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19 publications mentioning rno-mir-193a

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-193a. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 185
Williams et al. found that overexpression of mir-193a-3p inhibited malignant pleural mesothelioma (MPM) xenograft tumor growth by directly suppressing myeloid cell leukemia-1 (MCL1) expression, and was associated with increased apoptosis [8]. [score:10]
MiR-193 agomir injection into rats contributed to inhibition of ALDH2 expression, accumulation of 4-HNE, inhibition of TH expression and activity, accumulation of tyrosine, and decrease of dopamine. [score:9]
Consistent with our results from the rat mo del (Figure 1), miR-193 mimics significantly suppressed ALDH2 expression, while the miR-193 inhibitor significantly increased the expression of ALDH2 (Figure 3B and 3C). [score:9]
These data indicate that, consistent with our observations in rats, overexpression of miR-193 is associated with decreased expression of ALDH2 and increased accumulation of toxic aldehydes, while inhibition of miR-193 leads to increased expression of ALDH2 and a decrease in toxic aldehyde accumulation. [score:9]
In the present study, we found that ALDH2 is a potential target of miR-193 and demonstrated that miR-193 inhibits ALDH2 by directly targeting its 3′UTR (Figures 3 and 4). [score:8]
As shown in Figure 3A, transfection with miR-193 mimics significantly increased miR-193 expression, while the miR-193 inhibitor significantly decreased miR-193 expression, compared to controls. [score:6]
In the present study, we demonstrated that miR-193, which is overexpressed after cerebral I/R injury, directly suppresses ALDH2 (Figures 2– 4). [score:6]
We demonstrated that miR-193 directly inhibited the expression of ALDH2, which is partly responsible for clearance of toxic aldehydes. [score:6]
To determine whether high expression of miR-193 is associated with excessive aldehyde levels, PC-12 cells were treated with miR-193 mimics or an miR-193 inhibitor. [score:5]
In addition, altered expression of miR-193 is also found in cardiovascular and cerebrovascular diseases. [score:5]
Furthermore, the miR-193 inhibitor reversed the suppression caused by miR-193 mimics. [score:5]
Exogenous miR-193 mimics suppressed ALDH2 expression and increased aldehyde levels in PC-12 cells. [score:5]
With regard to toxic aldehyde levels, we found that miR-193 overexpression significantly increased the levels of toxic aldehydes 4-HNE and MDA, while the miR-193 inhibitor significantly decreased these levels, compared to controls (Figure 3D and 3E). [score:4]
Many studies have described downregulated miR-193 in rat cerebral endothelial cells after stroke [20]. [score:4]
These data indicate that miR-193 regulates the expression of ALDH2. [score:4]
Bioinformatic analysis revealed that ALDH2 may be a target of miR-193 (Figure 1D). [score:3]
To explore whether miR-193 overexpression is one of the factors of cerebral I/R injury, an in vivo experiment was conducted. [score:3]
To ensure the expected functioning of miR-193 agomir, we measured miR-193 expression before and after injection with miR-193 agomir and found that miR-193 expression significantly increased in rats treated with miR-193 agomir (Figure 6A). [score:3]
Taken together, these data indicate that cerebral I/R injury is associated with overexpression of miR-193, which, through its action on ALDH2, drives toxic aldehyde and tyrosine accumulation and subsequent dopamine insufficiency (Figure 1 and Supplementary Figure 1). [score:3]
Figure 1(A) miR-193 expression level; (B) ALDH2 mRNA level; (C) ALDH2 preotein level; (D) schematic diagram of interaction between miR-193 and ALDH2; (E) 4-HNE content; (F) MDA content. [score:3]
Plasmids containing the wild type 3′UTR of ALDH2 (ALDH2-WT, with the seed sequence “AAAACCC”), or mutated 3′UTR of ALDH2 (ALDH2-MU, with the seed sequence “AAAGCCC”), were co -transfected with the miR-193 mimics and/or inhibitor into PC-12 cells. [score:3]
