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8 publications mentioning gga-mir-33-2

Open access articles that are associated with the species Gallus gallus and mention the gene name mir-33-2. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 315
Other miRNAs from this paper: gga-mir-33-1
Since miR-33 inhibits the expression of FTO, it might play a role in mediating the nutritional regulation of FTO expression in chicken liver. [score:8]
Using LNA-anti-miR-33, we successfully reduced the expression of endogenous miR-33 in primary chicken hepatocytes, and this reduction was associated with an up-regulated expression of FTO mRNA. [score:8]
These results indicate that miR-33 can inhibit FTO expression by directly interacting with the predicted target site in the FTO 3′UTR. [score:8]
These inverse changes in miR-33 and FTO mRNA expression suggest that miR-33 may be one of the negative regulators of FTO mRNA expression in the chicken liver during development. [score:7]
miR-33 Knockdown Up-regulated FTO mRNA Expression in Primary Chicken Hepatocytes. [score:7]
miR-33 Knockdown Up-regulated FTO mRNA Expression in Primary Chicken HepatocytesThe FTO gene appears to play a role in lipid metabolism and energy homeostasis [23], [27]. [score:7]
However, our expression data did not support co-regulation of SREBF2 and miR-33 expression across 10 types of chicken tissues examined. [score:6]
Specifically, we determined if knockdown of miR-33 expression by LNA-anti-miR-33 would increase FTO mRNA expression in primary chicken hepatocytes. [score:6]
Computational prediction of partial miR-33 target genes by Targetscan. [score:5]
Inverse Correlation of miR-33 and FTO mRNA Expression in Chicken Liver at Different Developmental StagesTo further evaluate the possibility that FTO expression is negatively regulated by miR-33 in chicken liver, we quantified miR-33 and FTO mRNA in chicken liver at 8 different ages using real-time qRT-PCR. [score:5]
Expression of miR-33 and SREBF2 Gene in Various Chicken TissuesThe expression of miR-33 in 10 types of tissues from 4 week-old chickens was analyzed using real-time qRT-PCR. [score:5]
The objectives of this study were to determine whether miR-33 is expressed in the chicken, and, if so, to identify its target genes. [score:5]
The expression of miR-33 was normalized to 18S rRNA, and the expression of SREBF2 mRNA was normalized to β-actin mRNA. [score:5]
To determine whether the putative miR-33 target sequence in the FTO 3′UTR mediates translational repression by miR-33, we inserted the 3′UTR of the chicken FTO transcript downstream of a luciferase reporter gene to generate the reporter plasmid pMIR-FTO (Fig. 3). [score:5]
In addition, a variety of online target prediction software was used to predict the targets of miR-33. [score:5]
The chicken FTO 3′UTR encompassing the predicted miR-33 binding site was amplified by PCR and directionally inserted downstream of the luciferase expression cassette of the pMIR-reporter vector (Ambion, Carlsbad, CA) at the SacI and HindIII sites to construct the pMIR-FTO reporter vector. [score:4]
The correlation coefficient between miR-33 and FTO mRNA expression in chicken liver at different developmental stages was −0.669 (P = 0.07)(Fig. 6B). [score:4]
One of the predicted target genes of miR-33 named FTO is a member of the non-heme dioxygenase superfamily, and has been recently implicated in regulation of lipid and energy metabolism [22], [23]. [score:4]
microRNA-33 (miR-33) is transcribed from an intronic region within the sterol response element binding transcription factor 2 (SREBF2), also called sterol response element binding protein-2 gene [5], which directly activates the expression of more than 30 genes involved in the synthesis and uptake of cholesterol, fatty acids, triglycerides, and phospholipids [6], [7]. [score:4]
