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9 publications mentioning dre-mir-27b

Open access articles that are associated with the species Danio rerio and mention the gene name mir-27b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

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[+] score: 248
The overexpression of miR-27b mimics resulted in a significant increase in the expression of four lipogenic genes, PPAR-γ, ANGPTL3, N-deacetylase/Nsulfotransferase 1 (NDST1), and GPAM, and the inhibition of endogenous miR-27b significantly upregulated the same four genes. [score:10]
In their study, Kang et al., determined that the levels of both miR-27a and miR-27b were down-regulated following adipogenic induction of hMADS, while the overexpression of miR-27a or miR-27b inhibited PHB expression and adipocyte differentiation [20]. [score:10]
Collectively, these data suggest that miR-27b-SP can specifically inhibit miR-27b expression and sequester miR-27b activity on its target genes by eliminating miR-27b expression. [score:9]
Conversely, suppressing miR-27b function down-regulated expression of specific genes in brown adipose tissue [21]. [score:8]
Zou B. Ge Z. Zhu W. Xu Z. Li C. Persimmon tannin represses 3T3-L1 preadipocyte differentiation via up -regulating expression of miR-27 and down -regulating expression of peroxisome proliferator-activated receptor-γ in the early phase of adipogenesisEur. [score:7]
Chan et al., reported that ginsenoside-Rb1 can downregulate miR-27b activity, which in turn promotes PPAR-γ expression and adipogenesis [50]. [score:6]
Overexpression of miR-27b inhibited brown adipose differentiation and the energy expenditure of primary adipocytes. [score:5]
Molecular analysis revealed that gankyrin overexpression induced hepatic steatosis and modulated the expression profiles of four hepatic microRNAs, miR-16, miR-27b, miR-122, and miR-126 [30]. [score:5]
Karbiener et al., demonstrated that miR-27b levels decreased during adipogenesis of human adipose-derived stem (hMADS) cells and the overexpression of miR-27b repressed PPAR-γ and CCAAT enhancer binding protein-α (C/EBP-α) expression during early onset of adipogenesis and triglyceride accumulation at later stages [18, 19]. [score:5]
Excessive inhibition of miR-27b expression is associated with hyperlipidemia, NAFLD (or NASH), and obesity phenotypes. [score:5]
These results suggest that miR-27b depletion accelerates adipocyte differentiation in zebrafish through the upregulation of adipogenic transcriptional factors that are involved in adipogenesis. [score:4]
PPAR-γ has a highly conserved predicted binding site in its 3′ UTR and was confirmed to be a direct target of miR-27b [18]. [score:4]
Recent reports have identified miR-27b as a regulatory hub in lipid metabolism, with many confirmed metabolic targets [22, 34, 35, 37]. [score:4]
Zou et al., reported that persimmon tannin inhibited adipocyte differentiation of 3T3-L1 cells through regulation of PPAR-γ, C/EBP-α, and miR-27 in the early stage of adipogenesis [19]. [score:4]
Our results suggest parallel lipid metabolic pathways for miR-27b expression in vivo and strong similarities between the lipid metabolisms of miR-27b -mediated regulation in mammals and zebrafish. [score:4]
They demonstrate that hepatic miR-27b is responsive to lipid levels and regulates the expression of two key metabolic genes, angiopoietin-like 3 (ANGPTL3) and glycerol-3-phosphate acyltransferase 1 (GPAM), which have been previously implicated in the pathobiology of dyslipidemia [38, 39]. [score:4]
