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22 publications mentioning rno-mir-99a

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-99a. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 38
Female-biased expression of miR-29b and miR-152 occurred from 15 to 78 weeks of age while male-biased expression of miR-125b-5p and miR-99a occurred during this same age span. [score:5]
miR-125b-5p and miR-99a showed the most consistent male-biased expression with sex differences observed at 15, 21, 52, and 78 weeks of age and fold changes ranging from 1.5 to 2.3. miR-99a* exhibited similar significant male-biased expression of 1.7- to 2.3-fold at 15, 52, and 78 weeks of age. [score:5]
Despite only seven sexually dimorphic miRNAs being in common between the adult and the old rats (miR-125b-5p, miR-152, miR-29b, miR-374, miR-96, miR-99a*, and miR-99a), 91% (74/81) of the mRNA targets in the old rats were also mRNA targets in the adult rats. [score:5]
miR-99a appears to be a tumor suppressor in the liver [84] that possibly acts through inhibition of the RNA -induced silencing complex, Ago2 [85]. [score:5]
Using the same analysis described above, the expression of 2 miRNAs was found to associate with the presence and absence of liver bile duct hyperplasia, miR-99a and miR-203 (Table  4). [score:3]
miRNAs showing the most male-biased expression included miR-125b-5p, miR-99a*, miR-99a, miR-96, miR-221, and miR-183 (Fig.   3). [score:3]
Increased expression of both miR-99a and miR-203 was associated with the presence of hepatic bile duct hyperplasia, a common aging lesion [83]. [score:3]
The expression of specific miRNAs (miR-451, miR-18a, miR-99a, and miR-203) was found to associate with sexually dimorphic histopathology findings of basophilic foci and bile duct hyperplasia. [score:3]
The expression of miRNAs (miR-18a, miR-99a, and miR-203, miR-451) was also found to associate with specific sexually dimorphic hepatic histopathology. [score:3]
miR-125b-5p and miR-99a are suggested to be co-expressed in humans from chromosome 21 and play a role in vincristine resistance of leukemia cells [62]. [score:3]
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2
[+] score: 27
In acute cell culture mo dels, overexpressing members of the miR-99/100 family inhibits gene expression and protein translation of mTORC1 signaling proteins, downregulating the activity of the pathway and ultimately cellular proliferation (Jin et al., 2013; Wei et al., 2013; Jia et al., 2014). [score:12]
In human muscle, diminished miR-99 and miR-100 expression predict the anabolic response to a resistance exercise bout, with reduced expression of these miR upregulating mTORC1 signaling (Zacharewicz et al., 2014). [score:8]
miR that regulate targets in the mTORC1 pathway (hsa-miR-16-5p, hsa-miR-26b-5p, hsa-miR-99a-5p, hsa-miR-100-5p, hsa-miR-128a-3p, hsa-miR-133a-3p, hsa-miR-199a-3p, hsa-miR-221-3p) were analyzed using TaqMan® microRNA Assays (Applied Biosystems, Foster City, CA, USA). [score:3]
Findings from the present investigation indicate that alterations of mTORC1 signaling following sustained CR are not regulated by the expression of miR-99a or miR-100-5p. [score:2]
MicroRNA-99 family targets AKT/mTOR signaling pathway in dermal wound healing. [score:2]
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3
[+] score: 26
We found that up-regulated miRNAs (miR-346, miR-135b, miR-30ab, miR-344, miR-18a, miR-99a, miR-210, miR-207, miR-18a, and miR-129) in ARDS were inversely correlated with the expression of their predicted targets such as Gabrb1, Mdh1, Eif2ak1, Fbln5, and Tspan8. [score:8]
miR-99a and miR-30b were confirmed to be the up-regulated miRNAs in ARDS, while miR-126 and miR-26a were confirmed to be down-regulated miRNAs in ARDS (Figure  2). [score:7]
The down-regulated miRNAs included miR-24, miR-26a, miR-126, and Let-7a, b, c, f. The up-regulated miRNAs were composed of miR-344, miR-346, miR-99a, miR-127, miR-128b, miR-135b, and miR-30a/b. [score:7]
The up-regulated miRNAs included miR-99a, miR-127, miR-128b, miR-135b, miR-30a, and miR-30b. [score:4]
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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: 19