The expression levels of miR-33 and SREBF2 are closely paralleled in human or mouse hepatocytes and macrophages [5], [10], suggesting that they are coregulated at the transcriptional level. [score:4]
We also observed that miR-33 and FTO mRNA expression were inversely correlated in chicken liver at most of the developmental ages examined. [score:4]
miR-33 might be involved in lipid metabolism and energy homeostasis in the chicken by negatively regulating the expression of the FTO gene in the liver. [score:4]
This inverse relationship further supports the possibility that miR-33 negatively regulates FTO expression in chicken liver. [score:4]
0091236.g005 Figure 5Effect of miR-33 knockdown on the expression of miR-33 and FTO mRNA in primary chicken hepatocytes. [score:4]
These data suggest the possibility that miR-33 negatively regulates the expression of FTO mRNA in chicken liver. [score:4]
This suggests that the expression of FTO at these two stages may be regulated predominantly by mechanisms other than miR-33. [score:4]
We also provide evidence suggesting that miR-33 may regulate the expression of the FTO gene in the chicken liver. [score:4]
Effect of miR-33 knockdown on the expression of miR-33 and FTO mRNA in primary chicken hepatocytes. [score:4]
Inverse Correlation of miR-33 and FTO mRNA Expression in Chicken Liver at Different Developmental Stages. [score:4]
0091236.g002 Figure 2Expression profile of miR-33 and SREBF2 mRNA in chicken tissues. [score:3]
The PCR product was cloned into the pcDNA3.1 (+) vector (Invitrogen, Carlsbad, CA) at the HindIII and XhoI restriction sites to generate the chicken miR-33 over -expression vector pcDNA3.1-miR-33. [score:3]
The correlation coefficient (R) between miR-33 and SREBF2 mRNA expression in different chicken different tissues was −0.268 (P>0.05). [score:3]
Transfection of LNA-anti-miR-33 into chicken hepatocytes decreased miR-33 expression by 44% (Fig. 5A). [score:3]
The expression levels of miR-33 and SREBF2 mRNA in 10 tissues from 4-wk-old chickens were analyzed by real-time qRT-PCR. [score:3]
The expression level of miR-33 was detected by real-time qRT-PCR. [score:3]
Interacting sites with miR-33 in the 3′UTR of predicted target genes are in parentheses. [score:3]
A. The expression levels of miR-33 and FTO mRNA in chicken liver from 0 to 49 d of ages were analyzed by qRT-PCR. [score:3]
The expression of miR-33 in 10 types of tissues from 4 week-old chickens was analyzed using real-time qRT-PCR. [score:3]
Computational Prediction of miR-33 Target Genes. [score:3]
Expression profile of miR-33 and SREBF2 mRNA in chicken tissues. [score:3]
C2C12 cells were transfected with the control vector pcDNA3.1 or the miR-33 over -expression vector pcDNA3.1-miR-33. [score:3]
0091236.g006 Figure 6Expression levels of chicken miR-33 and FTO mRNA in chicken liver at different postnatal ages. [score:3]
Expression levels of chicken miR-33 and FTO mRNA in chicken liver at different postnatal ages. [score:3]
Of the 11,891 chicken 3′UTRs in the 3′UTR database, 378 were predicted to be targeted by miR-33. [score:3]
B. Expression levels of chicken miR-33 and FTO mRNA in liver from 0 to 49 d of ages are negatively correlated (P = 0.07), as determined by a regression analysis. [score:3]
The expression of miR-33 and FTO mRNA was detected 48 h post-transfection. [score:3]
The middle panel shows complementarity between miR-33 and predicted target site in the FTO 3′UTR. [score:3]
Top targets of miR-33 (total context score <−0. [score:3]
We found that the expression of miR-33 was increased, whereas that of FTO mRNA was decreased from 0 to 49 days of age (Fig. 6A). [score:3]
Successful overexpression of miR-33 was validated by real-time qRT-PCR (Fig. 4A). [score:3]
Expression of miR-33 and SREBF2 Gene in Various Chicken Tissues. [score:3]