Relative to the wild-type control, miR-27b was significantly down-regulated 15.4- and 7.8-fold in the livers of hC27bSP1 and hC27bSP2 lines, respectively. [score:4]
They demonstrated that hepatic miR-27b is responsive to lipid levels and regulates the expression (mRNA and protein) of key metabolic genes, including angiopoietin-like 3 (ANGPTL3) and glycerol-3-phosphate acyltransferase 1 (GPAM), which have been previously implicated in the pathobiology of lipid-related disorders [22]. [score:4]
Recent research has demonstrated that miRs are able to regulate the expression of key genes involved in lipid homeostasis, including miR-122, miR-33, miR-106, miR-758, miR-26, miR-370, miR-378, let-7, miR-27, miR-143, miR-34a, and miR-335 [7, 8, 9, 10, 11, 12, 13]. [score:4]
Karbiener et al., found that the anti-adipogenic effect of miR-27b in hMADS cells results from suppression of PPAR-γ [18]. [score:3]
The results demonstrate that the miR-27b-SP is able to block miR-27b expression in vivo. [score:3]
We performed stem-loop RT-PCR to detect expression levels of mature miR-27b in bC27bSPs and hC27bSPs. [score:3]
Consequently, targeting miR-27b may promote energy expenditure that is mediated by WAT conversion to brown adipose tissue (BAT), and potentially prevent obesity. [score:3]
To generate stable mCherry-fused miR-27b-SP expression in zebrafish, the pb-Act-mCherry-miR-27b-SP and LF2.8-mCherry-miR-27b-SP constructs were used to produce germline-transmitting transgenic zebrafish lines, C27bSPs (Figure 2A). [score:3]
They introduced miR-27b mimics or inhibitors (antagomiRs) into human hepatocytes (Huh7 cells). [score:3]
2.4. miR-27b Depletion Increases Expression of Genes Associated with Lipogenesis in C27bSPs. [score:3]
Expression of miR-27b cluster sponge elements (miR-27b-SP) was examined to evaluate its ability to function in vivo to reduce miR-27b expression. [score:3]
With the pb-Act-mCherry-miR-27b-SP construct, zebrafish transgenic lines, bC27bSPs (Tg(-2.5β-Act:mCherry-miR-27b-SP)), were generated in which miR-27b expression was globally eliminated (Figure 2B, panels 1, 2). [score:3]
To study the function of endogenous miR-27b in the zebrafish, we designed a miR-27b-sponge containing 10 copies of the miR-27b binding sites and four nucleotide spacers with mismatches opposite miRNA nucleotides 9–12 to block the inhibitory activity of miR-27b (Figure 1B). [score:3]
With the LF2.8-mCherry-miR-27b-SP construct, zebrafish transgenic lines, hC27bSPs (Tg(-2.8fabp10a:mCherry-miR-27b-SP)), were generated, in which miR-27b expression was specifically eliminated in the liver (Figure 2B, panels 3, 4). [score:3]
The mature miR-27b sequences containing the miR-30e stem-loop region [54] and the miR-27b targeting sequences (TS; 5′-TGCAGAACTTAGCCACTGTGAA-3′) and its mutant sequence (mTS; 5′-TGCAGAACTTAGCCACAAAGAA-3′) were synthesized as DNA oligonucleotides (Invitrogen, Waltham, MA, USA). [score:3]
To evaluate the suppressive activity of the sponge construct in vivo and in vitro, we evaluated whether the sequestration of miR-27b by the sponge products could disrupt the binding of miRNA-27b to target sites in the 3′ UTR of a target mRNA. [score:3]
We hypothesize that that miR-27b may mediate fat accumulation much better than fuel metabolism for inhibiting adipose tissue by energy expenditure. [score:3]
Inhibition of Endogenous miR-27b Increases Endotrophic and Intravascular Lipid Accumulation. [score:3]
Thus, miR-27b depletion resulted in hyperplasia of visceral adipocytes in zebrafish juvenile, implicating an effect of miR-27b expression on post-embryonic growth and larval adipocyte formation in zebrafish. [score:3]
