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23 publications mentioning rno-mir-193b

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

1
[+] score: 175
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]
According to Wu et al, deregulation of miR-193b affected cell growth in colon cancer via the TGF-β and SMAD3 signaling pathways [19]. [score:2]
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-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: 54
The downregulation of mR-193 is quantitatively comparable with the upregulation achieved in panel A. (D) HepG2 cells were transfected with GAPMER control or GAP1 alone or in association with anti-miR-193b, and cell viability assessed by CellTiter-Blue at 48 hours. [score:7]
Among these nine miRNAs, miR-615, miR-193b and miR-346 were upregulated after inhibition of uc. [score:6]
We have previously shown that miR-193b mediates apoptosis through targeting of mcl-1, 12 and the overexpression of uc. [score:5]
158− in Huh-7 cells induced downregulation of miR-193b (figure 7C). [score:4]
Indeed, miR-193b was shown to be downregulated in human HCC. [score:4]
158− in HCC nicely fits with these data as well as with the previous work that found downregulation of miR-193b in a subgroup of HCCs. [score:4]
miR-193b was found to be overexpressed in Huh-7 versus HepG2 cells (in line with uc. [score:3]
158− changed miR-193b expression in human malignant hepatocytes. [score:3]
158− in HepG2 cells, with miR-193b showing the most significant increase and having higher values of expression (figure 7A). [score:3]
158− inhibitor and anti-miR-193b rescued the effect of uc. [score:3]
In three independent experiments, miR-193b expression was higher in Huh-7 in comparison with HepG2. [score:3]
Bars represent logarithmic expression of miR-193b in Huh-7 versus HepG2. [score:3]
We then looked at the level of miR-193b in the sera of patients with HCC (n:10) who were naive for any treatment. [score:1]
Patients with low circulating miR-193b had mainly alpha-fetoprotein (AFP) negative tumours, in line with previous reports of observed lower levels of AFP in CTNNB1-mutated HCC 41 (figure 7E). [score:1]
Co-transfection of GAP1 and anti-miR-193b could rescue the biological effect of uc. [score:1]
miR-193b was predicted to have binding sites within the uc. [score:1]
χ [2] test was used to assess the correlation between miR-193b and alpha-fetoprotein (AFP) groups. [score:1]
158− and miR-193b was assessed by real-time PCR. [score:1]
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3
[+] score: 27
miRNA-193b-3p was found to be downregulated in the renal cortices from Cd -treated animals, and downregulation of this miRNA has been shown to promote autophagy and cell survival in mouse motor neuron-like cells [61]. [score:7]
The microarray results demonstrated significantly decreased expression of 54 miRNAs in the renal cortices from the Cd -treated group versus the saline control group, and miR-193b-3p, miR-455-3p, and miR-342-3p demonstrated a more abundant expression level and a two-fold or greater decreased expression in the Cd-treatment group versus the saline control group. [score:7]
Li C. Chen Y. Chen X. Wei Q. Cao B. Shang H. Downregulation of microRNA-193b-3p promotes autophagy and cell survival by targeting TSC1/mTOR signaling in NSC-34 cellsFront. [score:6]
miR-193b-3p, miR-455-3p, and miR-342-3p demonstrated more abundant expression and a two-fold or greater significant decreased expression with Cd treatment. [score:5]
Shin C. H. Lee H. Kim H. R. Choi K. H. Joung J. G. Kim H. H. Regulation of PLK1 through competition between hnRNPK, miR-149–3p and miR-193b-5pCell Death Differ. [score:2]
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4
[+] score: 24
In summary, the data analysis supports the view that the down-regulation of four miRs (miR-133b, miR-143, miR-335-5p, miR-1) appears to orchestrate the development of chronic neuropathic pain in Sural-SNI while the up-regulation of seven miRs (miR-133b, miR-145, miR-193b, miR-143, miR-335-5p, miR-191, miR-1) appear to orchestrate the recovery from post-nerve injury induced pain in Tibial-SNI. [score:8]