In the present study, although we did not observe altered expression of miR-99a or miR-144, we found that miR-99a-3p and miR-144-3p were significantly down-regulated in NAFLD rats and constructed a series of miRNAs- mRNAs regulatory pairs. [score:7]
Among these DEMs, miR-33, miR-33-5p, miR-33-3p, miR-144-3p and miR-99a-3p were down-regulated in NAFLD, whereas miR-200b, miR-200b-3p, miR-200b-5p, miR-200c-3p and miR-349 were up-regulated. [score:7]
We also observed that NAFLD-related genes Apln, Vcan, Cd36 and Cyp7a1 were targets of miR-99a-3p and miR-144-3p 26, 27, 31, 32. [score:3]
By integrated analysis, we observed 14 decreased miRNAs (such as miR-33, miR-33-5p, miR-33-3p, miR-144-3p, and miR-99a-3p) and constructed 459 miRNA and mRNA regulatory pairs in NAFLD rats. [score:2]
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6
[+] score: 16
When compared to T cells from peripheral blood, qRT-PCR analyses of purified TCRαβ [+] blood T cells from the same rats indicated a similar expression pattern, with upregulation of miR-21, miR-99a, miR-223, miR-326, and miR-345-5p (Figure 6D), indicating that the GvHD grade during sampling of T cells may be crucial in terms of miRNA expression. [score:7]
Moreover, we found that miR-99a, miR-326, and miR-345-5p, which were all indicated as downregulated by NanoString were detected as upregulated by qRT-PCR (Figure 6C). [score:7]
miR-99a, miR-345-5p, or miR-743b was not found associated with any of the other miRNAs or to genes related to T cell activation. [score:1]
As input for the analysis, we chose miR-21, miR-99a, miR-223, miR-326, miR-345-5p, and miR-743b, and also genes involved in GvHD pathogenesis as well as T cell activation, proliferation, and migration. [score:1]
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7
[+] score: 13
Interestingly, miR-9, miR-124a, miR-99a/b and miR-181b/c up-regulation during early cortical neurogenesis was negatively correlated with the expression level of their predicted targets, consistent with reports that have found a negative expression correlation between tissue-enriched miRNAs and their putative targets [17, 18]. [score:12]
These include miR-7, miR-9, miR-124a, miR-125a/b, miR-181b/c and miR-99a/b. [score:1]
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8
[+] score: 13
The summary of the miRNAs significantly differentially expressed are provided in Table 1. Our study revealed the significant downregulation of miR-99 family (Fig. 2A,B) that comprises of three miRNAs such as miR-99a, miR-99b and miR-100, which are present in 11, 1, 8 chromosomes respectively. [score:6]
This miR-99 family mainly targets Akt/mTOR/IGF1 axis that leads to increased apoptosis and decreased protein synthesis during cancer. [score:3]
Coppala et al.,[23] revealed that the miR-99a/let-7c cluster controls cardiomyogenesis process by altering the epigenetic factors. [score:1]
This is the first report to showcase the significant role of miR-99 family during cardiac hypertrophy. [score:1]
Recent evidence by Coppala et al.,[23] indicated that the miR-99a/let-7c cluster controls the cardiomyogeneic process by altering the epigenetic factors. [score:1]
We found that miR-99, miR-100, miR-208, miR-181, miR-19 and many others were associated to cardiac hypertrophy and apoptosis. [score:1]
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9
[+] score: 12
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-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-30a, hsa-mir-31, hsa-mir-96, hsa-mir-99a, hsa-mir-16-2, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-182, hsa-mir-183, hsa-mir-211, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-221, hsa-mir-222, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-132, hsa-mir-143, hsa-mir-145, hsa-mir-191, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-184, hsa-mir-190a, hsa-mir-195, rno-mir-322-1, rno-let-7d, rno-mir-335, rno-mir-342, rno-mir-135b, hsa-mir-30c-1, hsa-mir-299, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, hsa-mir-382, hsa-mir-342, hsa-mir-135b, hsa-mir-335, 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-15b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-26a, rno-mir-26b, 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-96, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-126a, rno-mir-132, rno-mir-143, rno-mir-145, rno-mir-183, rno-mir-184, rno-mir-190a-1, rno-mir-191a, rno-mir-195, rno-mir-211, rno-mir-217, rno-mir-218a-2, rno-mir-218a-1, rno-mir-221, rno-mir-222, rno-mir-299a, hsa-mir-384, hsa-mir-20b, hsa-mir-409, hsa-mir-412, hsa-mir-489, hsa-mir-494, rno-mir-489, rno-mir-412, rno-mir-543, rno-mir-542-1, rno-mir-379, rno-mir-494, rno-mir-382, rno-mir-409a, rno-mir-20b, hsa-mir-542, hsa-mir-770, hsa-mir-190b, hsa-mir-543, rno-mir-466c, rno-mir-17-2, rno-mir-182, rno-mir-190b, rno-mir-384, rno-mir-673, rno-mir-674, rno-mir-770, rno-mir-31b, rno-mir-191b, rno-mir-299b, rno-mir-218b, rno-mir-126b, rno-mir-409b, rno-let-7g, rno-mir-190a-2, rno-mir-322-2, rno-mir-542-2, rno-mir-542-3