bC27bSPs (Tg(-2.5β-Act:mCherry-miR-27b-SP)) showed global C27bSP expression when driven by the promoter of the β-actin1 gene (GenBank Accession No. [score:3]
Several miRNAs, including miR-27, have been implicated in the process of accelerating or inhibiting preadipocyte differentiation [42, 43, 44, 45, 46]. [score:3]
Correspondingly, an in vivo assay demonstrated that the decreased eGFP fluorescence of pb-Act-EGFP-miR-27b-TS/miR-27b co -expression could be rescued by miR-27b-SP expression in dose -dependent manner as compared with the control group (Figure 1D). [score:3]
Two bC27bSPs (bC27bSP1 and bC27bSP2) and two hC27bSPs (hC27bSP1 and hC27bSP2) transgenic lines were selected based on miR-27b expression (Figure 2C). [score:3]
The microRNA miR-27b is involved in numerous metabolic processes, which are implicated in several diseases, including lipid metabolism [22, 33], atherosclerosis [34, 35], insulin resistance, and type-2 diabetes [36]. [score:3]
Both in vivo and in vitro eGFP reporter assays were performed to confirm the direct interaction of miR-27b-SP and the miR-27b targeting sequence (miR-27b-TS). [score:3]
Because miR-27b depletion can induce endotrophic and intravascular lipid accumulation and hepatic steatosis in zebrafish, we next investigated the effect of miR-27b depletion on the expression of lipogenic and unfolded protein response (UPR) target genes. [score:3]
Kang et al., found that miR-27 is an anti-adipogenic microRNA in part by targeting prohibitin (PHB) and impairing mitochondrial function [20]. [score:3]
Our results are in agreement with a recent study, showing that miR-27b inhibition restored cytoplasmic lipid droplets in rat hepatic stellate cells (HSCs) [40]. [score:3]
Correspondingly, miR-27 was found to inhibit adipocyte differentiation, which is closely associated with the onset of obesity [19, 49]. [score:3]
Kang T. Lu W. Xu W. Anderson L. Bacanamwo M. Thompson W. Chen Y. E. Liu D. MicroRNA-27 (miR-27) targets prohibitin and impairs adipocyte differentiation and mitochondrial function in human adipose-derived stem cellsJ. [score:3]
The transgenic zebrafish line hC27bSPs (Tg(-2.8fabp10a:mCherry-miR-27b-SP)) showed liver-specific expression of mCherry and miR-27b-SP (C27bSP) when driven by the L-FABP 2.8 promoter [56]. [score:3]
Karbiener M. Fischer C. Nowitsch S. Opriessnig P. Papak C. Ailhaud G. Dani C. Amri E. -Z. Schei deler M. microRNA miR-27b impairs human adipocyte differentiation and targets PPAR-γBiochem. [score:3]
We report the novel finding that miR-27b depletion causes endotrophic and intravascular lipid accumulation and hyperlipidemia, as well as an increased expression of several lipogenic marker genes in zebrafish. [score:3]
Furthermore, Vickers et al., provided in silico, in vitro and in vivo evidence that miR-27b is a strong candidate to be a regulatory hub in lipid metabolism [22]. [score:2]
Correspondingly, we provided evidence that miR-27b depletion in the liver is responsible for the development of hepatic steatosis, and even steatohepatitis, which have further combinational effects on inflammatory response and ER stress. [score:2]
The results from this work reveal, for the first time, that miR-27b functions to regulate molecular pathologic signaling pathways that are involved in lipometabolic disorders in zebrafish. [score:2]
This finding highlights the potential importance of functional equivalences of miR-27b for zebrafish adipose tissue, which has also been shown to be closely related to the general development and size of zebrafish. [score:2]
