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50 publications mentioning hsa-mir-421

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-421. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 146
As both miR-421 and miR-30c were expressed in HUVEC, we cloned the entire PAI-1 3′UTR in the luciferase expression vector and over-expressed these two miRNAs. [score:7]
Interestingly, the introduction of mutations in the sequence complementary to miR-421 seed sequence from site 1 or site 2 were sufficient to abolish the miR-421 sensitive decrease of luciferase expression, indicating that the two close binding sites are necessary to obtain an inhibitory effect by miR-421 (Figure 3B ). [score:6]
MiR-421 was further shown to directly interact with PAI-1 mRNA to inhibit the expression of the associated protein in HUVEC. [score:5]
A homogeneous decrease in luciferase expression was observed when miR-30c and miR-421 were over-expressed (63% and 60%, respectively). [score:5]
MiR-421 and miR-30c overexpression did not show any additive effect on PAI-1 protein expression. [score:5]
According to bioinformatics tools such as Targetscan [15] and microSniper [16], the rs1050955 polymorphism is predicted to map in the close vicinity of target binding sites for several miRNAs including hsa-miR-300, hsa-miR-381, hsa-miR-548l, hsa-let7f-1*, has-let7-a* and hsa-miR-421. [score:5]
While hsa-miR-548l, hsa-miR-300, has-miR-381, has-let7f-1* and hsa-let7a* miRNAs were not or very poorly expressed in any of the aforementioned cell lines, both PAI-1 (see Table 1 ) and miR-421 (see Table 2 ) were homogeneously found expressed in these cell lines with the highest levels observed in HUVEC. [score:5]
MiR-421 and miR-30c inhibit SERPINE1 expression in HUVEC. [score:5]
Note that simultaneously co -expressing miR-421 and miR-30c did not reveal any additive effect on PAI-1 inhibition (Figure 2B ). [score:5]
At a first step, we over-expressed miR-421 by transfection of 3 nM of dedicated miRNA precursor (Pre-miR-421) and checked whether this was accompanied by a decrease in PAI-1 mRNA level or of PAI-1 protein translation. [score:5]
The mRNA inhibition was not observed with miR-421 and this could explain why the inhibitory effect on PAI-1 protein was stronger with miR-30c than with miR-421. [score:5]
Over -expression of miR-421 and miR-30c lead to a decrease in luciferase activity of 40% in both cases (Figure 3A ), indicating that both miRNAs can directly bind to PAI-1 3′UTR mRNA. [score:4]
Nevertheless, our work strongly suggests that miR-421 participates to the regulatory control of SERPINE1 expression. [score:4]
The second stage consisted in checking whether the observed miR-421 inhibitory effect on PAI-1 protein was due to a direct interaction between the miRNA and the PAI-1 mRNA sequence. [score:4]
However, as shown in Figure 2B, both over -expression of miR-421 and miR-30c were associated with a significant decrease in PAI-1 protein level, 59% and 32%, respectively. [score:3]
A. Quantification by qRT-PCR of PAI-1 mRNA level after over -expression of either Pre-miR-421, Pre-miR-30c or a Pre-miR Negative control (Pre-Neg) in HUVEC cells. [score:3]
Among the miRNAs predicted to bind the SERPINE1 region where rs1050955 lies, we demonstrated that only the miR-421 was jointly expressed with SERPINE1 in a variety of cell types. [score:3]
MiR-421 binding sites on PAI-1 3′UTR are poorly conserved among species but we showed that this miRNA has indeed a true inhibitory effect on PAI-1 in humans. [score:3]
This could be explained by the degradation of SERPINE1 mRNA by miR-30c before miR-421 could exert its inhibitory effect. [score:3]
However, our work did not provide support to our starting hypothesis about the role of the rs1050955 on SERPINE1 expression as we did not observe any evidence for a modulation of miR-421's binding efficiency according to the allele present at the rs1050955. [score:3]
Little is known about miR-421 and its pathophysiological role in human diseases. [score:3]
C. Comparison of miR-421 inhibitory effect on luciferase activity between SERPINE1 3′UTR wild-type or mutated at rs1050955 (n = 4). [score:3]
Graph shows renilla luciferase activity normalized to firefly luciferase activity and expressed as percentage of Pre-Neg transfected cells (n = 4 for miR-30c and n = 5 for miR-421; *, p<0.05; **, p<0.01)). [score:3]
We demonstrated that mir-421 binds to two sites and that its inhibitory effect is abolished as soon as the seed sequence of at least one of these sites is mutated. [score:3]
However it should be noted that many cell types could be responsible for PAI-1 (e. g. endothelial cells, hepatocytes, monocytes and platelet) and miR-421 plasma expression. [score:3]
Other cell lines used in the study to detect PAI-1 and miR-421 expression included human mammary epithelial cells (HMEC), human aortic endothelial cells (HAEC), human acute monocytic leukemia cells (THP1), and fresh monocytes preparation. [score:3]
Sequence complementary to miR-421 seed sequence were also directly searched along serpine1 3′UTR. [score:2]
B. Various 3′UTR SERPINE1 sequence containing both miR-421 site 1 and site 2 predicted binding sites or mutation of each seed sequence binding sites were fused to renilla luciferase. [score:2]
B. Western-Blot and quantification of PAI-1 and GAPDH protein level after over -expression of either Pre-miR-421, Pre-miR-30c or both compared to Pre- Neg transfected cells. [score:2]
