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45 publications mentioning hsa-mir-323a

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-323a. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 34
Quite unexpectedly, despite the reported increase in the circulating levels of this miRNA in ectopic pregnancy, our data evidenced that ectopic embryonic tissue actually expressed lower levels of mir-323-3p from week-7 onwards, so that the raise in mir-323-3p expression observed in normal gestation is not detected in ectopic pregnancies. [score:5]
Similarly, despite very recent findings on circulating mir-323-3p as putative biomarker of ectopic pregnancy [29], to our knowledge, no information has been so far reported on changes of expression in ectopic placental tissue of miRNAs in general, and of the elements of the LIN28/Let-7 system in particular. [score:3]
Targets analyzed were: LIN28B (A), Let-7a (B), mir-132 (C), mir-145 (D) and mir-323-3p (E). [score:3]
Expression profiles of mir-132, mir-145 and mir-323-3p in embryonic tissue from early ectopic pregnancies. [score:3]
Our comparative analyses revealed that, in contrast to Let-7a, mir-132 and mir-145, the embryonic expression of mir-323-3p increased during early pregnancy, with minimal levels being detected in ≤6-week embryonic tissue that raised thereafter. [score:3]
Interestingly, mir-323-3p levels were similar in normal and ectopic gestation at ≤6-weeks; yet, the rise of expression detected at later stages of normal early gestation was not observed in ectopic pregnancies, so that mir-323-3p levels in 7–9 week ectopic embryonic tissue were significantly lower than in the control group (Figure 3C ). [score:3]
In contrast, mir-323-3p expression levels raised in normal human embryonic tissue between ≤6-week and later stages of early gestation; a difference that was statistically significant due to the grouped analysis of the samples (≤6-week vs. [score:3]
On the other hand, an inverse trend was detected for mir-323-3p, whose expression levels were minimal in ≤6-week embryonic tissue, and increased thereafter, with maximal mean levels at week-9. Yet, due to some variability within groups, these differences did not reach statistical significance when compared on a weekly basis (Figure 1E ). [score:2]
For miRNA analyses, expression levels of Let-7a, mir-145, mir-132 and mir-323-3p were assayed, following a previously published procedure [19]. [score:2]
For comparative purposes, the embryonic expression levels of the recently proposed circulating biomarker of ectopic pregnancy, mir-323-3p [29], were also assayed in normal and ectopic gestations. [score:2]
In fact, the possibility that the source of circulating mir-323-3p in ectopic pregnancy might not be solely the embryonic tissue has been already suggested [29], [32]; our findings support the non-embryonic origin of this miRNA and call for independent confirmation of the usefulness of plasma levels of mir-323-3p as universal marker of ectopic gestation. [score:1]
29Zhao Z, Zhao Q, Warrick J, Lockwood CM, Woodworth A, et al. (2012) Circulating microRNA miR-323–3p as a biomarker of ectopic pregnancy. [score:1]
Thus, although mir-323-3p has been proposed as pregnancy-specific miRNA (32), our results cast doubt on the placental origin of the excess of this factor in ectopic gestation. [score:1]
On the latter, however, little attention have been paid so far to ectopic pregnancy, and to our knowledge only one study have been reported on the potential usefulness of circulating mir-323-3p as biomarker of ectopic pregnancy [29]. [score:1]
As mentioned above, mir-323-3p is the only putative biomarker of ectopic pregnancy reported to date [29]. [score:1]
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2
[+] score: 28
Other miRNAs from this paper: hsa-mir-21, hsa-mir-518b, hsa-mir-517a, hsa-mir-323b
miR-21, which is known to be wi dely expressed in various tissues/cells, was expressed at similar levels in CP-MSCs, CV-MSCs, and DB-MSCs (Fig. 3a), while expression of miR-323-3p, a representative C14MC miRNA, was significantly higher in CP-MSCs and CV-MSCs than in DB-MSCs (p < 0.001 vs. [score:7]