Figure 6The effect of in vivo infusion of miR-193 agomir on brain tissues(A) miR-193 expression level; (B) ALDH2 protein level; (C) 4-HNE content; (D) TH protein level; (E) TH enzyme activity; (F) tyrosine content in brain tissue; (G) Dopamine content. [score:3]
The effect of cerebral ischemia/reperfusion injury on the expression of miR-193, ALDH2, and the accumulation of toxic aldehydes. [score:3]
In conclusion, we have shown that overexpression of miR-193 in cerebral I/R injury was associated with the accumulation of toxic aldehydes and tyrosine. [score:3]
Figure 3(A) miR-193 expression level; (B) ALDH2 mRNA level; (C) ALDH2 protein level; (D) 4-HNE content; (E) MDA content. [score:3]
All values expressed as means ± S. E. M. [*] p < 0.05 vs +NC with +miR-193 mimics, [#] p < 0.05 vs +ALDH2-WT with +miR-193 mimics. [score:3]
In this study, we found that the expression of miR-193 was significantly increased in rats with cerebral ischemia/reperfusion injury. [score:3]
Rats treated with miR-193 agomir had significantly increased levels of 4-HNE, decreased expression and activity of TH, increased tyrosine levels, and decreased dopamine levels (Figure 6C–6G). [score:3]
Exogenous miR-193 mimics decreased expression of ALDH2 in a luciferase reporter gene construct. [score:3]
Before transfection, a mix including the transfection agent lip2000 and miR-193 mimics or inhibitor were prepared. [score:3]
To our knowledge, this study is the first to explore the role of miR-193 in cerebral I/R injury and may provide novel targets for the treatment of ischemic stroke. [score:3]
Decreased expression of miR-193 is usually associated with tumorigenesis, such as oral squamous cell carcinoma, acute myeloid leukemia, lung cancer, BRAF-mutated melanoma, etc [8]. [score:3]
The effect of exogenous miR-193 mimics on ALDH2 expression and aldehyde levels in PC-12 cells. [score:3]
Overexpression of miR-193 in vitro and in a rat mo del led to increased toxic aldehyde accumulation. [score:3]
We hypothesized that the mechanism of this accumulation involves direct action of miR-193 on ALDH2. [score:2]
To determine whether miR-193 regulates ALDH2 activity, a reporter gene was constructed as described in the methods section. [score:2]
In the I/R group, the expression of miR-193 significantly increased and ALDH2 (both mRNA and proteins) significantly decreased, compared to the sham procedure group (Figure 1A–1C). [score:2]
MiR-193 mimic and inhibitor transfection. [score:2]
MiR-193a-3p is also involved in multi-drug resistance or multi-chemoresistance of tumors, via presenilin 1 (PSEN1) gene or lysyl oxidase-like 4 (LOXL4) gene suppression [9]. [score:2]
MiR-193 mimic or inhibitor transfection experiments were conducted according to the instructions of the manufacturer. [score:2]
We explored the relationships between the metabolic abnormalities of aldehydes and tyrosine in cerebral I/R injury, and found that the underlying mechanism involved is the miR-193/ALDH2/4-HNE/TH/dopamine axis. [score:1]
Because ALDH2 is significantly decreased in brain tissue subjected to I/R injury while miR-193 is significantly increased, we focused on these. [score:1]
In the current study, we investigated whether overexpression of miR-193 results in the accumulation of toxic aldehydes and tyrosine. [score:1]
We therefore measured the expression of miR-193 and ALDH2 in a rat mo del of I/R injury. [score:1]
+MiR-193 agomir: tail vein infusion with miR-193 agomir (50 nmol/day) for two days. [score:1]
Cerebral ischemia/reperfusion injury induced increased miR-193, decreased ALDH2, and accumulation of toxic aldehydes. [score:1]
The effect of in vivo infusion of miR-193 agomir on brain tissues. [score:1]
In accordance with the manufacturer’s instructions, miR-193 agomir was dissolved in PBS at a concentration of 50 nmol/ml. [score:1]