Vickers et al., predicted miR-27b to be a regulatory hub in lipid metabolism [22]. [score:2]
Thus, we performed an eGFP reporter assay using the luciferase reporter pb-Act-eGFP-mir-27b-TS and a vector, with the 3′ UTR of eGFP mRNA containing a perfect target sequence for miR-27b. [score:2]
miR-27b acts as a negative regulator of adipogenesis in rat, mouse, and human cell mo dels [18, 19, 20, 44]. [score:2]
Kong et al., identified that miR-27b is a central upstream regulator of Prdm16 to control browning of WAT [21]. [score:2]
We additionally demonstrated that the hepatic overexpression of miR-27b-SP did not alter the level of endogenous mature miR-27b in other tissues in hC27bSPs when compared with the wild-type (WT) (Figure 2C). [score:2]
We determined the effect of miR-27b depletion on the regulation of pathways that govern lipogenesis and adipogenesis in zebrafish. [score:2]
Recently, results from three research groups have suggested that miR-27b is a negative regulator of adipocyte differentiation. [score:2]
In this study, we identified miR-27b functions as negative regulator for both lipogenesis and adipogenesis in zebrafish. [score:2]
We discovered that oxidative stress significantly increased the quantity of hepatic MDA and the release of H [2]O [2] in hC27bSPs and bC27bSPs; however, no or less effect of oxidative stress was observed in the liver of WT that was fed with the LFD (Figure 5D), suggesting that miR-27b depletion can significantly enhance oxidative stress in zebrafish livers. [score:1]
Real-Time RT-PCR and Quantification of Mature miR-27b. [score:1]
Our in vivo observations indicate that miR-27b depletion yielded adipocyte hyperplasia by the induction of several adipogenic marker genes, including PPAR-γ, C/EBP-α, and SREBP-1c, at terminal differentiation of adipocyte in bC27bSP1. [score:1]
We generated microRNA-sponge (miR-SP) transgenic zebrafish (C27bSP) to analyze the effects of miR-27b depletion on lipid homeostasis. [score:1]
The mutant version of miR-27b-SP (miR-27b-SP-mut) was generated with three nucleotides of the seed binding site sequence for the miR-7 binding site (AC TGTGA) were substituted (AC AAAGA). [score:1]
Despite these observations, to date, no reports are available regarding the impact of miR-27b on lipid metabolism in vivo. [score:1]
To more clearly define the physiological role of endogenous miR-27b in the hepatic response, we generated a liver-specific miR-27b-SP transgenic zebrafish mo del, hC27bSPs. [score:1]
Louis, MO, USA) to perform miR-27b gain-of-function experiments. [score:1]
The transgenic construct pLF2.8-mCherry-miR-27b-SP is similar to constructs that we previously used to generate transgenic zebrafish lines [29, 30, 31, 32, 55, 56] except that the GFP gene was replaced with the mCherry gene, and that miR-27b-SP was inserted at the 3′ end. [score:1]
The resulting vectors were designated as pb-Act-miR-27b, pb-Act-miR-27b-mut, pb-Act-miR-27b-SP, pb-Act-miR-27b-SP-mut, pb-Act-EGFP-miR-27b-TS, pb-Act-EGFP-miR-27b-TS-mut, pb-Act-mCherry-miR-27b-SP, pb-Act-mCherry-miR-27b-SP-mut, pb-Act-eGFP-miR-27b-TS, and pb-Act-eGFP-miR-27b-TS-mut. [score:1]
However, miR-27b has been found to promote adipogenesis. [score:1]
Designing and Testing the Functionality of the miR-27b Sponge. [score:1]
Chronic depletion of miR-27b leads to increased adipogenesis, which in turn, drove fat accumulation (adipocyte hyperplasia) and enhanced weight gain in zebrafish. [score:1]