On the other hand, the translation of these ion channels would be predicted to decrease in the Tibial-SNI primary sensory neurons due to the increase in expression of all seven identified miRs (miR-133b, miR-145, miR-193b, miR-143, miR-335-5p, miR-191, miR-1). [score:5]
By using the rationale from our dual SNI variants we interpret that the decrease in expression of four miRs (miR-133b-3p, miR-145, miR-143, and miR-1) contributes to pain while the increase in expression of two miRs (miR-193b-3p and miR-191-5p) limits the level of pain that develops following a sciatic nerve crush. [score:5]
In both the microarrays (Figure 3A) and qPCR (Figures 3B,C) seven miRs (miR-133b, miR-145, miR-193b, miR-143, miR-335-5p, miR-191, miR-1) had a significantly higher level of expression in Tibial-SNI than in Sural-SNI. [score:3]
Ct values were <30.60 for miR-133b, <27.78 for miR-145, <27.66 for miR-193b, <30.19 for miR-143, <33.69 for miR-335, <23.42 for miR-191, <37.89 for miR-130a, <36.00 for miR-325, <32.04 for miR-1. Reference miRs were: MammU6-4395470 (Ct values < 19.30), snoRNA135-4380912 (Ct values < 33.98), and U87-4386735 (Ct values < 28.32). [score:1]
In rats miR-1 differs in one nucleotide, and miR-193b is 3 nucleotides shorter (Supplement 2). [score:1]
The two exceptions, miR-1 and miR-193b are identical between mice and humans. [score:1]
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5
[+] 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]
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6
[+] 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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7
[+] score: 12
Some miRNAs have been shown to be important in diseases; for example, circulating miRNA-21 is a potential biomarker for IS in humans (Tsai et al., 2013), and miRNA-193b regulates amyloid precursor protein in Alzheimer's disease (Liu et al., 2014). [score:6]
For example, CSF exosomal miR-193b was proposed as a biomarker for Alzheimer's disease (Liu et al., 2014), CSF exosomal miR-15b and miR-21 as markers for gliomas (Baraniskin et al., 2012) and some miRNAs in CSF as biomarkers of stroke (Sørensen et al., 2014). [score:3]
Microrna-193b is a regulator of amyloid precursor protein in the blood and cerebrospinal fluid derived exosomal microrna-193b is a biomarker of alzheimer's disease. [score:3]
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8
[+] 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]
[1 to 20 of 1 sentences]
9
[+] score: 9
Serum was also analyzed by Q-RT-PCR for a panel of 20 tissue enriched and potential miRNA biomarkers, including those identified for liver (cfa-miR-122 and -885), heart/muscle (cfa-miR-1, -133, and -206), testis (miR-34b/c), pancreas (cfa-miR-216), brain (cfa-miR-212), and ubiquitously expressed cfa-miR-193b. [score:3]
Elevation of serum cfa-miR-193b in the two dogs with liver injury (Dogs 1 and 3) was likely due to the ubiquitous expression of the miRNA in the dog, including the liver. [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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10
[+] score: 8
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]
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]
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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11
[+] score: 5
CFTR suppresses tumor progression through miR-193b targeting urokinase plasminogen activator (uPA) in prostate cancer. [score:5]
[1 to 20 of 1 sentences]
12
[+] score: 5