Oligonucleotides corresponding to the serpine1 3′UTR surrounding the predicted miR-421 binding sites with or without mutation and miR-30c binding site were inserted into psiCHECK-2 using XhoI and NotI restriction enzyme (see Table 3 ). [score:2]
In conclusion, we demonstrated for the first time that miR-421 participates to the regulation of PAI-1 molecule. [score:2]
Data shown were normalized to GAPDH protein level and expressed as percentage compared to Negative control (n = 5 for miR-421 and miR-30c, n = 3 for miR-421+30c; *, p<0.05; **, p<0.01). [score:2]
B. Psicheck2 vector containing total 3′UTR SERPINE1 sequence with the mutated rs1050955-A allele fused to renilla luciferase was co -transfected with Pre-Neg, Pre-miR-421, Pre-miR-30c or both. [score:1]
In pulmonary artery smooth muscle cells, miR-421 was found inducible by transforming growth factor beta (TGFb) and bone morphogenetic protein 4 (BMP4) via a conserved Smad binding element (SBE) – like sequence [27]. [score:1]
This positive correlation between PAI-1 and miR-421 plasma levels could be considered as intriguing compared to the negative correlation we observed on the corresponding expressions in HUVECs. [score:1]
High miR-421 plasma levels could thus be an adaptative response to high PAI-1 levels or a sign of an inflammatory response. [score:1]
Interestingly a second binding site for hsa-miR-421 according to sequence similarity (called site 2) was found 23 bp further. [score:1]
A. Psicheck2 vector containing total 3′UTR SERPINE1 sequence fused to renilla luciferase was co -transfected with Pre-Neg, Pre-miR-30c, Pre-miR-421 or both Pre-miR-30c and Pre-miR-421. [score:1]
As a consequence, we pursued our investigations on the influence of rs1050955 on miR-421's binding to SERPINE1 3′UTR region and on SERPINE1 expression in HUVEC. [score:1]
Conversely, unlike miR-421, plasma levels of miR-30c were not associated with PAI-1 in our sample of venous thrombosis patients despite a trend for such association. [score:1]
Moreover in humans, hsa-miR-421 was predicted to bind close to the polymorphism sequence (this binding sequence was referred to as site 1 in this work) although this site was not conserved among species. [score:1]
Levels of miR-421 and of miR-30c were strongly correlated, the corresponding Spearman correlation coefficient being 0.51 and 0.66 in the low and high PAI-1 groups, respectively. [score:1]
Sequences of the 3′UTR of the PAI-1 mRNA surrounding the two close miR-421 potential binding sites (site 1 and site 2 described in Figure 1 ) containing the wild-type (G) or the mutated (A) allele at rs1050955 were subcloned in a luciferase reporter vector, as well as constructions with mutated seed sequence of either site 1 or site 2 miR-421 binding sites. [score:1]
MiR-421 and miR-30c were detected by qRT-PCR in plasma samples from two groups of 20 patients either with low (1.6+/−1 ui/ml) or high (40.5+/−13 ui/ml) PAI-1 plasma levels. [score:1]
Nevertheless, we further observed an association of plasma levels of miR-421 with those of PAI-1 in a sample of 40 patients with venous thrombosis. [score:1]
Plasma levels of miR-421 and miR-30c in plasma samples of venous thrombosis patients. [score:1]
Influence on luciferase activity of miR-421 and miR-30c binding to the 3′UTR SERPINE1 1704–1760 region. [score:1]
0044532.g005 Figure 5 MiR-421 and miR-30c were detected by qRT-PCR in plasma samples from two groups of 20 patients either with low (1.6+/−1 ui/ml) or high (40.5+/−13 ui/ml) PAI-1 plasma levels. [score:1]
Conversely, it could also be hypothesized that plasma circulating levels of miR-421 could reflect free miR-421 that had not bound to PAI-1 mRNA. [score:1]
SERPINE1 3′UTR is 1841 bp long and miR-30c and miR-421 binding sites are separated by more than 1000 bp (662–668/1722–1729 and 1746–1752 for sequence complementary to seed sequence of miR-30c or miR-421 respectively). [score:1]
Then cells were transfected either with 3 nM Pre-miR™ miRNA Precursor for miR-421 (Pre-421) or Pre-30c or Negative control (Pre-Neg) (Life Technologies, Villebon sur Yvette, France) with Lipofectamine transfection reagent (Life Technologies) according to the manufacturer's recommandations: 300 µl of Opti-MEM+Pre-miR+3 µl Lipofectamine were added to the cells. [score:1]
It is noteworthy that the miR-30c and miR-421 plasma variability tended to be higher in patients with high PAI-1 levels than in patients with extremely low levels of PAI-1. 10.1371/journal. [score:1]
The polymorphism rs1050955 allows a better base pairing for hsa-miR-421 on this site 2 although not on its seed sequence (Figure 1 ). [score:1]
C. Alignment of miR-421 onto SERPINE1 3′UTR 1704–1760 region which includes two predicted binding sites, site 1 and site 2, complementary to the miR-421 seed sequence. [score:1]
MiR-421 overexpression was not followed by any modulation of PAI-1 mRNA level compared to a negative control (Pre-Neg) (Figure 2A ). [score:1]
0044532.g004 Figure 4Influence of miR-421 and miR-30c binding to total 3′UTR SERPINE1 on luciferase activity. [score:1]
A. psicheck2 vector containing 3′UTR SERPINE1 sequence surrounding miR-30c predicted binding site or miR-421 predicted binding sites according to the allele present at rs1050955 fused to renilla luciferase were co -transfected with Pre-Neg, Pre-miR-30c or Pre-miR-421. [score:1]