We then measured the expression of ALDH2 before and after injection of miR-193 agomir and found a significant decrease in ALDH2 levels after miR-193 injection (Figure 6B). [score:1]
We therefore think that miR-193 plays an important but understudied role in cerebral I/R injury. [score:1]
These data suggest that miR-193 plays a pivotal role in oxidative stress. [score:1]
Considering the important role of miR-193 in cerebral ischemia/reperfusion injury, we conducted an in vivo experiment to explore the effects of miR-193 agomir on toxic aldehyde accumulation and tyrosine metabolism in rats. [score:1]
The effect of exogenous miR-193 mimics on relative luciferase activity. [score:1]
However, in the present study, we found that in rats subjected to 2 hours ischemia and 24 hours reperfusion, miR-193 significantly increased. [score:1]
Although many authors have reported that miR-193 is involved in the pathological processes of tumors [8, 9], scant information exists on its role in ischemic stroke. [score:1]
As shown in Figure 4, miR-193 mimics significantly decreased the relative luciferase activity in the ALDH2-WT group but not in the ALDH2-MU group. [score:1]
Taken together, these data suggest that, after I/R injury in rats, there is an increase in miR-193, a decrease in ALDH2, and an increase in toxic aldehyde accumulation. [score:1]
In the present study, we show that miR-193 is significantly increased in rats subjected to 2 hours ischemia and 24 hours reperfusion. [score:1]
Intracerebroventricular infusion of miR-193 agomir. [score:1]
To further confirm the interaction between miR-193 and ALDH2, a sequence including the seed region sequence was cloned into plasmid GV272 to construct a luciferase reporter gene. [score:1]
Then, 5 nmol of the miR-193 agomir solution was injected into rats’ right lateral ventricle of the brain following the methods described by Fei Zhu et al. for each of two consecutive days. [score:1]
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2
[+] score: 65
In contrast, Arc -regulating miR-34a, miR-326, miR-19 and miR-193a were not significantly regulated, although there was trend for miR-34a upregulation at 30 minutes post-BDNF (p = 0.07). [score:6]
miR-34a, miR-326 and miR-193a downregulate Arc protein expression in cultured hippocampal neurons. [score:6]
Inhibition of the Arc 3′UTR by miR-326 was not affected by co-transfection with miR-19a, yet significantly stronger inhibition was obtained when miR-326 was paired with miR-193a or miR-378. [score:5]
Ectopic expression of miR-193a, miR-326, and miR-34a all enhanced BDNF-evoked Arc protein expression. [score:5]
Mutation of the binding sites for miR-193, -378 and -512-5p also had no effect on reporter expression elicited by the respective miRNAs. [score:4]
A significant downregulation of Arc protein was seen in miR-193a and miR-326 transfected cells. [score:4]
Thus, at DIV10, expression of miR-19a, miR-34a, miR-326 and miR-193a were decreased while Arc mRNA was elevated. [score:3]
For further validation we selected the four miRNAs (miR-34a, miR-193, miR-378, and miR-512-5p) with strongest inhibitory effect on the Arc 3′UTR. [score:3]
After 7 days in vitro (DIV7), neurons were transfected with plasmids expressing DsRed only (empty vector), ds-Red-miR-150, DsRed-miR-326 or DsRed-miR-193a using Lipofectamine-2000 Reagent (Invitrogen). [score:3]
The following combinations: miR-34a/miR-193a, miR-326/378 and miR-326/193a gave enhanced inhibition of luciferase activity compared to miR-34a and miR-326 alone. [score:2]
Dramatic changes in mature miR-19a, miR-34a, miR-326 and miR-193a were observed during development, with maximum changes of more than 100-fold. [score:2]
In contrast, miR-19a, miR-34a, miR-326 and miR-193a were not significantly regulated. [score:2]
Collating results from mutation studies in HEK cells with effects of miRNA manipulation in hippocampal neurons, we provide evidence that miR-19a, miR-34a, miR-193a, and miR-326 are capable of modulating Arc. [score:2]