The miR-27b mimic and its negative control (miR-NC) were ordered from Ribobio (Guangzhou, China) Sigma-Aldrich (Sigma Genosys, St. [score:1]
These data suggest that miR-27b depletion can induce endotrophic and intravascular lipid accumulation in zebrafish larvae. [score:1]
We additionally examined whether miR-27b-SP modulates hypertrophy in the WAT of bC27bSPs accompanying adipogenesis. [score:1]
miR-27b-SP overexpression rescued the reduced GFP intensity of the miR-27b-TS in a consistent manner (Figure 1C) when compared with control GFPs (TS-mut or SP-mut) in in vitro assays. [score:1]
To determine whether miR-27b depletion might have functional relevance in adipose tissues, we examined the phenotype of the white adipose tissues (WAT) of adult bC27bSPs and found that they had a hypertrophic response to obesity or overweightness. [score:1]
In conclusion, our results show that chronic depletion of miR-27b causes an increase in total lipid contents resulting the early onset of hyperlipidemia and NAFLD phenotypes in zebrafish. [score:1]
There was a nearly 3.8- and 2.9-fold reduction in hepatic mature miR-27b in the livers of bC27bSP1 and bC27bSP2 lines, respectively. [score:1]
Antisense oligonucleotides (ASOs) were injected at a working dilution of 50 nM and miR-27b mimics were injected at a range of 0.05–0.2 ng into stage one embryos. [score:1]
The mature miR-27b sequence is perfectly conserved across many species with an identical seed sequence at the 5′ end (Figure 1A). [score:1]
To generate transgenic miR-27b cluster sponge elements (miR-27b-SP), we introduced 10 copies each of complementary sequences to miR-27b (MI0001929), each with mismatches at positions 9–12, into the 3′ UTR of mCherry in the beta-actin constructs [31]. [score:1]
Wang J. M. Tao J. Chen D. D. Cai J. J. Irani K. Wang Q. Yuan H. Chen A. F. MicroRNA miR-27b rescues bone marrow-derived angiogenic cell function and accelerates wound healing in type 2 diabetes mellitusArterioscler. [score:1]
It was demonstrated that miR-27b depletion is sensitive to HFD -induced adipocyte hyperplasia, which at least partially accounts for the weight gain or obesity in bC27bSPs, showing that the bC27bSPs can be used as a mo del for early-onset weight gain. [score:1]
2.6. miR-27b Depletion Induces Early Onset of Adipocyte Hyperplasia in Zebrafish. [score:1]
The aim of the present study was to explore the effects of depletion of miR-27b on the lipid metabolism of both larval and adult zebrafish. [score:1]
In addition, Kong et al., demonstrated that miR-27b plays a central role in the pathogenesis of glucocorticoid (GC) -induced central fat accumulation [21]. [score:1]
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[+] score: 29
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-20a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-92a-1, hsa-mir-92a-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-15b, mmu-mir-23b, mmu-mir-27b, mmu-mir-130a, mmu-mir-133a-1, mmu-mir-140, mmu-mir-24-1, hsa-mir-196a-1, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-206, hsa-mir-30c-2, hsa-mir-196a-2, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-200b, mmu-mir-301a, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-23b, hsa-mir-27b, hsa-mir-130a, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-140, hsa-mir-206, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-196a-1, mmu-mir-196a-2, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-18a, mmu-mir-20a, mmu-mir-24-2, mmu-mir-27a, mmu-mir-92a-2, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