In this study, 378 genes were predicted as the target genes of miR-33 among the total 11,891 chicken genes within the 3′UTR database using “miRanda”. [score:3]
In addition to regulating cholesterol transport, high-density lipoprotein metabolism and fatty acid β-oxidation, miR-33 was recently reported to regulate cell cycle progression and cellular proliferation [12], inflammatory response [13] and insulin signaling [14]. [score:3]
A: Verification of over -expression of miR-33 in C2C12 cells. [score:3]
Dual-luciferase reporter assays and site mutation analyses validated that chicken FTO was a target gene of miR-33. [score:3]
A number of miR-33 targets have been identified, including the ABCA1, ABCG1 and NPC-1 genes, which are involved in cholesterol efflux and high-density lipoprotein metabolism [5], [8], [11], and the CPT1A, CROT and HADHB genes, which are involved in fatty acid β-oxidation [11]. [score:3]
In conclusion, chicken miR-33 is transcribed from intron 16 of the chicken SREBF2 gene and is expressed in various chicken tissues. [score:3]
This association supports that the FTO gene is targeted by miR-33 in chicken hepatocytes. [score:3]
We also constructed a similar plasmid, pMIR-FTOmut, in which the putative miR-33 binding site in the FTO 3′UTR was partially mutated, and a chicken miR-33 over -expression vector named pcDNA3.1-miR-33. [score:3]
A: Expression levels of miR-33. [score:3]
miR-33 is expressed in numerous mammalian cell types and tissues [8], [9]. [score:3]
After 48 h, total RNA was isolated and used to quantify the expression level of miR-33. [score:3]
The expression levels of miR-33 and SREBF2 mRNA did not parallel in most of the tissues analyzed (Fig. 2). [score:3]
miR-33 is an intronic miRNA, and its expression levels paralleled those of its host gene SREBF2 in diverse cell types, including hepatocytes and macrophages in the human and mouse [8], [10]. [score:3]
Because in chickens de novo fatty acid synthesis occurs primarily in the liver, we further studied the possibility that miR-33 targets FTO in the chicken liver. [score:3]
Verification of the Interaction between miR-33 and the FTO 3′UTROne of the predicted miR-33 targets is the FTO gene. [score:3]
To determine if miR-33 targets the FTO 3′UTR, C2C12 cells were seeded in 24-well plates for 24 h before transfection. [score:3]
At day 35 and day 42 of age, the expressions of miR-33 and FTO mRNA were not inversely correlated. [score:3]
miR-33 expression was detected in all 10 chicken tissues with the highest level in the heart (Fig. 2). [score:3]
To overexpress miR-33, cells were seeded at a density of 1.5×10 [5] cells/ml in 6-well plates for 24 h and transfected with pcDNA3.1-miR-33 using the X-tremeGENE 9 DNA Transfection Reagent (Roche) as described previously [25]. [score:3]
To predict the target genes of chicken miR-33, the chicken 3′UTRs were analyzed for potential binding sites of miR-33 by the computational algorithm “miRanda”. [score:3]
One of the predicted miR-33 targets is the FTO gene. [score:3]
In this paper, we provide computational and experimental evidence demonstrating that miR-33 is expressed in the chicken. [score:3]
The expression of miR-33 was quantified by real-time qRT-PCR according to the protocol of TaqMan MicroRNA Assay (Applied Biosystems, Foster City, CA). [score:2]
Point mutations in the seed region of the predicted miR-33 binding sequence within the 3′UTR of chicken FTO were generated using overlap-extension PCR, and the resulting plasmid was named pMIR-FTOmut. [score:2]
Research by multiple groups has shown that miR-33 analogs regulate cholesterol and fatty acid metabolism in mammalian systems, corresponding with the function of its host gene [10], [11]. [score:2]
Co-transfection of pcDNA3.1-miR-33 resulted in a decrease in luciferase activity expressed from pMIR-FTO, compared with co-transfection of pcDNA3.1 (P<0.05, Fig. 4B). [score:2]