Among the miRNAs examined, 79 miRNAs (24%) responded to the hyperandrogenic condition and interestingly, 80% of which were upregulated compared to the control group supporting the notion that hyperandrogenic condition down-regulates androgen receptors in the granulosa cells [35] which could be mediated by these upregulated miRNAs (rno-miR-379*, rno-let-7d, rno-miR-24, rno-miR-673, rno-miR-26b, rno-miR-335, rno-miR-382*, rno-miR-412, rno-miR-99a*, rno-miR-543, rno-miR-674-3p, rno-miR-409-3p). [score:9]
A list of differentially expressed miRNAs (Fold change ≥ 2 and their corresponding P value) is presented in Figure  4. Beside this group, miRNAs which were also highly abundant in DHT -treated ovaries are rno-miR-221, rno-miR-222, rno-miR-25, rno-miR-26b, rno-miR-379*, rno-let-7d, rno-miR-24, rno-miR-673, rno-miR-26b, rno-miR-335, rno-miR-382*, rno-miR-412, rno-miR-99a*, rno-miR-543, rno-miR-674-3p, rno-miR-409-3p. [score:3]
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10
[+] score: 10
Of the 46 increased miRNA, sICAM-1 was the predicted target of 6 (miR-23b, miR-27a, miR-99a, miR-100, miR-324-5p, miR-363); PAI-1 was the predicted target of 4 (miR-30a, miR-30d, miR-182, miR-384-5p), E selectin the predicted target of 2 (miR-16; miR-195) and the alpha chain of fibrinogen the predicted target of miR-29c [26]. [score:9]
Most had peak increases relative to controls at the 8-hour (n = 21) or 24-hour (n = 21) post-treatment time points, with one miRNA (miR-23a) having peak increase at the 1-hour time point, one miRNA (miR-363) having a peak increase at the 4-hour time point, and 2 miRNAs (miR-21, miR-99) with peak increases at the 48 hour time point. [score:1]
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11
[+] score: 9
Recent data have shown numerous miRNA dysregulations during MI, for example, MiR-210 and miR-1 were proven to improve cardiac function following MI by enhancing angiogenesis and inhibiting cardiomyocyte apoptosis [10, 11]; MiR-150 was shown to be downregulated in patients with acute myocardial infarction (AMI), atrial fibrillation, dilated cardiomyopathy and ischemic cardiomyopathy [12– 14]; and overexpression of microRNA-99a attenuates heart remo deling and improves cardiac performance following myocardial infarction [15]. [score:9]
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12
[+] 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-17, hsa-mir-18a, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-26a-1, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-106a, hsa-mir-107, mmu-let-7g, mmu-let-7i, mmu-mir-99a, mmu-mir-101a, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-126a, mmu-mir-127, mmu-mir-145a, mmu-mir-146a, mmu-mir-129-1, mmu-mir-206, hsa-mir-129-1, hsa-mir-148a, mmu-mir-122, mmu-mir-143, hsa-mir-139, hsa-mir-221, hsa-mir-222, hsa-mir-223, mmu-let-7d, mmu-mir-106a, hsa-let-7g, hsa-let-7i, hsa-mir-122, hsa-mir-125b-1, hsa-mir-143, hsa-mir-145, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-129-2, hsa-mir-146a, hsa-mir-206, mmu-mir-148a, 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-18a, mmu-mir-20a, mmu-mir-21a, mmu-mir-22, mmu-mir-26a-1, mmu-mir-129-2, mmu-mir-103-1, mmu-mir-103-2, rno-let-7d, rno-mir-335, rno-mir-129-2, rno-mir-20a, mmu-mir-107, mmu-mir-17, mmu-mir-139, mmu-mir-223, mmu-mir-26a-2, mmu-mir-221, mmu-mir-222, mmu-mir-125b-1, hsa-mir-26a-2, hsa-mir-335, mmu-mir-335, 