Other miRNAs from this paper: hsa-let-7a-2, hsa-let-7c, hsa-let-7e, hsa-mir-15a, hsa-mir-16-1, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-2, hsa-mir-100, hsa-mir-29b-2, mmu-let-7i, mmu-mir-99b, mmu-mir-125a, mmu-mir-130a, mmu-mir-142a, mmu-mir-144, mmu-mir-155, mmu-mir-183, hsa-mir-196a-1, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, hsa-mir-148a, mmu-mir-143, hsa-mir-181c, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-181a-1, hsa-mir-200b, mmu-mir-298, mmu-mir-34b, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-130a, hsa-mir-142, hsa-mir-143, hsa-mir-144, hsa-mir-125a, mmu-mir-148a, mmu-mir-196a-1, mmu-let-7a-2, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-mir-15a, mmu-mir-16-1, mmu-mir-21a, mmu-mir-22, mmu-mir-23a, mmu-mir-24-2, rno-mir-148b, mmu-mir-148b, hsa-mir-200c, hsa-mir-155, mmu-mir-100, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-181c, hsa-mir-34b, hsa-mir-99b, hsa-mir-374a, hsa-mir-148b, rno-let-7a-2, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7i, rno-mir-21, rno-mir-22, rno-mir-23a, rno-mir-24-2, rno-mir-29b-2, rno-mir-34b, rno-mir-99b, rno-mir-100, rno-mir-124-1, rno-mir-124-2, rno-mir-125a, rno-mir-130a, rno-mir-142, rno-mir-143, rno-mir-144, rno-mir-181c, rno-mir-183, rno-mir-199a, rno-mir-200c, rno-mir-200b, rno-mir-181a-1, rno-mir-298, hsa-mir-193b, hsa-mir-497, hsa-mir-568, hsa-mir-572, hsa-mir-596, hsa-mir-612, rno-mir-664-1, rno-mir-664-2, rno-mir-497, mmu-mir-374b, mmu-mir-497a, mmu-mir-193b, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-568, hsa-mir-298, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, hsa-mir-664a, mmu-mir-664, rno-mir-568, hsa-mir-664b, mmu-mir-21b, mmu-mir-21c, rno-mir-155, mmu-mir-142b, mmu-mir-497b, rno-mir-148a, rno-mir-15a
Among them are two polycistronic transcripts (miR-15a~16-1 and miR-193b~365-1), and two expressing single miRNAs (miR-148a and miR-155). [score:3]
Cluster Mapped ESTs Mapped cDNAs mir-497~195 Human: CR737132, DB266639, DA2895925, BI752321, AA631714 Human: AK098506.1 Rat: CV105515 mir-144-451 Human: R28106 Mouse: AK158085.1 Rat: AW919398, BF2869095, AI008234 mir-99b~let-7e~mir-125a Human: DB340912 Human: AK125996 mir-143~145 Human: BM702257 mir-181a-1~181b-1 Human: DA528985, BX355821 Mouse: BE332980, CA874578 mir-29b-2~29c Human: BF089238 Mouse: AK081202, BC058715 mir-298~296 Human: W37080 mir-183~96~182 Human: CV424506 mir-181c~181d Human: AI801869, CB961518, CB991710, BU729805, CB996698, BM702754 Mouse: CJ191375 mir-100~let-7a-2 Human: DA545600, DA579531, DA474693, DA558986, DA600978 Human: AK091713 Mouse: BB657503, BM936455 Rat: BF412891, BF412890, BF412889, BF412895 Mouse: AK084170 mir-374b~421 Human: DA706043, DA721080 Human: AK125301 Rat: BF559199, BI274699 Mouse: BC027389, AK035525, BC076616, AK085125 mir-34b~34c Human: BC021736 mir-15a-16-1 Human: BG612167, BU932403, BG613187, BG500819 Human: BC022349, BC022282, BC070292, BC026275, BC055417, AF264787 Mouse: AI789372, BY718835 Mouse: AK134888, AF380423, AF380425, AK080165 mir-193b~365-1 Human: BX108536 hsa-mir-200c~141 Human: AI969882, AI695443, AA863395, BM855863.1, AA863389 mir-374a~545 Human: DA685273, AL698517, DA246751, DA755860, CF994086, DA932670, DA182706 Human: AK057701 Figure 2 Predicted pri-miRNAs, their lengths, and features that support the pri-miRNA prediction. [score:1]
Cluster Mapped ESTs Mapped cDNAs mir-497~195 Human: CR737132, DB266639, DA2895925, BI752321, AA631714 Human: AK098506.1 Rat: CV105515 mir-144-451 Human: R28106 Mouse: AK158085.1 Rat: AW919398, BF2869095, AI008234 mir-99b~let-7e~mir-125a Human: DB340912 Human: AK125996 mir-143~145 Human: BM702257 mir-181a-1~181b-1 Human: DA528985, BX355821 Mouse: BE332980, CA874578 mir-29b-2~29c Human: BF089238 Mouse: AK081202, BC058715 mir-298~296 Human: W37080 mir-183~96~182 Human: CV424506 mir-181c~181d Human: AI801869, CB961518, CB991710, BU729805, CB996698, BM702754 Mouse: CJ191375 mir-100~let-7a-2 Human: DA545600, DA579531, DA474693, DA558986, DA600978 Human: AK091713 Mouse: BB657503, BM936455 Rat: BF412891, BF412890, BF412889, BF412895 Mouse: AK084170 mir-374b~421 Human: DA706043, DA721080 Human: AK125301 Rat: BF559199, BI274699 Mouse: BC027389, AK035525, BC076616, AK085125 mir-34b~34c Human: BC021736 mir-15a-16-1 Human: BG612167, BU932403, BG613187, BG500819 Human: BC022349, BC022282, BC070292, BC026275, BC055417, AF264787 Mouse: AI789372, BY718835 Mouse: AK134888, AF380423, AF380425, AK080165 mir-193b~365-1 Human: BX108536 hsa-mir-200c~141 Human: AI969882, AI695443, AA863395, BM855863.1, AA863389 mir-374a~545 Human: DA685273, AL698517, DA246751, DA755860, CF994086, DA932670, DA182706 Human: AK057701 Figure 2 Predicted pri-miRNAs, their lengths, and features that support the pri-miRNA prediction. [score:1]