This decrease was abolished by mutation of the miR-33 binding site in the FTO 3′UTR (Fig. 4B). [score:2]
To further evaluate the possibility that FTO expression is negatively regulated by miR-33 in chicken liver, we quantified miR-33 and FTO mRNA in chicken liver at 8 different ages using real-time qRT-PCR. [score:2]
The miR-33 family has been predicted to be present in several mammalian species, including human, rat, mouse, and cow. [score:1]
We transfected C2C12 cells with the pMIR-FTO or pMIR-FTOmut reporter vector, and pcDNA3.1-miR-33 or pcDNA3.1 (empty vector). [score:1]
8 m: An exact match to positions 1–8 of miR-33; 7m+m8: An exact match to positions 2–8 of miR-33; 7m+1A: An exact match to positions 2–7 of miR-33 followed by an ‘A’. [score:1]
Chicken hepatocytes were transfected with 80 nM miRCURY LNA-anti-miR-33 or LNA scramble control (Exiqon, Woburn, USA) utilizing X-tremeGENE HP DNA transfection reagent (Roche, Mannheim, Germany). [score:1]
Wild type and the miR-33 binding site-mutated FTO 3′UTR were cloned into the reporter vector. [score:1]
A miR-33 stem-loop is predicted from intron 16 of SREBF2, and the sequence of this part of the SREBF2 gene is highly conserved across mammalian species (mmu: mouse; rno: rat; bta: cow; hsa: human) and chicken (gga: chicken). [score:1]
0091236.g004 Figure 4Verification of the interaction between miR-33 and the FTO 3′UTR. [score:1]
Prediction of transcription of chicken miR-33 from the chicken SREBF2 gene. [score:1]
miR-33 is Predicted from Intron 16 of the Chicken SREBF2 GeneThe miR-33 family has been predicted to be present in several mammalian species, including human, rat, mouse, and cow. [score:1]
org/) were employed to predict miR-33 binding sites in chicken 3′UTRs. [score:1]
miR-33 is Predicted from Intron 16 of the Chicken SREBF2 Gene. [score:1]
pMIR-FTO (Firefly luciferase) or pMIR-mutFTO, pcDNA3.1-miR-33 or pcDNA3.1-NC-miRNA and transfection efficiency control pRL-CMV (Renilla luciferase) were mixed and co -transfected into the cells using X-tremeGENE 9 DNA Transfection Reagent (Roche). [score:1]
0091236.g001 Figure 1Prediction of transcription of chicken miR-33 from the chicken SREBF2 gene. [score:1]
B: Reporter gene analysis of the interaction between miR-33 and FTO 3′UTR. [score:1]
miR-33 and FTO mRNA were quantified by real-time qRT-PCR 48 h after transfection. [score:1]
Primary chicken hepatocytes were transfected with LNA-anti-miR-33 or LNA scramble control. [score:1]
Verification of the interaction between miR-33 and the FTO 3′UTR. [score:1]
Aligning the chicken SREBF2 and SREBF1 DNA sequences with the corresponding human, mouse, rat, and cow sequences revealed that intron 16 of the chicken SREBF2 gene might encode the chicken miR-33 (Fig. 1). [score:1]
In some species there is a single member of this family which gives the mature product miR-33. [score:1]
Verification of the Interaction between miR-33 and the FTO 3′UTR. [score:1]
C2C12 cells were co -transfected with pMIR-FTO or pMIR-FTOmut and pcDNA3.1 or pcDNA3.1-miR-33. [score:1]
A DNA fragment containing the predicted miR-33 and 150 bp upstream and 150 bp downstream sequences was amplified by PCR from chicken genomic DNA. [score:1]
In the present study we predicted computationally and validated experimentally the transcription of miR-33 from intron 16 of the chicken SREBF2 gene. [score:1]
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2
[+] score: 19