Influence of miR-421 and miR-30c binding to total 3′UTR SERPINE1 on luciferase activity. [score:1]
0044532.g003 Figure 3Influence on luciferase activity of miR-421 and miR-30c binding to the 3′UTR SERPINE1 1704–1760 region. [score:1]
Plasmids were transfected with Pre-Neg or Pre-miR-421. [score:1]
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[+] score: 45
The significance of the differences in the expression was confirmed for six of the miRNAs, including two down-regulated miRNAs namely miR-181d-5p and miR-206 and four up-regulated miRNA namely miR-1233-3p, miR-183-5p, miR-421 and miR-625-5p) (P < 0.05) (Fig.   3). [score:9]
Specifically, O’Brien et al. [10] identified 61 miRNAs with significantly altered expression levels and Bittel et al. [9] found that miR-421 exhibited the most significant expressed miRNA in the RVOT myocardial tissue of infants with TOF. [score:5]
Moreover, differential expression levels of miR-421, miR-1233-3p and miR-625-5p were found in TOF-noHF and TOF-HF patients with significantly reduced expression levels in TOF patients with symptomatic right heart failure (Fig.   4). [score:5]
Expression levels of miR-421, miR-1233-3p and miR-625-5p are lower in TOF patients with symptomatic right heart failure and thus may indicate disease progression in these patients. [score:5]
We found that expression levels of circulating miR-421, miR-1233-3p and miR-625-5p were significantly lower in TOF patients with as compared to those without symptomatic right heart failure indicating a potential role of these miRNAs in identifying disease progression in TOF patients. [score:4]
The RT-qPCR showed the same direction of expression changes as the microarray analysis for six miRNAs namely miR-181d-5p, miR-1233-3p, miR-183-5p, miR-206, miR-421 and miR-625-5p. [score:4]
In the latter group, altered expression levels of miR-421, miR-1275, miR-27b, miR-1201 and miR-122 have been reported. [score:3]
In addition, we selected three miRNAs (miR-1233-3p, miR-140-3p and miR-421) with low or moderate expression levels in the three comparisons and miR-421 that had been identified in TOF [9]. [score:3]
For further analysis of the patient group, we additionally selected three miRNAs (miR-1233-3p, miR-140-3p and miR-421) with low or moderate expression levels in the three comparisons and miR-421 that had been identified in myocardial tissue of TOF patients [9]. [score:3]
Moreover, expression levels of miR-625-5p, miR-1233-3p and miR-421 were lower in TOF-HF compared to TOF-noHF (P = 0.012). [score:2]
However, weak correlations were observed between miR-421 and miR-1233-5p and right ventricular volumes, ejection fraction as well as hsTNT (Table  3). [score:1]
Nevertheless, miR-421 was also significantly altered in the blood of patients after long-term repair of TOF suggesting a specific role of miR-421 in the early pathology of TOF as well as during long-term follow-up. [score:1]
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[+] score: 28
Other miRNAs from this paper: hsa-mir-17, hsa-mir-21
hsa-miR-21-5p negatively regulates the expression of p21 protein in the p53 network (30), and hsa-miR-421, is a miRNA that downregulates the ataxia telangiectasia mutated (ATM) gene expression inducing changes at S-phase level of cell cycle checkpoint and an increasing of sensitivity to ionizing radiation (31, 32). [score:9]
miR-421 regulates the cell cycle S-phase checkpoint and cellular radiosensitivity by suppressing ATM expression, a serine/threonine protein kinase that regulates DNA damage -induced at the G1-S and S phases of the cell cycle checkpoints (31). [score:7]
The increased expression of hsa-miR-421 downregulates ATM so reducing the capacity of T98G cells to repair radiation damage. [score:6]
In the present study, we aimed to evaluate the in vitro effect of gallic acid (3,4,5-trihydroxybenzoic acid) on the T98G glioma cell line and to correlate the anti-proliferative and cell death effects with the expression of the miRNAs hsa-miR-17-3, hsa-miR-21-5p and hsa-miR-421-5p, already proven to be involved in the regulation of cancer cell pathways. [score:2]
In conclusion, based on the present study, GA at low concentrations inhibits all the three miRNAs considered, indicating that the increase in mitochondrial antioxidant capacity (decrease of 17-3p), increases cell proliferation by stimulating the regeneration of cells and tissues (decrease of miR-21), and increases the ability to repair damage caused by chemicals and radiation (decrease of miR-421). [score:2]
Gallic acid at high doses causes a reduction in mitochondrial antioxidant activity (increased miR-17 levels); slows cell proliferation (increased miR-21 levels) and decreases the ability to repair the damage (increased miR-421 levels). [score:1]
miR-17-3p LNA probe (ACUGCAGUGAAGGC ACUUGUAG), miR-21-5p LNA probe (UAGCUUAUCAGAC UGAUGUUGA), miR-421-5p LNA probe (AUCAACAGAC AUUAAUUGGGCGC), provided by Exiqon, using the following reaction conditions: a first step at 95°C for 10 min, 45 amplification cycles of 95°C for 10 sec followed by a step at 60°C for 1 min. [score:1]
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[+] score: 21