Furthermore, expression levels of miR-518b and miR-323-3p were effectively facilitated and suppressed by transfection with miRNA mimic and miRNA inhibitor, respectively (Fig. 7b). [score:7]
The relative expression levels of miR-323-3p varied between primarily expanded MSCs and their original tissues (Fig. 4a), while expression levels of C19MC miRNAs (miR-518b and -517a) were significantly higher in CP and CV tissues than in twice-passaged CP-MSCs and CV-MSCs (p < 0.001 vs. [score:5]
Similarly, MSCs primarily expanded from umbilical cord blood (UCB-MSCs) and Wharton’s jelly tissue (WJ-MSCs) both expressed miR-323-3p (Fig. 3b) but not miR-518b and miR-517a (Fig. 3c,d). [score:3]
However, first-trimester CV-MSCs showed relatively higher expression of miR-323-3p compared with third-trimester CV-MSCs, though the difference was not significant (Fig. 6c), while miR-518b and -517a levels were similar in cells from both trimesters (Fig. 6c). [score:2]
The expression of miR-323-3p in CP-MSCs and CV-MSCs was significantly higher in later (p8) compared with earlier passage (p2) cells (p < 0.001 vs. [score:2]
Fold changes in expression levels of miR-518b (b) and miR-323-3p (c) compared with scramble control in CP-MSCs and CV-MSCs. [score:2]
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3
[+] score: 25
Thus miR-98, miR-323-3p, miR-330-3p, miR-376a, miR-494, miR-598 were down-regulated by UVA and UVB, while miR-191, miR-376c and miR-501-5p were up-regulated by both. [score:7]
Among the 6 down-regulated miRNAs after UVA- and UVB-irradiation (miR-98, miR-323-3p, miR-330-3p, miR-376a, miR-494, miR-598) 3 miRNAs (miR-98, miR-330-3p and miR-376a) shared the common regulator element Hox-2.3-undefined-site-2 (gggggtgggggggag) in their promoter regions. [score:5]
Interestingly, of these ten commonly regulated microRNAs miR-98, miR-191, miR-323-3p, miR-330-3p, miR-494, and miR-598 were reported to be also deregulated after ionizing radiation [29], [30], [31] and miR-376a was shown to be a regulator of apoptosis in response to arsenic trioxide treatment [32]. [score:4]
The down-regulated miRNA-set consists of miR-98, miR-323-3p, miR-330-3p, miR-376a, miR-494 and miR-598. [score:4]
Down-regulation was most pronounced in miR-494 (–9.8, UVA; –2.0, UVB) and miR-323-3p (–3.4, UVA; –7.7, UVB) (see Table 1, 2 and Fig. 2). [score:4]
miR-23a (–25.0) and miR-323-3p (–7.7) showed the strongest reductions (Table 2). [score:1]
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4
[+] score: 19
This pattern included the two created target sites for ssc-miR-34a and ssc-miR-34c, both predicted by TargetScan and PACMIT in SLA-1 (Figure 3 A); the disrupted target site for ssc-miR-148a in HSPA1A predicted by PACMIT and TargetSpy (Figure 3 B); the ssc-miR-133b (TargetScan and PACMIT), ssc-miR-133a-3p (TargetScan) and ssc-miR-323 (TargetSpy) created target sites in RNF5 (Figure 3 C); and the disrupted site for ssc-miR-2320 predicted by TargetSpy in SLA-1 (Figure 3D). [score:19]
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5
[+] score: 19
Insulin appeared in Network 2 as indirectly controlling the expression of miR-206, 324-5p, 432, and 95. miR-323-3p and 495, both belonging to cluster 14q32, were chosen for validation by RT-qPCR. [score:4]
Our miRNA profile (84) Chromosomal localization Fold change Reference DOWNREGULATED hsa-miR-206 6p12.2 −7.53(29) hsa-miR-219-2-3p 9q33.3 −6.64(52) hsa-miR-383 8p22 −6.56(12, 55, 56) hsa-miR-138 16q13.3/3p21.32 −5.16(12, 14) hsa-miR-323-3p 14q32.2 −4.96(12, 52) hsa-miR-122 18q21.31 −4.82 hsa-miR-105 Xq28 −4.66 hsa-miR-129-5p 11p11.2/7q32.1 −4.56(23) hsa-miR-935 19q13.43 −4.53(52) hsa-miR-329 14q32.2 −4.48 hsa-miR-129-3p 11p11.2/7q32.1 −4.43 hsa-miR-650 22q11.21 −4.19 hsa-miR-184 15q24.3 −4.14 hsa-miR-370 14q32.2 −3.99(12) hsa-miR-433 14q32.2 −3.96(29) hsa-miR-138-2* 16q13. [score:4]