Other miRNAs from this paper: hsa-let-7d, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-17, hsa-mir-21, hsa-mir-22, hsa-mir-30a, hsa-mir-32, hsa-mir-33a, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-147a, hsa-mir-34a, hsa-mir-187, hsa-mir-204, hsa-mir-205, hsa-mir-200b, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-138-2, hsa-mir-142, hsa-mir-144, hsa-mir-125b-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-190a, hsa-mir-200c, hsa-mir-155, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-365b, hsa-mir-328, gga-mir-33-1, gga-mir-125b-2, gga-mir-155, gga-mir-17, gga-mir-148a, gga-mir-138-1, gga-mir-187, gga-mir-32, gga-mir-30d, gga-mir-30b, gga-mir-30a, gga-mir-30c-2, gga-mir-190a, gga-mir-204-2, gga-mir-138-2, gga-let-7d, gga-let-7f, gga-mir-146a, gga-mir-205b, gga-mir-200a, gga-mir-200b, gga-mir-34a, gga-mir-30e, gga-mir-30c-1, gga-mir-205a, gga-mir-204-1, gga-mir-23b, gga-mir-142, hsa-mir-449a, hsa-mir-489, hsa-mir-146b, hsa-mir-548a-1, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-33b, hsa-mir-449b, gga-mir-146b, gga-mir-147, gga-mir-489, gga-mir-449a, hsa-mir-449c, gga-mir-21, gga-mir-144, gga-mir-460a, hsa-mir-147b, hsa-mir-190b, gga-mir-22, gga-mir-460b, gga-mir-1662, gga-mir-1684a, gga-mir-449c, gga-mir-146c, gga-mir-449b, gga-mir-2954, hsa-mir-548aa-1, hsa-mir-548aa-2, 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-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, gga-mir-365b, gga-mir-125b-1, gga-mir-190b, gga-mir-449d, gga-mir-205c
We noticed the miR-33-5p, miR-460a-5p, miR-365b-5p, miR-125b-5p and miR-2954 correlated with inflammatory genes including MEOX2, IL-1BETA, TRAF2, TNFRSF1B and MAP3K8, and except for the up-regulated miR-33-5 correlated with under expression of MEOX2, other down-regulated miRNAs all correlated with overexpression targets. [score:13]
Likewise, from the miRNA-mRNA association, the under expressed genes LZTFL1, JAZF1, THBS2 and RPS14 were associated with microRNAs (miR-146b-5p, miR-1684a-3p, miR-460b-3p, miR-30e-5p, miR-33-5p, miR-148a-5p, miR-32-5p, miR-155 and miR-144-3p) that were down-regulated in pulmonary arteries (Figure 4). [score:6]
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3
[+] score: 17
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-15a, hsa-mir-18a, hsa-mir-33a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, mmu-mir-27b, mmu-mir-126a, mmu-mir-128-1, mmu-mir-140, mmu-mir-146a, mmu-mir-152, mmu-mir-155, mmu-mir-191, hsa-mir-10a, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, mmu-mir-297a-1, mmu-mir-297a-2, hsa-mir-27b, hsa-mir-128-1, hsa-mir-140, hsa-mir-152, hsa-mir-191, hsa-mir-126, hsa-mir-146a, mmu-let-7a-1, mmu-let-7a-2, mmu-mir-15a, mmu-mir-18a, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-342, hsa-mir-155, mmu-mir-107, mmu-mir-10a, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-33, mmu-mir-211, hsa-mir-374a, hsa-mir-342, gga-mir-33-1, gga-let-7a-3, gga-mir-155, gga-mir-18a, gga-mir-15a, gga-mir-218-1, gga-mir-103-2, gga-mir-107, gga-mir-128-1, gga-mir-140, gga-let-7a-1, gga-mir-146a, gga-mir-103-1, gga-mir-218-2, gga-mir-126, gga-let-7a-2, gga-mir-27b, mmu-mir-466a, mmu-mir-467a-1, hsa-mir-499a, hsa-mir-545, hsa-mir-593, hsa-mir-600, hsa-mir-33b, gga-mir-499, gga-mir-211, gga-mir-466, mmu-mir-675, mmu-mir-677, mmu-mir-467b, mmu-mir-297b, mmu-mir-499, mmu-mir-717, hsa-mir-675, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-297c, 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-466d, hsa-mir-297, mmu-mir-467e, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-467f, mmu-mir-466j, mmu-mir-467g, mmu-mir-467h, hsa-mir-664a, hsa-mir-1306, hsa-mir-1307, gga-mir-1306, hsa-mir-103b-1, hsa-mir-103b-2, gga-mir-10a, mmu-mir-1306, mmu-mir-3064, 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-466, hsa-mir-3173, hsa-mir-3618, hsa-mir-3064, hsa-mir-499b, mmu-mir-466q, hsa-mir-664b, gga-mir-3064, mmu-mir-126b, mmu-mir-3618, mmu-mir-466c-3, gga-mir-191
Several independent studies in chicken have similarly indicated that gga-mir-33 and its host gene SREBF2 are highly expressed in the liver, suggesting involvement in expression upregulation of genes related to cholesterol biosynthesis [80], [81]. [score:8]
