20 of 1 sentences]
10
[+] score: 5
However, the maternally inherited miR-17–92 cluster, which has similar seed sites as miR-430 and human embryonic regulator miRNA (miR-302/miR-467) (44), may be of great importance to developmental biologist in studying their potential roles in degradation of maternal transcripts during early embryogenesis. [score:3]
As an illustrative example, primary transcript of the intergenic miR-17–92 cluster is shown with full-length transcript, CAGE tags and H3K4me3 peaks (Figure 1B). [score:1]
Six pre-miRNAs of the miR-17–92 cluster are encoded by a single primary transcript, as reported in human (6). [score:1]
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11
[+] score: 5
For example, miR-590 and miR-17/92 clusters promote cardiomyocyte proliferation by inhibiting the proliferation repressors Homer protein homolog 1 (Homer1) and Homeodomain-only protein x (Hopx), whereas miR-15 family represses cardiomyocyte proliferation by inhibiting the proliferative activator Checkpoint kinase 1 (Check1). [score:5]
[1 to 20 of 1 sentences]
12
[+] score: 4
Nature Publishing Group; 2003; 21: 818– 21. doi: 10.1038/nbt836 51 Abramov R, Fu G, Zhang Y, Peng C. Expression and regulation of miR-17a and miR-430b in zebrafish ovarian follicles. [score:4]
[1 to 20 of 1 sentences]
13
[+] score: 4
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, mmu-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-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
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]
Hypothalamus miR-17, miR-29c, miR-124a-1, miR-128a, miR-150, miR-199a, miR-217, miR-223, miR-329, miR-429. [score:1]
Dorsal root ganglion let-7c, miR-17, miR-145, miR-150, miR-199a, miR-223, miR-365, miR-451. [score:1]
Brain stem let-7c-1, miR-17, miR-135b, miR-150, miR-199a, miR-218-1, miR-223, miR-329. [score:1]
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14
[+] score: 3
The figure shows predicted binding alignment of miR-125a, miR-125b, miR-125c, miR-17a*, miR-20*, miR-210*, miR-29a, miR-29b and miR457a with predicted zebrafish lncRNA. [score:1]
The miRanda software identified potential binding sites of miR-125a, miR-125b, miR-125c, miR-17a*, miR-20a*, miR-210*, miR-2187, miR-29a, miR-29b and miR-457a in the predicted zebrafish 7sl lncRNA (Figure 2). [score:1]
0053823.g002 Figure 2 The figure shows predicted binding alignment of miR-125a, miR-125b, miR-125c, miR-17a*, miR-20*, miR-210*, miR-29a, miR-29b and miR457a with predicted zebrafish lncRNA. [score:1]
[1 to 20 of 3 sentences]
15
[+] score: 3
In line with this results, Han et al., characterizing an allelic series of genetically engineered mice harboring selective targeted deletions of individual components of the miR-17 ~ 92 cluster, showed that the cardiac defects observed in the miR-17~92–null mice 27 were only detected upon deletion of the entire cluster 40. [score:1]
More specifically, limb and digit malformations are some of the consequences of monoallelic micro deletions involving the miR-17 ~ 92 cluster in a subset of individuals with Feingold syndrome 40 41. [score:1]
Moreover, very recently, Han et al. 40 reported also forelimb defects in miR-17 ~ 92 deleted mice. [score:1]
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[+] score: 2