Functional studies using mimic miR-129-5p (11p11.2/7q32.1), miR-206 (6p12.2), and miR-323-3p (14q32.2) and the DAOY cell line, suggested a suppressive role for miR-129-5p in MB proliferation. [score:3]
As expected, miR-206 (p = 0.0001; Mann–Whitney test), miR-129-5p (p = 0.002), miR-323-3p (p = 0.014), and miR-495 (p = 0,054), had lower expression in MB in comparison to normal cerebellum (Figure 3), thus confirming our microarray findings. [score:3]
No significant differences were found on cell viability or apoptosis after miR-206, miR-129-5p, and miR-323-3p transfections in comparison to control (Figure 4; Figure A3 in, respectively). [score:1]
Transfection of miRVana miRNA mimics (Invitrogen Ambion, Austin, TX, USA) of miR-206, miR-129-5p, miR-323-3p, or miRVana miRNA mimic negative control #1 (referred to as scrambled) was carried out 24 h after seeding, in a final concentration of 3 nM, using Lipofectamine RNAiMAX reagent (Invitrogen) according to the manufacturer’s recommendation. [score:1]
73(12) hsa-miR-377* 14q32.2 −2.72 hsa-miR-7 15q25.3/19p13.3/9q21.32 −2.72(12, 14) hsa-miR-124 20p23.1/8q12.3/8p23.1 −2.71(12, 14, 29, 48, 49) hsa-miR-323-5p 14q32.31 −2.69(12) hsa-miR-873 9p21.1 −2.65 hsa-miR-129* 11p11.2/7q32.1 −2.63 hsa-miR-338-5p 17q25.3 −2.61(14) hsa-miR-409-5p 14q32.2 −2.61 hsa-miR-874 5q31.2 −2.46 hsa-miR-495 14q32.2 −2.46(52) hsa-miR-885-5p 3p25.3 −2.45 hsa-miR-376c 14q32.2 −2.43(52) hsa-miR-299-5p 14q32.2 −2.41 hsa-miR-539 14q32. [score:1]
Briefly, mimic-miR-206, mimic-miR-129-5p, and mimic-miR-323-3p or mimic -negative control #1 transfected cells were harvested 20 h after transfection and seeded in triplicate in 96-well plate (1,500 cells/well) in serum-free RPMI-1640 (Cultilab). [score:1]
As shown in Figure 4, no consistent differences in proliferation were found in transfections with miR-206 and miR-323-3p. [score:1]
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6
[+] score: 17
By contrast, recent evidence points towards miR-323 as a positive regulator of Wnt/cadherin signaling to upregulate pro-inflammatory mechanisms and potentiate cell migration, proliferation and adhesion in the pathogenesis of rheumatoid arthritis [79], [80]. [score:5]
However, in line with potentially protective effects of miR-323 upregulation, mouse studies have also found that maternal stress may enhance anti-viral immunity, for example by promoting the protection against herpes simplex virus [85], [86]. [score:4]
Both miR-323 and miR-98 upregulation in brains of prenatally stressed offspring may indicate an altered pro-inflammatory state in the brain. [score:4]
Further changes in miRNA profiles included miR-323, which modulates host-pathogen interactions, such as those involved in HIV-1 [76] and H1N1 Influenza A [31]. [score:1]
miR-323 binds to the PB1 virus gene and may assist in the defense against viral replication [31] and thus have protective functions against stress -induced vulnerability to pathogens [77], [78]. [score:1]
The following miRNAs were analyzed (5′ to 3′): mirR-181 and miR-186 (dams); miR-103, miR-151, miR-323, miR-145, miR-425, miR-98 (newborns). [score:1]
Non-stress groups), as observed by microarray analyses, the following candidates were selected for verification by qRT-PCR analysis: miR-151, miR-145, miR-425 (all down) and miR-103, miR-323, miR-98 (up) (Figure 3C). [score:1]
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7
[+] score: 16
Interestingly, CBX7 seems to positively regulate miR-323: this can account for the reduced miR-323 expression in prostate cancer where CBX7 is drastically downregulated [38] and miR-323 has a tumor suppressor activity by targeting AdipoRI [39]. [score:11]
Equally, we observe that a potential oncosuppressor gene, such as miR-137, is regulated negatively, whereas another one, such as miR-323, is regulated positively. [score:5]
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8
[+] score: 16
With respect to specific functions that are attributable to RASF, we can include bone resorption, which is related to the expression of Wnt proteins in RASF; the mRNA of such proteins is a target for positive regulation by miR-323, considered to be another target to modulate cellular functions in RASF [14]. [score:7]