Out of the 26 miRNA/host gene pairs with coordinated expression, 11 have been found to be coordinately expressed in both, human and mouse [19], [27], [59], [61]– [64], [67]– [69], [71], [73]– [79]: mir-103/ PANK3, mir-107/ PANK1, mir-126/ EGFL7, mir-128-1/ R3HDM1, mir-140/ WWP2, mir-211/ TRPM1, mir-218-1/ SLIT2, mir-218-2/ SLIT3, mir-27b/ C9orf3, mir-33/ SREBF2, and mir-499/ MYH7B. [score:5]
Moreover, two miRNA/host gene pairs have been found to have expression patterns associated with the same phenotype in both species: mir-499/ MYH7B with heart development [79] and mir-33/ SREBF2 with cholesterol homeostasis [74], [75], [77]. [score:4]
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4
[+] score: 14
Other miRNAs from this paper: hsa-let-7c, hsa-mir-33a, gga-mir-33-1, gga-let-7c, hsa-mir-33b
Moreover, miR-33 [*] targets the key transcriptional regulators of lipid metabolism, including SRC1, SRC3, NFYC, and RIP140 [10]. [score:4]
Together, these data support a regulatory role for miR-33a-3p and suggest that miR-33 inhibits tumor cell proliferation and metastasis by both arms of the miR-33a /miR-33a-3p duplex. [score:4]
Members of miR-33 family are intronic miRNAs that are located within the sterol regulatory element -binding protein (SREBP) genes and function as regulators of glucose and lipid metabolism [10, 11]. [score:3]
Research from Goedeke et al. showed that miR-33 [*] and miR-33 share the same targets involved in cholesterol efflux (ABCA1 and NPC1), fatty acid metabolism (CROT and CPT1a), and insulin signaling (IRS2) [10]. [score:3]
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5
[+] score: 11
MiR-33, which is expressed from an intron of the SREBP-2 gene, represses expression of SREBP-1c in mice [34], and it reduces fatty acid oxidation in human hepatic cells [35]. [score:4]
One novel miRNA identified, nc- miR-33 was shown to regulate expression of FASN. [score:4]
Subsequently, chicken miR-33 was shown to repress expression of the chicken fat mass and obesity associated gene [17]. [score:3]
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6
[+] score: 9
In mammals, a number of miRNAs have been demonstrated to target genes involved in adipogenesis and lipid metabolism, such as the regulation on the proliferation of adipose tissue-derived mesenchymal stem cells by miR-21 and miR-196a [4– 6]; the enhancement of adipogenesis by miR-103, miR-224 and the miR-17–92 cluster [7– 9]; the impairment of adipogenesis by the let-7 family, miR-448, miR-15a and miR-27 [10– 13]; the regulation of adipocyte lipid metabolism by miR-27a and miR-143 [13– 15]; and the important role of miR-33 on the repression of sterol transporters reported in numerous studies [16– 24]. [score:5]
One study examined the role of miR-33 on the regulation of FTO gene, which is important in adipose tissue development [24]. [score:3]
The most interesting miRNA could be miR-33, reported in a number of studies [16– 24], which is highly important on cholesterol homeostasis by repressing sterol transporters. [score:1]
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7
[+] score: 6
miR-33 is another miRNA involved in liver metabolism: it regulates cholesterol efflux and high-density lipoprotein metabolism by targeting ATP -binding cassette, sub -family A (ABC1), member 1 and ATP -binding cassette, sub -family G (WHITE), member 1 [19], and it reduces fatty acid degradation by targeting multiple genes involved in fatty acid β-oxidation [20]. [score:6]
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8
[+] score: 5
More than 50 miRNAs have been identified in chicken liver [27- 29], but only miR-33 has been experimentally verified to target the FAS gene in chicken fibroblast cells [30]. [score:3]
Recently, miR-33, which is located in the intron of SREBPs, was reported to regulate cholesterol metabolism [23, 24]. [score:2]
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