-17, mmu-mir-19a, mmu-mir-200c, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-19b-1, mmu-mir-92a-1, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-301a, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, hsa-mir-196b, mmu-mir-196b, dre-mir-196a-1, dre-mir-199-1, dre-mir-199-2, dre-mir-199-3, hsa-mir-18b, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-1-2, dre-mir-1-1, dre-mir-15a-1, dre-mir-15a-2, dre-mir-15b, dre-mir-17a-1, dre-mir-17a-2, dre-mir-18a, dre-mir-18b, dre-mir-18c, dre-mir-19a, dre-mir-20a, dre-mir-23b, dre-mir-24-4, dre-mir-24-2, dre-mir-24-3, dre-mir-24-1, dre-mir-27a, dre-mir-27c, dre-mir-27d, dre-mir-27e, dre-mir-30c, dre-mir-92a-1, dre-mir-92a-2, dre-mir-92b, dre-mir-130a, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-140, dre-mir-196a-2, dre-mir-196b, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-206-1, dre-mir-206-2, dre-mir-301a, dre-let-7j, hsa-mir-92b, mmu-mir-666, mmu-mir-18b, mmu-mir-92b, mmu-mir-1b, dre-mir-196c, dre-mir-196d, mmu-mir-3074-1, mmu-mir-3074-2, hsa-mir-3074, mmu-mir-133c, mmu-let-7j, mmu-let-7k, dre-mir-24b
miRNA Embryonic age Expression profile mir15a 48 and 72 hpf Midbrain, MHB, notochord mir15b 48 and 72 hpf Midbrain, neurocranium, notochord mir23b 30, 48, and 72 hpf Somites, lens, pharyngeal arches, notochord mir27b 48 and 72 hpf mir30c 48 and 72 hpf Brain, neurocranium, eye, heart mir130a 48 and 72 hpf Brain, gut tube, heart, eye mir133b 30, 48, and 72 hpf Notochord mir301a 48 and 72 hpf Forming cartilage Midbrain, neurocranium, eye, trigeminal ganglia Figure 5 Expression of mir23b in zebrafish embryos. [score:5]
miRNA Embryonic age Expression profile mir15a 48 and 72 hpf Midbrain, MHB, notochord mir15b 48 and 72 hpf Midbrain, neurocranium, notochord mir23b 30, 48, and 72 hpf Somites, lens, pharyngeal arches, notochord mir27b 48 and 72 hpf mir30c 48 and 72 hpf Brain, neurocranium, eye, heart mir130a 48 and 72 hpf Brain, gut tube, heart, eye mir133b 30, 48, and 72 hpf Notochord mir301a 48 and 72 hpf Forming cartilage Midbrain, neurocranium, eye, trigeminal ganglia Figure 5 Expression of mir23b in zebrafish embryos. [score:5]
One of the interesting aspects our data analysis (Figure 1) is that Mir27b expression is also present in the developing midface, with its expression mirroring that of Mir23b. [score:5]
mir23b and mir27b are separated by less than 200 bp, though it is not clear that their expression is co-regulated. [score:4]
Cardiomyocyte overexpression of miR-27b induces cardiac hypertrophy and dysfunction in mice. [score:3]
MicroRNA profiling during mouse ventricular maturation: a role for miR-27 modulating Mef2c expression. [score:3]
This is especially true for Mir23b and Mir27b, as while both work concurrently to drive cardiomyocyte development from ES cells in vitro, Mir23b subsequently controls the later beating phenotype of differentiated cells while Mir27b functions to inhibit this event (Chinchilla et al., 2011; Wang et al., 2012). [score:3]
In mouse, Mir23b is part of a miRNA cluster that includes Mir23b, Mir27b, Mir3074.1, and Mir24.1. [score:1]
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[+] score: 7
Zhou J. H. Zhou Q. Z. Lyu X. M. Zhu T. Chen Z. J. Chen M. K. Xia H. Wang C. Y. Qi T. Li X. The Expression of Cysteine-Rich Secretory Protein 2 (CRISP2) and Its Specific Regulator miR-27b in the Spermatozoa of Patients with AsthenozoospermiaBiol. [score:4]
It has been demonstrated that high expression of miR-27b has a significant relationship with low sperm progressive motility in humans [30]. [score:3]