For example, miRNA-205 increased NPC cells radioresistance by directly targeting PTEN [15], miRNA-221 and miRNA-222 regulated gastric carcinoma cells radioresistance by targeting PTEN [16], downregulation of miRNA-210 expression enhanced radiosensitivity in hypoxic human hepatoma cells [17], overexpression of miRNA-421 lead to a pronounced DSB repair defect and clinical hypersensitivity in SKX squamous cell carcinoma [18], silencing of miRNA-21 increased radiosensitivity through inhibiting a PI3K/AKT pathway and enhancing autophagy in malignant glioma cells [19], and upregulation of NF-κB -dependent miRNA-125b promoted cell survival by targeting p38α upon ultraviolet radiation [20]. [score:21]
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[+] score: 13
In addition, seven of the 12 most significant 5’ moRNAs shown in Table 5 are expressed from a miRNA hairpin opposite to the major miRNA stem (3p) and one of them, moR-421-5p, is expressed alone without expression of its adjacent miRNA miR-421. [score:7]
Interestingly, many moRNA-deriving, cancer -associated hairpins are also expressed in oocytes such as mir-17-92 cluster, miR-20, miR-21, miR-15a/16 and miR-103 [50] whereas miR-421 from mir-374b-421 cluster has been reported to be up-regulated in ovarian teratomas [60]. [score:6]
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[+] 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-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-98, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-192, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-210, hsa-mir-215, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-30b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-137, hsa-mir-138-2, hsa-mir-143, hsa-mir-144, hsa-mir-145, hsa-mir-152, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-138-1, hsa-mir-146a, hsa-mir-193a, hsa-mir-194-1, hsa-mir-206, hsa-mir-320a, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-194-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-302a, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-369, hsa-mir-371a, hsa-mir-340, hsa-mir-335, hsa-mir-133b, hsa-mir-146b, hsa-mir-519e, hsa-mir-519c, hsa-mir-519b, hsa-mir-519d, hsa-mir-519a-1, hsa-mir-519a-2, hsa-mir-499a, hsa-mir-504, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-190b, hsa-mir-301b, hsa-mir-302e, hsa-mir-302f, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-320e, hsa-mir-371b, hsa-mir-499b
Hu H. Du L. Nagabayashi G. Seeger R. C. Gatti R. A. ATM is down-regulated by N-Myc-regulated microRNA-421 Proc. [score:5]
Firstly, the DNA damage transducer genes, ATM is itself targeted by miR-421 in Hela cells [23], whilst H2AX is regulated by miR-24 in terminally differentiated human blood cells [24]. [score:4]
Ectopic expression of miR-421 causes a phenotype resembling that seen in ATM patients characterized by cellular checkpoint changes and radiosensitivity [23], whereas miR-24 mediated suppression of H2AX causes sensitivity to gamma-radiation and genotoxic drugs [24]. [score:3]
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[+] score: 11
As expected, most majority of the miRNAs, either upregulated in the cancer tissues, such as miR-223-3p [61], miR-421 [62], miR-424-5p [63], miR-1260b [64] etc, or downregulated in the penile cancer, such as miR-205-5p [65], miR-211-5p [65– 66], miR-365-3p [67] and miR-1247 [68] etc, were entitled the similar roles in carcinogenesis of bladder cancer, retinoblastoma, breast cancer, nasopharyngeal cancer, pancreatic cancer and several other cancer types [61– 68]. [score:7]
miR-421 induces cell proliferation and apoptosis resistance in human nasopharyngeal carcinoma via downregulation of FOXO4. [score:4]
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[+] score: 10
Mansour W. Y. Bogdanova N. V. Kasten-Pisula U. Rieckmann T. Kocher S. Borgmann K. Baumann M. Krause M. Petersen C. Hu H. Aberrant overexpression of miR-421 downregulates ATM and leads to a pronounced DSB repair defect and clinical hypersensitivity in SKX squamous cell carcinoma Radiother. [score:6]
miR-421 has also been described as negatively regulating ATM expression, leading to clinically manifest tumor radiosensitivity [22]. [score:4]
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[+] score: 9
119) used real-time PCR to analyse miR-421 expression levels in gastric juice from patients with gastric cancer or benign gastric disease. [score:5]
The results showed that gastric juice levels of miR-421 in patients with gastric cancer differed significantly from the levels observed in patients with benign gastric disease. [score:3]
Several miRNAs circulating in blood of gastric cancer patients can be applied as diagnosis biomarkers, including let-7a, miR-1, miR-17-5p, miR-21, miR-20a, miR-27a, miR-34, miR-106a/b, miR-196a, miR-199a-3p, miR-218, miR-221, miR-223, miR-370, miR-376c, miR-378, miR-421, miR-423-5p, miR-451 and miR-486 (Refs 64, 76, 111, 112, 113, 114, 115, 116, 117). [score:1]
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[+] score: 9
For example, upregulation of miR-421 inhibits FOXO signaling pathway by directly targeting 3’-UTR of FOXO4 [88]. [score:9]
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[+] score: 9
Of the 186 miRNAs the expression of which was altered, nine were up-regulated at both time points (miR-125a-3p, miR-297c, miR-421, miR-452, miR-483, miR-574-3p, miR-574-5p, miR-669a, miR-720) and 11 were down-regulated at both time points (let-7g, miR-107, miR-10a, miR-15a, miR-15b, miR-199b*, miR-26a, miR-29c, miR-324-5p, miR-331-3p, miR-342-3p). [score:9]