miR-326 and miR-193a experiments were similarly analyzed but in this series mean values of cytoplasmic pixels from the 20 highest DsRed expressing cells were compared with the 20 lowest. [score:2]
We chose to study miR-34a and miR-326 as strong candidates from the point mutation analysis and miR-193a because of its synergistic effects. [score:2]
B) Quantitative relative real-time PCR of miR- miR-133, 19a, miR-34a, miR-326 and miR-193a. [score:1]
Mean Arc levels were comparable between cells transfected with empty vector and miR-150 controls, but were significantly reduced in neurons transfected with miR-34a, miR-326, or miR-193a (Figure 4C and E). [score:1]
Unstimulated hippocampal neurons were transfected at DIV8 with PNA-AS complementary to miR-34a, miR-326 and miR-193a and cells were harvested 48 hours later for qPCR or western blot. [score:1]
While little is currently known about mir-193a and miR-19a, new studies have shed light on miR-34 and miR-326 function in the nervous system. [score:1]
The microRNAs included were miR-19a, miR-34a, miR-193a and miR-326. [score:1]
However, the combination of miR-34a and miR-193a significantly enhanced repression relative to miR-34a alone. [score:1]
0041688.g004 Figure 4 Cultured hippocampal neurons were transfected with either empty vector-DsRed, miR150-DsRed, miR34a-DsRed, miR326-DsRed or miR193a-DsRed. [score:1]
Transfection of miR-193a AS resulted in a small but insignificant increase in Arc mRNA. [score:1]
miR-193a enhanced repression by both miR-34a and miR-326. [score:1]
For miR-326 and miR-193a, CellProfiler threshold detection was used to separate the nuclear and cytoplasmic signals. [score:1]
B) Quantitative relative real-time PCR of miR-19a, miR-34a, miR-326, miR-193a and miR-132. [score:1]
Cultured hippocampal neurons were transfected with either empty vector-DsRed, miR150-DsRed, miR34a-DsRed, miR326-DsRed or miR193a-DsRed. [score:1]
The seed binding site of miR-193a is close (5 nts) to the first miR-326 site but 360 nts distant from miR-34a. [score:1]
We confirmed that PNA-AS transfection almost completely eliminated PCR-detectable miR-326, miR-34a and miR-193 (Figure 5B). [score:1]
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3
[+] score: 23
0037395.g003 Figure 3(A) Serum miR-122 expression levels; (B) Serum miR-192 expression levels; (C) Serum miR-193 expression levels; (D) Biochemical parameter: serum ALT levels; (E) Biochemical parameter: serum AST levels. [score:7]
0037395.g004 Figure 4(A) Serum miR-122 expression levels; (B) Serum miR-192 expression levels; (C) Serum miR-193 expression levels; (D) Biochemical parameter: serum ALT levels; (E) Biochemical parameter: serum AST levels; The absolute concentrations of target miRNAs were calculated by referring to calibration curves developed with corresponding synthetic miRNA oligonucleotides. [score:7]
By individual TaqMan qRT-PCR analysis of dysregulated serum miRNAs uncovered by serum TLDA and dysregulated liver tissue miRNAs uncovered by microarray hybridization in primary screening, 6 serum miRNAs, including miR-122, miR-192, miR-193, miR-200a, miR-21 and miR-29c, exhibited a high correlation with primary screening results. [score:3]
In the dose -dependent analysis of the serum miRNAs miR-122, miR-192 and miR-193, miR-122 showed extremely high sensitivity in both 2 DILI mo del groups (fold change >50.0), while serum biochemical parameters (e. g., ALT and AST) displayed only mild sensitivity (fold change <20.0) in the high-dose group. [score:1]
Our results demonstrate that a new panel of serum miRNAs (miR-122, miR-192 and miR-193) could have the potential to serve as sensitive, specific and noninvasive biomarkers for the diagnosis of DILI. [score:1]
In summary, serum miR-122, miR-192 and miR-193 constitute a new panel for compound- and herb -induced liver injury diagnosis. [score:1]