Other miRNAs from this paper: dre-mir-10a, dre-mir-10b-1, dre-mir-204-1, dre-mir-181a-1, dre-mir-214, dre-mir-222a, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, 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-10b-2, dre-mir-10c, dre-mir-10d, dre-mir-17a-2, dre-mir-21-1, dre-mir-21-2, dre-mir-22a, dre-mir-22b, dre-mir-25, dre-mir-26a-1, dre-mir-26a-2, dre-mir-26a-3, dre-mir-30d, dre-mir-92a-1, dre-mir-92a-2, dre-mir-92b, dre-mir-100-1, dre-mir-100-2, dre-mir-125a-1, dre-mir-125a-2, dre-mir-125b-1, dre-mir-125b-2, dre-mir-125b-3, dre-mir-125c, dre-mir-126a, dre-mir-143, dre-mir-146a, dre-mir-462, dre-mir-202, dre-mir-204-2, dre-mir-430c-2, dre-mir-430c-3, dre-mir-430c-4, dre-mir-430c-5, dre-mir-430c-6, dre-mir-430c-7, dre-mir-430c-8, dre-mir-430c-9, dre-mir-430c-10, dre-mir-430c-11, dre-mir-430c-12, dre-mir-430c-13, dre-mir-430c-14, dre-mir-430c-15, dre-mir-430c-16, dre-mir-430c-17, dre-mir-430c-18, dre-mir-430a-2, dre-mir-430a-3, dre-mir-430a-4, dre-mir-430a-5, dre-mir-430a-6, dre-mir-430a-7, dre-mir-430a-8, dre-mir-430a-9, dre-mir-430a-10, dre-mir-430a-11, dre-mir-430a-12, dre-mir-430a-13, dre-mir-430a-14, dre-mir-430a-15, dre-mir-430a-16, dre-mir-430a-17, dre-mir-430a-18, dre-mir-430i-1, dre-mir-430i-2, dre-mir-430i-3, dre-mir-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, dre-let-7j, dre-mir-181a-2, dre-mir-1388, dre-mir-222b, dre-mir-126b, dre-mir-181a-4, dre-mir-181a-3, dre-mir-181a-5, dre-mir-204-3
The miR-17/92 cluster is well conserved and has been linked to regulating the cell cycle, proliferation, and apoptosis 55. [score:2]
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For example, in the GSM416733 dataset, the five most abundant microRNAs and their RPM are: hsa-miR-106b-5p (4101), hsa-miR-103a-3p (5222), hsa-miR-20a-5p (5316), hsa-miR-16-5p (9630) and hsa-miR-17-5p (9883). [score:1]
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Functional requirement of dicer1 and miR-17-5p in reactive astrocyte proliferation after spinal cord injury in the mouse. [score:1]
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Furthermore, the manipulation of some of these miRs in vitro (miR-1 and miR-499) and in vivo (the miR-17/92 cluster), was shown to be able to modulate CP cell fate [135, 136] (Figure 6). [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-17, hsa-mir-25, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-105-1, hsa-mir-105-2, dme-mir-1, dme-mir-10, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-124-3, mmu-mir-134, mmu-mir-10b, hsa-mir-10a, hsa-mir-10b, dme-mir-92a, dme-mir-124, dme-mir-92b, mmu-let-7d, dme-let-7, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-134, 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-92a-2, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-10a, mmu-mir-17, mmu-mir-25, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-92a-1, hsa-mir-379, mmu-mir-379, mmu-mir-412, gga-let-7i, gga-let-7a-3, gga-let-7b, gga-let-7c, gga-mir-92-1, gga-mir-17, gga-mir-1a-2, gga-mir-124a, gga-mir-10b, gga-let-7g, gga-let-7d, gga-let-7f, gga-let-7a-1, gga-mir-1a-1, gga-mir-124b, gga-mir-1b, gga-let-7a-2, gga-let-7j, gga-let-7k, dre-mir-10a, dre-mir-10b-1, dre-mir-430b-1, hsa-mir-449a, mmu-mir-449a, 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-10b-2, dre-mir-10c, dre-mir-10d, dre-mir-17a-2, dre-mir-25, dre-mir-92a-1, dre-mir-92a-2, dre-mir-92b, 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-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, hsa-mir-412, hsa-mir-511, dre-let-7j, hsa-mir-92b, hsa-mir-449b, gga-mir-449a, hsa-mir-758, hsa-mir-767, hsa-mir-449c, hsa-mir-802, mmu-mir-758, mmu-mir-802, mmu-mir-449c, mmu-mir-105, mmu-mir-92b, mmu-mir-449b, mmu-mir-511, mmu-mir-1b, gga-mir-1c, gga-mir-449c, gga-mir-10a, gga-mir-449b, gga-mir-124a-2, mmu-mir-767, mmu-let-7j, mmu-let-7k, gga-mir-124c, gga-mir-92-2, gga-mir-449d, mmu-mir-124b, gga-mir-10c, gga-let-7l-1, gga-let-7l-2
The family defining bootstrap cutoff values are tree-specific, and are set to be the smallest bootstrap value of the reference miRNA families (let7, mir-124, mir-17 and mir-1, See additional file 3: Reference miRNA families) in each input tree. [score:1]
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