Ten miRNAs (let-7e, miR-128, miR-323-3p, miR-133b, miR-18b, miR-144, miR-451, miR-150, miR-486-3p, and miR-196b-5p) reflected a fourfold differential expression, and three miRNAs (miR-130b-5p, miR-452, and miR-579) were only identified in plasma from RA patients. [score:3]
Chondrocytes also participate in the catabolic process of joints characterized by cartilage degradation and bone erosions; several pathways have been postulated for this process including the activation of Wnt/cadherin signaling, as well as a constitutive upregulation of β-catenin; a common component for the regulation in both pathways is miR-323. [score:3]
A study showed that miR-323-3p was upregulated in RA synovium compared to control subjects and, by enhancing Wnt and cadherin signaling, produced higher levels of Wnt and Fz. [score:3]
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9
[+] score: 12
In DLB, we detected coincident gene expression regulations with sCJD for miRNA-877-5p and miRNA-323a-5p (both with decreased expression levels) (Fig 6C). [score:6]
Among these, the deregulated expression levels of miRNA-195-5p, miRNA-877-5p and miRNA-323a-5p (marked in red) were previously validated by qPCR in the FC of sCJD cases (Fig 2). [score:4]
There is virtually no information on the functions of the two commonly regulated miRNAs in the brain of the three dementias (miRNA-877-5p and miRNA-323a-5p). [score:2]
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10
[+] score: 11
Our study identified 8 new differentially expressed miRNAs: mir-323, mir-138, mir-9*, mir-211, mir-149, mir-373, mir-135a and mir-184; that have not been reported in literature so far. [score:3]
Moreover, miR-323 was recently described to target EED, a component of the polycomb repressive complex 2 (PRC2) [25], that plays an essential role in GC formation; in fact, the modulation of miR-323 in the follicles was reported as a critical and relevant event of the adaptive immune response [26]. [score:3]
Moreover, miR-323, mir-138 and miR-204 were more highly expressed in naïve and SE B cells. [score:3]
We discovered that miR-323 expression was reduced in activated mature B cells compared to naïve and GC B cells. [score:2]
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11
[+] score: 10
Other miRNAs from this paper: hsa-mir-29a, hsa-mir-101-1, hsa-mir-139, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-142, hsa-mir-144, hsa-mir-127, hsa-mir-154, hsa-mir-185, hsa-mir-195, hsa-mir-29c, hsa-mir-101-2, hsa-mir-380, hsa-mir-381, hsa-mir-520e, hsa-mir-520a, hsa-mir-518c, hsa-mir-520d, hsa-mir-518a-1, hsa-mir-518d, hsa-mir-518a-2, hsa-mir-519a-1, hsa-mir-519a-2, hsa-mir-513a-1, hsa-mir-513a-2, hsa-mir-509-1, hsa-mir-576, hsa-mir-548a-1, hsa-mir-586, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-599, hsa-mir-548a-3, hsa-mir-607, hsa-mir-613, hsa-mir-548c, hsa-mir-625, hsa-mir-634, hsa-mir-642a, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-656, hsa-mir-509-2, hsa-mir-509-3, hsa-mir-1208, hsa-mir-548e, hsa-mir-548j, hsa-mir-1290, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-1247, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-1324, hsa-mir-1825, hsa-mir-548q, hsa-mir-548s, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-323b, hsa-mir-548w, hsa-mir-548x, hsa-mir-548y, hsa-mir-642b, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-548am, hsa-mir-548an, hsa-mir-548ao, hsa-mir-548ap, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-548ay, hsa-mir-548az, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc
We found one miRNA, miR-323-3p, which preferentially targets the down-regulated genes and was identified in all four databases (Figure 2 ; Table S2). [score:6]
Among the seven miRNAs belonging to this cluster that we identified in this study, miR-323-3p has been shown to be expressed in the mouse hippocampus and to play a role in learning, memory, anxiety and exploratory behaviors [39]. [score:3]