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[+] score: 4
Other miRNAs from this paper: rno-mir-21, rno-mir-96, rno-mir-152, rno-mir-193a, rno-mir-210
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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[+] 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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[+] score: 3
Other miRNAs from this paper: rno-mir-193a
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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[+] score: 3
Other miRNAs from this paper: hsa-mir-193b, hsa-mir-596, mmu-mir-193b
158- was activated by the Wnt/β-catenin pathway in liver cancer and drove cellular growth and migration, possibly by modulating miR-193b expression [18]. [score:3]
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[+] score: 3
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-18a, hsa-mir-21, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-30a, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-30a, mmu-mir-99a, mmu-mir-126a, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-138-2, hsa-mir-192, mmu-mir-204, mmu-mir-122, hsa-mir-204, hsa-mir-1-2, hsa-mir-23b, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-138-1, mmu-mir-192, mmu-let-7a-1, mmu-let-7a-2, mmu-mir-18a, mmu-mir-21a, mmu-mir-23a, mmu-mir-26a-1, mmu-mir-103-1, mmu-mir-103-2, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-26a-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, hsa-mir-26a-2, hsa-mir-376c, hsa-mir-381, mmu-mir-381, mmu-mir-133a-2, rno-let-7a-1, rno-let-7a-2, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-18a, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-26a, rno-mir-30a, rno-mir-99a, rno-mir-103-2, rno-mir-103-1, rno-mir-122, rno-mir-126a, rno-mir-133a, rno-mir-138-2, rno-mir-138-1, rno-mir-192, rno-mir-204, mmu-mir-411, hsa-mir-451a, mmu-mir-451a, rno-mir-451, hsa-mir-193b, rno-mir-1, mmu-mir-376c, rno-mir-376c, rno-mir-381, hsa-mir-574, hsa-mir-652, hsa-mir-411, bta-mir-26a-2, bta-mir-103-1, bta-mir-16b, bta-mir-18a, bta-mir-21, bta-mir-99a, bta-mir-126, mmu-mir-652, bta-mir-138-2, bta-mir-192, bta-mir-23a, bta-mir-30a, bta-let-7a-1, bta-mir-122, bta-mir-23b, bta-let-7a-2, bta-let-7a-3, bta-mir-103-2, bta-mir-204, mmu-mir-193b, mmu-mir-574, rno-mir-411, rno-mir-652, mmu-mir-1b, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-1-2, bta-mir-1-1, bta-mir-133a-2, bta-mir-133a-1, bta-mir-138-1, bta-mir-193b, bta-mir-26a-1, bta-mir-381, bta-mir-411a, bta-mir-451, bta-mir-9-1, bta-mir-9-2, bta-mir-376c, bta-mir-1388, rno-mir-9b-3, rno-mir-9b-1, rno-mir-126b, rno-mir-9b-2, hsa-mir-451b, bta-mir-574, bta-mir-652, mmu-mir-21b, mmu-mir-21c, mmu-mir-451b, bta-mir-411b, bta-mir-411c, mmu-mir-126b, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
Several miRNAs were found to be highly expressed in particular tissues: miR-204, -218, and -129-2-3p in brain tissues, miR-30a, -30e, -30d, -200a and -200b in kidney, miR-192 in liver, miR-451 in spleen, miR-21 in spleen and thymus, miR-193b, -378 in LDM muscle. [score:3]
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[+] 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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[+] score: 2
In comparison with lung recipients without BOS, clear dysregulation of miR-34a, miR-193b, miR-9 and miR-15a, likewise present in the VTM list in Fig 5, was also detected in peripheral mononuclear cells obtained from BOS patients in a RT-PCR evaluation of miRNA expression by Xu at al. [3]. [score:2]
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[+] 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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[+] 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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[+] 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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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]
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