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-17-1, rno-mir-18a, rno-mir-21, rno-mir-22, rno-mir-26a, rno-mir-101a, rno-mir-103-2, rno-mir-103-1, rno-mir-107, rno-mir-122, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-126a, rno-mir-127, rno-mir-129-1, rno-mir-139, rno-mir-143, rno-mir-145, rno-mir-146a, rno-mir-206, rno-mir-221, rno-mir-222, rno-mir-223, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, hsa-mir-20b, hsa-mir-451a, mmu-mir-451a, rno-mir-451, hsa-mir-486-1, hsa-mir-499a, mmu-mir-486a, mmu-mir-20b, rno-mir-20b, rno-mir-499, mmu-mir-499, mmu-mir-708, hsa-mir-708, rno-mir-17-2, rno-mir-708, hsa-mir-103b-1, hsa-mir-103b-2, mmu-mir-486b, rno-mir-126b, hsa-mir-451b, hsa-mir-499b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-130c, mmu-mir-21c, mmu-mir-451b, mmu-let-7k, hsa-mir-486-2, mmu-mir-129b, mmu-mir-126b, rno-let-7g, rno-mir-148a, rno-mir-196b-2, rno-mir-486
After 6 and 12 wks of E [2] exposure, 15 miRNAs were down-regulated, e. g., miR-22, miR-99a, miR-106a, miR-127, miR-499, and 19 miRNAs were-up-regulated, e. g., miR-17-5p, miR-20a, miR-21, miR-129-3p, miR-106a, miR-22, and miR-127. [score:7]
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13
[+] score: 7
miR-99, which regulates the expression of AKT [30] along with miR-155 [31], got downregulated in HSD, UNX and UNX+HSD (Fig 5E). [score:7]
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14
[+] score: 5
For example, it has been reported that Igf1r is a target of miR-1 [55], miR-139 [56], miR-378 [57], miR-99a [58], and miR-497 [59]. [score:3]
On the other hand, miR-99a [23] and miR-486 [24, 25] are involved in myocardial remo deling through the regulation of different types of signaling pathways. [score:2]
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15
[+] score: 4
In agreement with their results, we observed the downregulation of miR-127, miR-181a, miR-411, miR-99a, miR-34a, miR-30b, and miR-30c, which according to Liu [6] should lead to increased inflammation. [score:4]
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16
[+] score: 4
In mouse and human hematopoietic stem cells, the miR-99a/100∼125b miRNAs have been implicated in the regulation of stem and intermediate progenitor cell homeostasis by controlling the balance between TGFβ and Wnt signaling (Emmrich et al., 2014). [score:2]
miR-99a/100∼125b tricistrons regulate hematopoietic stem and progenitor cell homeostasis by shifting the balance between TGFbeta and Wnt signaling. [score:2]
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17
[+] score: 4
The extent of downregulation can be categorized into three groups: one retaining less than 5% of the basal miRNA level in naïve animal (miR-10a, -98); one maintaining 5~15% (miR-99, -124a, -183) and one showing more than 25% left (miR-29a, -134). [score:4]
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18
[+] score: 3
Validation confirmed that both BMFC and BMFC +  KOC supplementation modulated the expression of 11 miRNAs in the hippocampus: miR-99a-5p, -128-3p, -148a- 3p, -379-5p, -381-3p, -146a-5p, -30e-3p, -370-3p, -106b-3p, -770-3p and let-7f-5p (Fig.   4E). [score:3]
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19
[+] score: 2
MicroRNA-100 (miR-100), a member of miR-99 family (including miR-99a, miR-99b, miR-100), is a key apoptotic regulator in various cell types [24, 25]. [score:2]
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20
[+] score: 2
At 24 hours, five miRNAs (rno-miR-214, rno-miR-99a, rno-miR-363*, rno-miR-100 and rno-miR-340–5p) and at 48 hrs 6 miRNAs (rno-miR-34b, rno-miR-500, rno-miR-24-1*, rno-miR-29b, rno-miR-199a-3p, rno-let-7a) showed the most prominent dysregulation (P < 0.001) (Fig.   7B). [score:2]
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21
[+] score: 1
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-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, rno-mir-193b, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
A-to-G transitions potentially caused by A-to-I editing were mainly identified in miR-99a and miR-376c (Figure 2), which have been reported to undergo A-to-I editing in human and mouse, respectively [22, 23]. [score:1]
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[+] score: 1
The microRNAs filtered in intact comparison but not filtered in HFD comparison and no-T2D comparison, including miR-143-3p, miR-99a-5p, miR-138-5p, miR-1304-3p, and miR-33b-5p, might involve the progress of T2D fed with normal diets only. [score:1]
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