miR-323-3p is conserved across species, from rodents to humans. [score:1]
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12
[+] score: 9
For the efficient target SEMA6D, miR-323-3p repressed it only in normal stage, and it had contribution to the ‘ventricular system development’ process only in CIN I stage. [score:4]
For the efficient target DSC2, miR-323-3p and miR-92a repressed it only in normal stage, and it had contribution to the process of ‘bundle of His cell to Purkinje myocyte communication’ only in CIN I stage. [score:3]
Our finding suggests that induced by miR-323-3p’s differential regulation on SEMA6D, the angiogenesis may be enhanced in CIN I stage. [score:2]
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13
[+] score: 8
In the present study on an obese population, we found that the exposure to Zr levels traced in hair is associated with a distinct signature of 7 miRNAs (miR-99b, miR-142-5p, miR-152, miR-193a-5p, miR-323-3p, miR-335, miR-494) expressed in peripheral blood. [score:3]
The seven miRNAs (miR-99b, miR-142-5p, miR-152, miR-193a-5p, miR-323-3p, miR-335, miR-494) associated with Zirconium levels with FDR P < 0.1, were selected for downstream target prediction analysis. [score:3]
Seven miRNAs (miR-99b, miR-142-5p, miR-152, miR-193a-5p, miR-323-3p, miR-335, miR-494) resulted specifically associated with Zr levels. [score:1]
Using an FDR linear step-up adjustment for multiple comparisons (FDR P < 0.1), we found 7 miRNAs (miR-99b, miR-142-5p, miR-152, miR-193a-5p, miR-323-3p, miR-335, miR-494) specifically associated with Zr levels traced in the hair (Table 2). [score:1]
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14
[+] score: 8
Several cellular miRNAs, such as miR-323, miR-491, miR-654, and Let-7c have recently been reported to inhibit H1N1 influenza A virus replication by downregulating the viral gene expression in infected MDCK or A549 cells [19, 20]. [score:8]
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15
[+] score: 8
Another interesting factor concluded was the similar levels of expression of mir-323-3p in embryonic tissue of normal and ectopic pregnancies at ≤ 6 weeks. [score:3]
In another study conducted in 2015 by Nagasaki University Graduate School of Biomedical Sciences in Japan, the researchers discovered that plasma concentration of cell-free pregnancy associated miRNAs—miR-323-3p, miR-515-3p, miR-517a, miR-517c, miR-518b—and the concentration of hCG have significant statistical differences in women with SA, EP and normal pregnancies (NP). [score:1]
Out of the 21 miRNAs, miR-873 and miR-223 were significantly lower in EP than in SA and VIP, while miR-323 was significantly higher in EP. [score:1]
They also concluded that the combination of hCG and progesterone and miR-323-3p constitute a significant diagnostic accuracy with 96.3% sensitivity and 72.6% specificity [13]. [score:1]
Serum miR-323-3p concentrations determined by real-time PCR were significantly elevated in EP and revealed more promising results than miR-517a, miR-519d, and miR-525-3p, with a 37% sensitivity rate (at a fixed-specificity of 90%) when used as a single marker. [score:1]
Moreover, there was no significant statistical difference of cell-free serum concentration of miR-21 between three groups and they reported no relationship between serum levels of hCG and plasma cell free of miR-323-3p, miR-515-3p, miR-517a, miR-517c, miR-518b, and miR-21. [score:1]
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16
[+] score: 7
They identified 13 miRNAs that were differentially expressed in OSCC when compared to healthy controls and, among them, 11 miRNAs were down-regulated (miRNA-136, miRNA-147, miRNA-1250, miRNA-148a, miRNA-632, miRNA-646, miRNA-668, miRNA-877, miRNA-503, miRNA-220a, miRNA-323-5p), and two miRNAs were over-expressed (miRNA-24, miRNA-27b). [score:7]
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17
[+] score: 7
Several of the miRNAs down-regulated in glioblastoma (including miR-124-3p and miR-323-3p) exhibited 5′ truncations or additions while one up-regulated miRNA, miR-10b-5p, exhibited 5′ variations (Table S8). [score:7]