Among this set of serum miRNAs, miR-122, miR-192 and miR-193 presented a significant change in both DILI mo del groups within the threshold of a fold change >10 and P-value<0.05 (Table 1). [score:1]
The panel of aberrantly expressed serum miRNAs (miR-122, miR-192 and miR-193) all exhibited time- and dose -dependent characteristics. [score:1]
In the time -dependent analysis of the serum miRNAs miR-122, miR-192 and miR-193, all of these serum miRNAs exhibited an ascending trend 3 h after administration in both DILI mo del groups (fold change >2.0); while serum biochemical parameters (e. g., ALT and AST) remained at baseline levels (fold change <1.5). [score:1]
[1 to 20 of 9 sentences]
4
[+] score: 21
24-Hour Acute ZT06 Expression 24-Hour Chronic ZT06 Expression 2-Week chronic ZT06 Expression rno-miR-142-5p Over rno-miR-126a-5p Under rno-miR-146a-5p Under rno-miR-150-5p Over rno-miR-30b-5p Under rno-miR-24-3p Under rno-miR-335 Under rno-let-7b-5p Over rno-miR-130a-3p Over rno-miR-15b-5p Over rno-miR-99a-5p Over rno-miR-127-3p Under rno-miR-133a-3p Under rno-miR-10a-5p Over rno-miR-672-5p Over rno-miR-l-3p Under rno-let-7c-5p Over rno-miR-193-3p Over rno-miR-142-5p Under rno-miR-146b-5p Under rno-miR-150-5p Over Of the three ZT06 groups that illustrated differential expression of miRNAs due to CD, emphasis was placed on the two-week chronic ZT06 group due to the differential expression of miRs 146a and 146b, and miR-127 (Figures 5A-5B and 6A). [score:11]
24-Hour Acute ZT06 Expression 24-Hour Chronic ZT06 Expression 2-Week chronic ZT06 Expression rno-miR-142-5p Over rno-miR-126a-5p Under rno-miR-146a-5p Under rno-miR-150-5p Over rno-miR-30b-5p Under rno-miR-24-3p Under rno-miR-335 Under rno-let-7b-5p Over rno-miR-130a-3p Over rno-miR-15b-5p Over rno-miR-99a-5p Over rno-miR-127-3p Under rno-miR-133a-3p Under rno-miR-10a-5p Over rno-miR-672-5p Over rno-miR-l-3p Under rno-let-7c-5p Over rno-miR-193-3p Over rno-miR-142-5p Under rno-miR-146b-5p Under rno-miR-150-5p Over Differentially expressed miRNAs based on Illumina sequencing in all the circadian-disrupted samples and their links to breast cancer development and circadian rhythms. [score:10]
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5
[+] score: 11
miR-193a was used as an endogenous control to normalize the expression levels of targets. [score:5]
The miR-193a served as a good choice for endogenous control because its expression was almost uniform in all the samples on the miRNA-chips (0.99 ± 0.026) and it was not differentially regulated among the tested samples. [score:4]
Consistency in expression of miR-193a across all the samples was evident in qPCR assays (mean CT-value 29.51 ± 0.19). [score:2]
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6
[+] score: 10
Almost all the up-regulated miRNAs (22 our of 25 miRNAs) such as miR-122, miR-192, miR-685, miR-193, and miR-29c were also up-regulated in our rat mo del, suggesting that common plasma miRNAs seem to be up-regulated in APAP -induced liver injury independent of species. [score:10]
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7
[+] score: 7
For example, miR-193a has been identified as a potent regulator of focal segmental glomerulosclerosis (FSGS), a disease impacting the glomeruli [3]. [score:4]
In FSGS, podocyte function is severely disrupted by miR-193a inhibition of Wilms tumor 1/WT1, an important transcription factor in podocyte homeostasis. [score:3]
[1 to 20 of 2 sentences]
8
[+] 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-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, mmu-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-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
For instance, among the 66 uniformly expressed miRNAs for which IPA assigned functions, we identified 12 candidates that have been implicated in androgen regulation, including: let-7a-5p, miR-15a-5p, miR-17-5p, miR-19b-3p, miR-23a-3p, miR-24-3p, miR-27b-3p, miR-30a-5p, miR-34a-5p, miR-140-5p, miR-193a-3p, miR-205-5p (S1 Fig). [score:4]