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[+] score: 8
To date, miR-17, miR-18a\b, miR-19a, miR-20a\b, miR-21, miR-106a\b, miR-340, miR-421, and miR-658 have been shown to be highly expressed in gastric cancer tissues[17– 20], whereas the expression of miR-34b, miR-34c, and miR-128a is upregulated in undifferentiated gastric cancer tissues[21]. [score:8]
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[+] score: 8
On the one hand, microRNAs might function as tumor suppressor via inducing apoptosis, i. e. miR-421, which induces cell proliferation and apoptosis resistance in human nasopharyngeal carcinoma via down-regulation of FOXO4 [49]; miR-149, which induces apoptosis by inhibiting Akt1 and E2F1 in human cancer cells [50] and miRNA-31, which induces apoptosis in human neuroblastoma cells [51]. [score:8]
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[+] score: 7
For example, miR-221-3p (28), miR-421 (8 ), miR-21 (27), miR-150 (20), miR-199a (3), and miR-106b (29) have been reported to be up-regulated in GC. [score:4]
For instance, miR-9, miR-421, miR-27a, and miR-143 have been reported to be involved in the development and progression of the GC by regulating tumor cells proliferation, apoptosis, invasion, and metastasis (7– 11). [score:3]
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[+] score: 7
The transcription of miR-9-3 is upregulated by myc in human breast cancer cells [40]; miR-421/-374 cluster is upregulated by myc in HeLa cells [41]. [score:7]
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[+] score: 7
Other miRNAs from this paper: hsa-mir-19a, hsa-mir-92a-1, mmu-mir-19a, mmu-mir-92a-1, mmu-mir-421
Interestingly, N-myc downregulates ATM through the induction of miR-421 [9], suggesting that ATM downregulation is part of the MYCN dictated cellular transformation program in NB. [score:7]
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[+] score: 6
Li Y, Li W, Zhang JG, Li HY, Li YM: Downregulation of tumor suppressor menin by miR-421 promotes proliferation and migration of neuroblastoma. [score:6]
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[+] score: 6
Other miRNAs from this paper: hsa-mir-203a, hsa-mir-219b, hsa-mir-203b
It has been demonstrated that the aberrant overexpression of miR-421 may down-regulated ATM, therefore, can lead to SKX squamous cell carcinoma [35]. [score:6]
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[+] score: 6
Dashwood et al. demonstrated that a single intake of cruciferous vegetables inhibits HDAC activity in mononuclear cells of peripheral blood promoting H3 and H4 acetylation [141], while other studies demonstrated that exposure to cigarette smoke causes a down-regulation of mir-34b, mir-421, mir450-b, mir-466, and mir-469 [142]. [score:6]
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[+] score: 6
Van Jaarsveld et al. compared the miR expression profiles of cisplatin-sensitive and -resistant ovarian cancer cells, revealing that high expression of miR-141, miR-200c, miR-215, and miR-421 and low expression of miR-492-5p correlated with increased cisplatin resistance [61]. [score:6]
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[+] score: 6
These authors showed that miRNAs 20-b, miR-20a, miR-17, miR-21, miR-106a, miR-18a, mir-21, miR106b, mir-18b, miR-421, miR-340, miR-19a and miR-658 were highly expressed in GC. [score:3]
Among them, miR-340*, miR-421 and miR-658 were first found highly expressed in cancer cells. [score:3]
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[+] score: 6
In regards to age, we discovered that the expression levels of 14 miRNAs (miR-654-5p, miR-493*, miR-410, miR-376a*, miR-758, miR-381, miR-543, miR-539, miR-487b, miR-337-5p, miR-136*, miR-154*, miR-330-3p, and miR-421) were significantly higher in HCC up to 66 years old than in HCC over 67 years old. [score:3]
o.   fold changep-valuehsa-miR-654-5p3.880.00014hsa-miR-493*3.100.00016hsa-miR-4102.930.00029hsa-miR-376a*2.660.00072hsa-miR-7582.870.00073hsa-miR-3812.390.00094hsa-miR-5432.070.00119hsa-miR-5393.060.00124hsa-miR-487b2.020.00186hsa-miR-337-5p2.540.00195hsa-miR-136*2.790.00246hsa-miR-154*2.270.00337hsa-miR-330-3p2.440.00759 hsa-miR-421 2.45 0.01282We also identified miRNAs with expression levels that varied according to gender and age. [score:3]
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[+] score: 5
Other miRNAs from this paper: cel-let-7, cel-lin-4, 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-29a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, mmu-let-7g, mmu-let-7i, mmu-mir-29b-1, mmu-mir-101a, mmu-mir-128-1, mmu-mir-9-2, mmu-mir-132, mmu-mir-138-2, mmu-mir-181a-2, mmu-mir-199a-1, hsa-mir-199a-1, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-199a-2, hsa-mir-181a-1, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-128-1, hsa-mir-132, hsa-mir-138-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-138-1, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-29a, mmu-mir-29c, mmu-mir-92a-2, rno-let-7d, rno-mir-7a-1, rno-mir-101b, mmu-mir-101b, hsa-mir-181b-2, mmu-mir-17, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-181c, mmu-mir-128-2, hsa-mir-128-2, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-29c, hsa-mir-101-2, cel-lsy-6, mmu-mir-181b-2, 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-7a-2, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-17-1, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-92a-1, rno-mir-92a-2, rno-mir-101a, rno-mir-128-1, rno-mir-128-2, rno-mir-132, rno-mir-138-2, rno-mir-138-1, rno-mir-181c, rno-mir-181a-2, rno-mir-181b-1, rno-mir-181b-2, rno-mir-199a, rno-mir-181a-1, rno-mir-421, hsa-mir-181d, hsa-mir-92b, mmu-mir-181d, mmu-mir-421, mmu-mir-92b, rno-mir-17-2, rno-mir-181d, rno-mir-92b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, mmu-mir-101c, mmu-let-7j, mmu-let-7k, rno-let-7g, rno-mir-29c-2, rno-mir-29b-3, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