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18
[+] score: 6
de web portal, we found that the short-lived mRNAs were enriched for predicted targets of the miRNAs miR-410, miR-323.3p, miR-200b, miR-200c, and miR-429 (see Supplemental Table 2, available on the Arthritis & Rheumatology web site at http://onlinelibrary. [score:3]
The miRNA miR-323.3p was among these highly expressed miRNAs. [score:3]
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19
[+] score: 6
In contrast, 11 miRNAs (hsa-miR-206, hsa-miR-34a, hsa-miR-374, hsa-miR-424, hsa-miR-100, hsa-miR-101, hsa-miR-323, hsa-miR-368, hsa-miR-137, hsa-miR-138 and hsa-miR-377) were abundantly expressed in day 9 neuronal progenitors (Figures 1B and 2A). [score:3]
Another 11 miRNAs (miR-206, miR-34a, miR-374, miR-424, miR-100, miR-101, miR-323, miR-368, miR-137, miR-138 and miR-377) were abundantly expressed in transdifferentiated neuronal progenitors. [score:3]
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20
[+] score: 6
For example, a few miRNAs, such as let-7c, miR-2911, miR-323, miR-491, and miR-654 had been found to inhibit IAV replication by directly targeting viral genes (Song et al., 2010; Ma et al., 2012; Zhou et al., 2015). [score:6]
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21
[+] score: 5
The majority of the miRNAs had alterations in expression that were consistent between the two species, except for miR-323-3p, miR-369-5p, miR-410, miR-411, miR-433, miR-494 and miR-130a, which were expressed discordantly in the tumors from the two different species (Table 1). [score:5]
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22
[+] score: 5
Many semaphorins and their receptors are predicted targets of brain-expressed miRNAs (e. g., let-7c, miR-125b, miR-153, miR-103, miR-323, miR-326, and miR-337). [score:5]
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23
[+] score: 4
miR-323 20.5Downregulated after spinal cord injury [38]. [score:4]
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24
[+] score: 4
In this context, we observed a preferential down-regulation in region 14q32.31 including miRNA miR-127, miR-370, miR-299, miR-154, miR-154*, miR-323, miR-134, miR-368 and miR-337. [score:4]
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25
[+] score: 4
As shown in Table 2, 15 miRNAs (miR-222, miR-320, miR-24, miR-132, let-7b, miR-106a, miR-19b, miR-16, miR-186, miR-339-3p, miR-17, miR-323-3p, miR-197, miR-20a, and miR-382) were down-regulated in Group 2 and were chosen for subsequent verification analysis. [score:4]
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26
[+] score: 3
Recently, many antiviral miRNAs (miR-323, miR-491, miR-654, and Let-7c) have been found to reduce IAV replication by targeting the viral genome 10 11. [score:3]
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27
[+] score: 3
Cahill and colleagues have shown that human derived BRAFT1799A- and RET/PTC-bearing thyroid tumor cells, KAT10 and TPC-1 respectively, express lower levels of 14q32-encoded miRNAs miR-323-3p, miR-370-5p, miR-127-3p, miR-299 and miR-154 [22, 23]. [score:3]
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28
[+] score: 3
It also has been shown that cellular miR-323, miR-491, and miR-654 could inhibit replication of the H1N1 influenza A virus through binding to the PB1 gene [6]. [score:3]
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29
[+] score: 3
Song et al. screened host miRNAs and found that miR-323, miR-491 and miR-654 inhibit the replication of the H1N1 IAV in MDCK cells by binding to the 3′ coding region rather than the 3′-UTR of the PB1 gene. [score:3]
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30
[+] score: 3
Overexpression of miR-221/222, miR-323-3p, and miR-203 has been noted in synovial fibroblasts in the arthritic phenotype of RA. [score:3]
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31
[+] score: 3