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[+] score: 6
Different members of these miRNA families were presented in different lineages ranging from urochordates to mammals, as we can see in Table 2. miR-27 was not found in sea squirt or any other invertebrates, indicating that the miR-27 gene likely originated in fishes. [score:1]
Sequence comparison of miR-27, miR-30 and miR-181 family members in zebrafish and human. [score:1]
Up to now, five members of the miR-27 family have been found. [score:1]
Alignments were carried out within miR-27, miR-30 and miR-181 family of zebrafish and human, respectively (Figure 7). [score:1]
miR-27, miR-30 and miR-181 family members in different lineages. [score:1]
Three miRNA families, miR-27, miR-30 and miR-181, were analyzed to determine gain and loss of miRNA family members and changes in their sequences (miRNA sequences were downloaded from miRBase). [score:1]
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[+] score: 5
In mammals, miR-27 plays regulatory roles during megakaryocytic and granulocytic differentiation by attenuating Runx1 expression and engaging in feedback loops with Runx1 [64]. [score:4]
Conservation of miR-27 binding sites, coupled with the presence of miR-27 in the elephant shark (GenBank Accession number JX994340) suggests that CmRunx1 may similarly be post-transcriptionally controlled by miR-27 in hematopoietic lineages of the elephant shark. [score:1]
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[+] score: 3
miRNA mimics (miR-27 a and miR-24), miRNA inhibitors (Anti-27a and Anti-24) and negative control molecules (Scramble) were obtained from Dharmacon (Austin, TX, USA) and transfected with DharmFECT1 (Dharmacon, Austin, TX, USA) at a final concentration of 60 nM. [score:3]
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[+] score: 3
Compared with their results, which were performed by microarray screening, we also identified similar miRNAs up- or down-regulated in early EPC (up: let-7 g-5p, miR-16-5p, miR-26b-5p, miR-30b-3p, miR-140-5p, miR-146a-5p, miR-146a-3p and miR-338-3p) or in late EPC (miR-27a-3p, miR-27b-5p, miR-27b-3p, miR-151a-5p and miR-193a-5p). [score:3]
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8
[+] score: 2
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-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-31, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10b, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-204, hsa-mir-212, hsa-mir-181a-1, hsa-mir-221, hsa-mir-23b, hsa-mir-27b, hsa-mir-128-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-200c, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-200a, hsa-mir-30e, hsa-mir-148b, hsa-mir-338, hsa-mir-133b, dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-10b-1, dre-mir-181b-1, dre-mir-181b-2, dre-mir-199-1, dre-mir-199-2, dre-mir-199-3, dre-mir-203a, dre-mir-204-1, dre-mir-181a-1, dre-mir-221, dre-mir-222a, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7e, dre-mir-7a-3, dre-mir-10b-2, dre-mir-20a, dre-mir-21-1, dre-mir-21-2, dre-mir-23a-1, dre-mir-23a-2, dre-mir-23a-3, dre-mir-23b, dre-mir-24-4, dre-mir-24-2, dre-mir-24-3, dre-mir-24-1, dre-mir-26b, dre-mir-27a, dre-mir-29b-1, dre-mir-29b-2, dre-mir-29a, dre-mir-30e-2, dre-mir-101b, dre-mir-103, dre-mir-128-1, dre-mir-128-2, dre-mir-132-1, dre-mir-132-2, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-143, dre-mir-148, dre-mir-181c, dre-mir-200a, dre-mir-200c, dre-mir-203b, dre-mir-204-2, dre-mir-338-1, dre-mir-338-2, dre-mir-454b, hsa-mir-181d, dre-mir-212, dre-mir-181a-2, hsa-mir-551a, hsa-mir-551b, dre-mir-31, dre-mir-722, dre-mir-724, dre-mir-725, dre-mir-735, dre-mir-740, hsa-mir-103b-1, hsa-mir-103b-2, dre-mir-2184, hsa-mir-203b, dre-mir-7146, dre-mir-181a-4, dre-mir-181a-3, dre-mir-181a-5, dre-mir-181b-3, dre-mir-181d, dre-mir-204-3, dre-mir-24b, dre-mir-7133, dre-mir-128-3, dre-mir-7132, dre-mir-338-3