The human and mouse genomic sequences for candidate miR-421 precursors are identical. [score:1]
We have not been able to detect miR-421 in mouse brain using northern blots. [score:1]
A file (Additional data file 2) containing precursor sequences and secondary structure predictions for the novel microRNA miR-421. [score:1]
An alignment of the predicted precursor sequences from human and mouse of the novel microRNA miR-421, which we identified from rat, is shown. [score:1]
We named this new microRNA rno-miR-421 (Figure 1 and). [score:1]
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Furthermore, a comparison was made in their negative regulatory effects on FOXO4 protein expression between miR-150 and several other potential up-stream miRNAs of FOXO4 (miR-421, miR-664a-3p, miR-499a-5p). [score:4]
miR-150, miR-421, miR-664a-3p, miR-499a-5p mimics and miRNA mimic NC were synthesized by Ribobio Technology Co. [score:1]
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MiR-421 can inhibit prostate cancer progression by attenuating NRAS protein expression [46]. [score:4]
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Over -expression of miR-9, let-7 g [54], miR-100, miR-101, miR-181a, or miR-421 has been shown to enhance the vulnerability of cells to IR -induced injury [55] and direct cells towards an apoptotic pathway. [score:4]
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For instance, a catalytic subunit of DNA -dependent protein kinase (DNA-PKs) is inhibited by miR-7 and miR-101 (Yan et al., 2010; Lee et al., 2011), and ataxia telangiectasia mutated protein (ATM) is regulated with miR-18a, miR-100, miR-101, and miR-421 (Ng et al., 2010; Yan et al., 2010). [score:4]
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One newly published paper revealed that CBX7 might be negatively regulated by miRNA421 in gastric cancer cell line [15], though the expression and function of CBX7 in gastric cancer are still unclear. [score:4]
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For example, runt related transcription factor 1 (RUNX1) and lysine methyltransferase 2A (MLL1) are essential for chromosomal translocations in acute myeloid leukemia [52, 53], which were predicted as targets of val-miR1086, val-miR765, val-miR615; and val-miR834 val-miR765, val-miR550, val-miR1127, val-miR954, val-miR1086, val-miR421, respectively. [score:3]
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Increased expression of miR-421 in human gastric carcinoma and its clinical association. [score:3]
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miRNAs [a]Presence in samples [b]Median editing (in %) Seed editing event Position in precursor Target Prediction [c]Overlap (%) Before/After editing hsa-mir-598-3p 6/5/0 0.49/0.34/0 Yes 62 11/9 0 (0) hsa-mir-376a-1-5p 6/6/0 11.24/8.43/0 Yes 9 131/166 4 (3.05) hsa-mir-337-3p* 4/1/0 4.21/−/0 Yes 66 146/197 11 (7.53) hsa-mir-376c-3p 6/5/2 3.72/1.9/− Yes 48 156/192 11 (7.05)hsa-mir-1301-3p [#,*] 6/6/2 7.59/3.94/− Yes 52 230/7 2 (0.87) hsa-mir-421 6/6/3 1.40/0.61/0.57 Yes 54 271/4 1 (0.37) hsa-mir-99b-3p* 6/6/2 3.61/1.65/− Yes 47 33/21 0 (0) hsa-mir-641-5p 6/6/3 5.62/7.08/3.35 Yes 18 355/128 11 (3.1) hsa-let-7e-3p* 4/0/0 2.09/0/0 Yes 57 5/3 0 (0)hsa-mir-1251-5p [#,*] 4/4/0 11.98/11.87/0 Yes 10 58/305 4 (6.9)hsa-mir-381-3p [#] 6/6/5 6.87/7.15/3.07 Yes 52 638/302 48 (7.52) hsa-mir-411-5p 6/6/5 27. [score:3]
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34 hsa-miR-335 −0.35hsa-miR-345 [44], [53], [71] 1.16 hsa-miR-363 0.99 hsa-miR-371-5p 0.55 hsa-miR-421 0.50 hsa-miR-483-5p 1.33 hsa-miR-494 0.87 hsa-miR-505* −0.40 hsa-miR-513a-5p 1.06 hsa-miR-513b 1.19 hsa-miR-513c 1.22 hsa-miR-551b −0.40 hsa-miR-574-5p 0.97hsa-miR-630 [68], [73] 0.96 hsa-miR-769-5p −0.34 hsa-miR-801 0.66 hsa-miR-873 −0.64 hsa-miR-877* 0.72 hsa-miR-923 0.89 hsa-miR-940 0.49 hsa-miR-95 −0.44 hsa-miR-99a −0.64Irradiated and non-irradiated PBL of the same donors were incubated in static gravity (1 g) for 4 and 24 h, and miRNA expression profile was analyzed at the end of each incubation time. [score:3]
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Conversely, HIF-1 promotes the expression of several hypoxamiRs including miR-210 [97], miR-146a [98], miR-145 [99], miR-382 [100], miR-191 [101], miR-363 [102], miR-421 [103] in tumor cells, miR-204 in neuronal cells [104], miR-30a and miR-21 in cardiomyocytes [105, 106], miR-687 in embryonic kidney cells [107], miR-155 in intestinal epithelial cells [108], and miR-429 [109] and miR-19a [110] in endothelial cells. [score:3]