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9
[+] score: 4
Based on qRT-PCR analysis, the expression of miR-451, miR-148a, miR-21, miR-205 and miR-193a were not different between the sexes and therefore contrasted the microarray results. [score:3]
However, miR-451, miR-148a and miR-193 have recently been detected in liver by a high-throughput sequencing approach (Sarah Leigh-Brown, personal communication). [score:1]
[1 to 20 of 2 sentences]
10
[+] score: 4
Other miRNAs from this paper: rno-mir-21, rno-mir-96, rno-mir-152, rno-mir-210, rno-mir-193b
Previous studies showed that expression of four miRNAs, including miR-96, miR-193-3p, miR-210, and miR-21, were correlated with the skin flap mo del in rat [9]. [score:3]
In Figure 1G, the results of laser Doppler velocimetry showed that relatively low blood flow in Part C. Positive correlation between ischemia-reperfusion injury in the skin flap of rat and four miRNAs (miR-21, miR-96, miR-193, and miR-210) has been demonstrated in previous studies [9]. [score:1]
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11
[+] score: 3
Interestingly, in the “early” and “late” response phases, Ets1 and Nfat5, are targeted by only a single miRNA, i. e., miR-193 and miR-494, respectively. [score:3]
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12
[+] score: 3
Other miRNAs from this paper: rno-mir-193b
Cismasiu VB et al. [4] found that miR-193 was highly expressed in telocytes rather than other stromal cells and suggested that telocytes could be specialized and characterized by the expression of miR-193, if the morphologies could be clarified. [score:3]
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13
[+] score: 3
The mir-193a was chosen as an endogenous control because of its uniform expression in PKD/Mhm [34]. [score:3]
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14
[+] score: 3
Q-RT-PCR ΔCt values (y-axis) line plot per animal for duration of Day 1, 7, and 14 treatment samples tested highlights the elevation of both liver enriched miRNAs (miR-122 and miR-885) and ubiquitously expressed miR-193 in the 2 dogs with elevated ALT and AST. [score:3]
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15
[+] score: 2
Several miRNAs including miR-140, miR-199a, mir-193 and mir-29a/29b control the anabolic and catabolic regulation in cartilage [42]. [score:2]
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16
[+] score: 1
miRNAs miR-298* and 532-3p in comparison P8 vs P14.4 and miR-193-3p in comparison P14.4 vs P21.4 are out of plots. [score:1]
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17
[+] score: 1
Meanwhile, the biological functions of five differentially expressed miRNAs, including miR-193-5p, miR-872-3p, miR-3559-3p, miR-3473, and let-7d-3p, in C. sinensis infection need to be further investigated. [score:1]
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18
[+] score: 1
Two miRNAs (miR-181a and miR-193a) were undetectable in the control dentate gyrus because their Ct values were greater than 40, and were therefore excluded from the analyses. [score:1]
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19
[+] score: 1
5 mmu-miR-214 -1.7 -6.1 -10.9 mmu-miR-137 -31.7 -6.8 -144.8 mmu-miR-29c -1.8 -10.5 -10.7 rno-miR-532–5p -2.0 -59.1 -126.9 mmu-miR-466d-3p -2.7 -4.2 -9.9 mmu-miR-466d-5p -23.2 -64.7 -105.7 mmu-miR-22 -1.6 -4.6 -9.9 mmu-miR-582–5p -21.3 -59.4 -97.1 mmu-miR-690 -1.9 -2.1 -9.7 rno-miR-421 -21.3 -59.3 -97.0 mmu-miR-193 -4.9 -3. 5 -8.1 mmu-miR-369–5p -20.9 -58.3 -95.3 mmu-miR-27b* -2.1 -2.9 -8.0 mmu-miR-684 -20.8 -58.1 -94.9 mmu-miR-378 -1.6 -4.6 -7.7 mmu-miR-375 -20.6 -57.6 -94.2 mmu-miR-9* -1.9 -18.4 -7.7 mmu-miR-337–5p -20.5 -57.4 -93.8 mmu-miR-204 -2.5 -5.3 -7.5 mmu-miR-15a* -20.3 -56.8 -92.8 mmu-miR-28* -1.9 -3.2 -6.5 mmu-miR-532–5p -19. [score:1]
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