Influenza virus infection modulates multiple cellular miRNAs, and miR-323, miR-491, and miR-654 have been shown to inhibit viral replication by binding to the viral PB1 gene [48], while miR-507 and miR-136 have potential binding sites within the viral PB2 and HA genes [49]. [score:3]
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32
[+] score: 3
In another report, results showed that miR-323, miR-491 and miR-654 could inhibit replication of H1N1 influenza A virus through binding to the conserved region of the PB1 gene [16]. [score:3]
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33
[+] score: 3
Moreover, several studies have demonstrated that cellular microRNAs (miR-323, miR-491, miR654, miR-146a) inhibit influenza virus replication or propagation [23, 24]. [score:3]
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34
[+] score: 3
In 2010, Song’s group reported that miR-323, miR-491 and miR-654 could target the viral PB1 gene [34]. [score:3]
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35
[+] score: 2
Compared to F0-N controls, rno-miR-138-1-3p* was significantly induced in the frontal cortex of F0-S dams whereas rno-miR-323-5p was significantly suppressed (P <0.01, n = 3). [score:2]
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About their regulating miRNA, hsa-miR-10a has been already proposed as a candidate circulating biomarker for PC patients [60], while, for the other two miRNAs (hsa-miR-552 and hsa-miR-323-3p), no publication is available. [score:2]
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0008514hsa-miR-39413.390.0064610hsa-miR-39386.030.008213hsa-miR-4983.470.048419hsa-miR-374c-3p6.040.00125Xhsa-miR-548as-3p3.490.0065713hsa-miR-377-5p6.290.0002414hsa-miR-323a-3p3.700.0035014hsa-miR-43246.390.0066919hsa-miR-550a-3p3.710.000747hsa-miR-4436b-5p6.569.0E-052hsa-miR-30e-3p3.750.01335Unknownhsa-miR-11846.640.00266Xhsa-miR-1273e3.830.00201Unknownhsa-miR-56907.226.6E-056hsa-miR-200b-3p3.830.001481hsa-miR-125b-2-3p7.680. [score:1]
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45 (33) CDK6, DAPK1, MET, MELK, TRIB20.0314HSA-MIR-323–3P. [score:1]
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The set includes miR-127, miR-154, miR-154*, miR-299, miR-323, miR-368, and miR-370. [score:1]
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40
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The set includes miR-127, miR-154, miR-154*, miR-299, miR-323, miR-368, and miR-370. [score:1]
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41
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Zhao Z. Zhao Q. Warrick J. Lockwood C. M. Woodworth A. Moley K. H. Gronowski A. M. Circulating microRNA miR-323–3p as a biomarker of ectopic pregnancyClin. [score:1]
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Keeping on non-cardiac-specific miRNAs, in September 2014, Pilbrow et al. defined through a validation cohort counting 200 patients two circulating miRNAs, miR-323-3p, and miR-652, as candidate markers for the presence and progression of acute coronary syndromes (50). [score:1]
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Furthermore, this cluster has a complex composition, containing other related sequences {hsa-mir-323, HP-33, HP-34, HP-35, HN-6} whereas the corresponding mouse cluster {mmu-mir-323, mmu-mir-329, MP-35, MN-7, MP-37} additionally contains a rodent-specific sequence, MN-7, which is not related to the other sequences in the cluster. [score:1]
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Other miRNAs found in our study to be affected during senescence (Fig. 3), but not reported in previous senescence studies, include miR-1246, miR-584 and miR-323, which are implicated in certain cancers [55]– [57]. [score:1]
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A previous report discovered that three miRNAs: miR-323, miR-491, and miR-654, were able to decrease H1N1 production in madin darby canine kidney (MDCK) cells via binding to a same conservative site on PB1 mRNA and subsequently inducing mRNA degradation [26]. [score:1]
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