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Bioinformatics and system biology validation indicated that five of the nine miRs, that is, miR-142-5p, miR-19b, miR-1928, miR-223 and miR-421-3p may have a role in the regulation of genes associated with delayed and exaggerated fear. [score:2]
The nine stress-responsive miRs, miR-142-5p, miR-19b, miR-1928, miR-223-3p, miR-322 [∗], miR-324, miR-421-3p and miR-463 [∗] identified may have potential as biomarkers for PTSD. [score:1]
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Pre-clinical studies in healthy mice and in vitro studies using estrogen have identified miRNAs either regulated by estrogen (miR-203, miR-126, miR-23a, miR-21, miR-24, miR-27a and b, and miR-106a and b) or encoded by X-chromosome (miR-98, miR-652, miR-221, miR-222, miR-223, miR-361, miR-421, miR-325, miR-188, miR-92a, miR-424, miR-503, miR-505). [score:2]
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From the prediction, the experimental data from cow milk study validated 9 transportable milk miRNAs in human blood, including bta-miR-487b, miR-181b, miR-421, miR-215, let-7c, miR-301a, miR-432, miR-127, and miR-184. [score:1]
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severe (p<0.05) cfa-let-7a, cfa-let-7b, cfa-let-7c, cfa-let-7f, cfa-miR-127, cfa-miR-1271, cfa-miR-130a, cfa-miR-139, cfa-miR-17, cfa-miR-1836, cfa-miR-1837, cfa-miR-20a, cfa-miR-23a, cfa-miR-25, cfa-miR-26a, cfa-miR-29b, cfa-miR-378, cfa-miR-421, cfa-miR-502, cfa-miR-503, cfa-miR-542, cfa- miR-652, cfa-miR-653, cfa-miR-872 Normal and mild vs. [score:1]
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Recent studies have reported microRNAs (miR-26a, miR-141, miR-210, miR-31, miR-21 and miR-421) having oncogenic function in CCAs by modulating cell proliferation signaling pathways [6] [7]. [score:1]
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In this condition, the TEs were inserted in the proximity of appropriate sequences that are similar to the complementary sequences of the TE head or tail to form the hairpin structure of pre-miRNAs, such as hsa-mir-326, hsa-mir-421 and hsa-mir-619 (S2 Table). [score:1]
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A study also reported that miR-421 can be used as a biomarker to detect circulated tumor cells of gastric cancer patients [5]. [score:1]
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This is the case of RP-97, which is close to rno-mir-421. [score:1]
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The top ten miRNAs with the highest absolute loadings for the second principal component (PC2) were hsa-miR-320a, hsa-miR-26b-5p, hsa-miR-421, hsa-miR-29a-3p, hsa-miR-450b-5p, hsa-miR-155-5p, hsa-miR-26a-5p, hsa-miR-30c-5p, hsa-miR-32-5p and hsa-miR-361-5p. [score:1]
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Lerebours’ et al. showed that a 5-miRNA signature comprising miR-421, miR-486, miR-503, miR-720 and miR-1303 was shown to be predictive for inflammatory BC phenotype with an overall accuracy of 89% [16]. [score:1]
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Scare bar = 50 μm To explore whether circHIPK3 can function as “miRNA sponge” in CRC cells, we selected the top ten (miR-599, miR-93-3p, miR-365a-5p, miR-365b-5p, miR-421, miR-570-3p, miR-597-5p, miR-7, miR-1207-3p, miR-124-5p) candidate miRNAs through CircNet database [21]. [score:1]
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miR-421 induces cells to become hypersensitive to ionizing radiation, which is dependent on ATM [12]. [score:1]
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Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7e, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-27a, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-99a, hsa-mir-100, hsa-mir-101-1, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-106a, hsa-mir-16-2, hsa-mir-192, hsa-mir-196a-1, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-10a, hsa-mir-196a-2, hsa-mir-199a-2, hsa-mir-203a, hsa-mir-215, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-200b, hsa-mir-1-2, hsa-mir-15b, hsa-mir-27b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-141, hsa-mir-143, hsa-mir-145, hsa-mir-152, hsa-mir-191, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-194-1, hsa-mir-195, hsa-mir-320a, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-128-2, hsa-mir-194-2, hsa-mir-200a, hsa-mir-101-2, hsa-mir-130b, hsa-mir-302c, hsa-mir-375, hsa-mir-378a, hsa-mir-148b, hsa-mir-324, hsa-mir-451a, hsa-mir-483, hsa-mir-484, hsa-mir-486-1, hsa-mir-500a, hsa-mir-92b, hsa-mir-595, hsa-mir-596, hsa-mir-378d-2, hsa-mir-744, hsa-mir-885, hsa-mir-939, hsa-mir-940, hsa-mir-1229, hsa-mir-1233-1, hsa-mir-1290, hsa-mir-1246, hsa-mir-103b-1, hsa-mir-103b-2, hsa-mir-718, hsa-mir-378b, hsa-mir-378c, hsa-mir-4306, hsa-mir-4286, hsa-mir-500b, hsa-mir-1233-2, hsa-mir-3935, hsa-mir-642b, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-3976, hsa-mir-4644, hsa-mir-203b, hsa-mir-451b, hsa-mir-378j, hsa-mir-486-2
Several circulating miRNAs were identified as biomarkers for the detection and diagnosis of GC: miR-21, miR-200c, miR-421, miR-199a, miR-122, miR-192, miR-222, miR-16, miR-25, miR-92a, miR-451, miR-486-5p, miR-940, miR-223, miR-19b, miR-194, miR-141, and miR-1233, with a reasonable degree of diagnostic ability [25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36]. [score:1]