26 +2.14 miR-132 +1.83 (1.71e-3) +0.52 miR-2184 -2.63 (2.54e-5) -2.25 -2.50 miR-222a +1.54 (1.13e-2) +3.24 miR-24 -1.36 (1.9e-2) -1.41 -0.73 miR-454b +1.14 (4.93e-2) +0.14 miR-133a -1.72 (2.67e-3) -4.25 -5.07 miR-101b -2.52 (3.44e-5) -3.43 miR-338 -2.23 (1.90e-4) -2.90 -1.57 miR-26b -1.91 (1.84e-3) -3. 67 miR-204 -2.60 (4.76e-5) -0.57 -2.36 miR-203b -1.77 (3.45e3 -0.21 miR-10b -1.36 (2.90e-2) -1.78 miR-725 -1.29 (3.23e-2) -1.62 Zebrafish + Axolotl Zebrafish SymbolZebrafish log [2] Fold-change (p-value)Axolotl log [2] Fold-change SymbolZebrafish log [2] Fold-change (p-value) miR-27a +1.57 (7.96e-3) +2.15 miR-27b +1.38 (2.44e-2) miR-29b -2.05 (1.28e-2) -0.97 miR-143 +1.31 (2.89e-2) miR-30e +1.18 (4.80e-2) miR-200c -1.85 (1.72e-3) miR-200a -1.74 (3.66e-3) miR-23a -1.35 (2.05e-2) 10. [score:1]
26 +2.14 miR-132 +1.83 (1.71e-3) +0.52 miR-2184 -2.63 (2.54e-5) -2.25 -2.50 miR-222a +1.54 (1.13e-2) +3.24 miR-24 -1.36 (1.9e-2) -1.41 -0.73 miR-454b +1.14 (4.93e-2) +0.14 miR-133a -1.72 (2.67e-3) -4.25 -5.07 miR-101b -2.52 (3.44e-5) -3.43 miR-338 -2.23 (1.90e-4) -2.90 -1.57 miR-26b -1.91 (1.84e-3) -3. 67 miR-204 -2.60 (4.76e-5) -0.57 -2.36 miR-203b -1.77 (3.45e3 -0.21 miR-10b -1.36 (2.90e-2) -1.78 miR-725 -1.29 (3.23e-2) -1.62 Zebrafish + Axolotl Zebrafish SymbolZebrafish log [2] Fold-change (p-value)Axolotl log [2] Fold-change SymbolZebrafish log [2] Fold-change (p-value) miR-27a +1.57 (7.96e-3) +2.15 miR-27b +1.38 (2.44e-2) miR-29b -2.05 (1.28e-2) -0.97 miR-143 +1.31 (2.89e-2) miR-30e +1.18 (4.80e-2) miR-200c -1.85 (1.72e-3) miR-200a -1.74 (3.66e-3) miR-23a -1.35 (2.05e-2) 10. [score:1]
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9
[+] score: 1
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-18a, hsa-mir-21, hsa-mir-27a, hsa-mir-96, hsa-mir-99a, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30b, mmu-mir-99a, mmu-mir-124-3, mmu-mir-125b-2, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-181a-2, mmu-mir-182, mmu-mir-183, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, hsa-mir-181a-2, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-181a-1, hsa-mir-200b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-18a, mmu-mir-21a, mmu-mir-27a, mmu-mir-96, mmu-mir-135b, mmu-mir-181a-1, mmu-mir-199a-2, mmu-mir-135a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-125b-1, hsa-mir-200a, hsa-mir-135b, dre-mir-182, dre-mir-183, dre-mir-181a-1, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-15a-1, dre-mir-15a-2, dre-mir-18a, dre-mir-21-1, dre-mir-21-2, dre-mir-27a, dre-mir-27c, dre-mir-27d, dre-mir-27e, dre-mir-30b, dre-mir-96, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-125b-1, dre-mir-125b-2, dre-mir-125b-3, dre-mir-135c-1, dre-mir-135c-2, dre-mir-200a, dre-mir-200b, dre-let-7j, dre-mir-135b, dre-mir-181a-2, dre-mir-135a, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, dre-mir-181a-4, dre-mir-181a-3, dre-mir-181a-5, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
A few miRNAs were identified in the enrichment analysis, such as miR-181a, miR114, miR-200a and miR-27, suspected as being active miRNAs in the regeneration. [score:1]
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