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The results revealed potentially conserved sites for approximately nine miRNA family candidates (miR-30c, miR-34a/c, miR-449b, miR-181, miR-301a, miR-421, miR-299-5p, miR-609 and miR-99a) in the PAI-1 mRNA 3′ UTR. [score:1]
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The precursor of miR-421, for example, was located on chromosome X and was clustered with the known miRNA ssc-miR-374a within a distance of 107 bp, while no obvious hairpin was detected in between (Table 2). [score:1]
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Other miRNAs from this paper: hsa-mir-25, hsa-mir-28, hsa-mir-95, mmu-mir-151, mmu-mir-290a, mmu-mir-297a-1, mmu-mir-297a-2, mmu-mir-130b, mmu-mir-340, mmu-mir-25, mmu-mir-28a, hsa-mir-130b, hsa-mir-367, hsa-mir-372, hsa-mir-378a, mmu-mir-378a, hsa-mir-340, hsa-mir-151a, mmu-mir-466a, mmu-mir-467a-1, hsa-mir-505, hsa-mir-506, mmu-mir-367, hsa-mir-92b, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-648, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-659, hsa-mir-151b, hsa-mir-1271, hsa-mir-378d-2, mmu-mir-467b, mmu-mir-297b, mmu-mir-505, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-297c, mmu-mir-421, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-467c, mmu-mir-467d, mmu-mir-92b, mmu-mir-466d, hsa-mir-297, mmu-mir-467e, mmu-mir-466l, mmu-mir-669g, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-467f, mmu-mir-466j, mmu-mir-467g, mmu-mir-467h, mmu-mir-1195, hsa-mir-548e, hsa-mir-548j, hsa-mir-1285-1, hsa-mir-1285-2, hsa-mir-1289-1, hsa-mir-1289-2, hsa-mir-548k, hsa-mir-1299, hsa-mir-548l, hsa-mir-1302-1, hsa-mir-1302-2, hsa-mir-1302-3, hsa-mir-1302-4, hsa-mir-1302-5, hsa-mir-1302-6, hsa-mir-1302-7, hsa-mir-1302-8, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-1255a, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-1268a, 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-1255b-1, hsa-mir-1255b-2, mmu-mir-1906-1, hsa-mir-1972-1, hsa-mir-548q, mmu-mir-466m, mmu-mir-466o, mmu-mir-467a-2, mmu-mir-467a-3, mmu-mir-466c-2, mmu-mir-467a-4, mmu-mir-466b-4, mmu-mir-467a-5, mmu-mir-466b-5, mmu-mir-467a-6, mmu-mir-466b-6, mmu-mir-467a-7, mmu-mir-466b-7, mmu-mir-467a-8, mmu-mir-467a-9, mmu-mir-467a-10, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, hsa-mir-3116-1, hsa-mir-3116-2, hsa-mir-3118-1, hsa-mir-3118-2, hsa-mir-3118-3, hsa-mir-548s, hsa-mir-378b, hsa-mir-466, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-3156-1, hsa-mir-3118-4, hsa-mir-3174, hsa-mir-3179-1, hsa-mir-3179-2, hsa-mir-3179-3, hsa-mir-548w, hsa-mir-3156-2, hsa-mir-3156-3, hsa-mir-548x, mmu-mir-3470a, mmu-mir-3470b, mmu-mir-3471-1, mmu-mir-3471-2, hsa-mir-378c, hsa-mir-1972-2, hsa-mir-1302-9, hsa-mir-1302-10, hsa-mir-1302-11, mmu-mir-1906-2, hsa-mir-3683, hsa-mir-3690-1, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-1268b, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-378f, hsa-mir-378g, 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-378h, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-378i, hsa-mir-548am, hsa-mir-548an, mmu-mir-28c, mmu-mir-378b, mmu-mir-28b, hsa-mir-548ao, hsa-mir-548ap, mmu-mir-466q, 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-378j, mmu-mir-378c, mmu-mir-378d, hsa-mir-548ay, hsa-mir-548az, hsa-mir-3690-2, mmu-mir-290b, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-3179-4, mmu-mir-466c-3, hsa-mir-548bc, mmu-mir-1271
The functional networks of miR-92b (PRdmiR, mir-25 family, derived from GC rich tandem repeats), miR-28 (RdmiR, mir-28 family, derived from LINE), miR-151 (RdmiR, mir-28 family, derived from LINE), miR-421 (RdmiR, mir-95 family, derived from LINE), miR-1271 (RdmiR, mir-1271 family, derived from LINE), miR-340 (RdmiR, mir-340 family, derived from DNA transportable element) and miR-378 (RdmiR, mir-378 family, derived from SINE) have been reconstructed (Figure 8). [score:1]
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Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-101-1, hsa-mir-106a, hsa-mir-107, hsa-mir-16-2, hsa-mir-192, hsa-mir-196a-1, hsa-mir-199a-1, hsa-mir-129-1, hsa-mir-148a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-196a-2, hsa-mir-199a-2, hsa-mir-203a, hsa-mir-210, hsa-mir-212, hsa-mir-214, hsa-mir-215, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-27b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-141, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-153-1, hsa-mir-153-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-129-2, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-195, hsa-mir-206, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-181b-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-200a, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-130b, hsa-mir-376c, hsa-mir-375, hsa-mir-378a, hsa-mir-148b, hsa-mir-338, hsa-mir-335, hsa-mir-423, hsa-mir-20b, hsa-mir-429, hsa-mir-449a, hsa-mir-433, hsa-mir-451a, hsa-mir-193b, hsa-mir-520d, hsa-mir-503, hsa-mir-92b, hsa-mir-610, hsa-mir-630, hsa-mir-650, hsa-mir-449b, hsa-mir-449c, hsa-mir-378d-2, hsa-mir-744, hsa-mir-1207, hsa-mir-1266, hsa-mir-378b, hsa-mir-378c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-4512, hsa-mir-378i, hsa-mir-203b, hsa-mir-451b, hsa-mir-378j
Zhang X. Cui L. Ye G. Zheng T. Song H. Xia T. Yu X. Xiao B. Le Y. Guo J. Gastric juice microRNA-421 is a new biomarker for screening gastric cancer Tumour Biol. [score:1]
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