Ignet

Gene Information

Gene symbol: MIRN93

Gene name: microRNA 93

HGNC ID: 31645

Related Genes

#	Gene Symbol	Number of hits
1	ADIPOQ	1 hits
2	INS	1 hits
3	MCM7	1 hits
4	MIRN223	1 hits
5	SLC2A4	1 hits
6	UCP1	1 hits
7	VEGFA	1 hits

Related Sentences

#	PMID	Sentence
1	20501654	Identification of microRNA-93 as a novel regulator of vascular endothelial growth factor in hyperglycemic conditions.
2	20501654	Here, we provide evidence that microRNA-93 (miR-93) regulates VEGF expression in experimental models of diabetes both in vitro and in vivo.
3	20501654	We identified VEGF-A as a putative target of miR-93 in the kidney with a perfect complementarity between miR-93 and the 3'-untranslated region of vegfa in several species.
4	20501654	We showed that forced expression of miR-93 in cells abrogated VEGF protein secretion.
5	20501654	Conversely, anti-miR-93 inhibitors increased VEGF release.
6	20501654	Transfection of miR-93 also prevented the effect of high glucose on VEGF downstream targets.
7	20501654	Using transgenic mice containing VEGF-LacZ bicistronic transcripts, we found that inhibition of glomerular miR-93 by peptide-conjugated morpholino oligomers elicited increased expression of VEGF.
8	20501654	Our findings also indicate that high glucose decreases miR-93 expression by down-regulating the promoter of the host MCM7 gene.
9	20501654	Taken together, our findings provide new insights into the role of miR-93 in VEGF signaling pathway and offer a potentially novel target in preventing the progression of diabetic nephropathy.
10	20501654	Identification of microRNA-93 as a novel regulator of vascular endothelial growth factor in hyperglycemic conditions.
11	20501654	Here, we provide evidence that microRNA-93 (miR-93) regulates VEGF expression in experimental models of diabetes both in vitro and in vivo.
12	20501654	We identified VEGF-A as a putative target of miR-93 in the kidney with a perfect complementarity between miR-93 and the 3'-untranslated region of vegfa in several species.
13	20501654	We showed that forced expression of miR-93 in cells abrogated VEGF protein secretion.
14	20501654	Conversely, anti-miR-93 inhibitors increased VEGF release.
15	20501654	Transfection of miR-93 also prevented the effect of high glucose on VEGF downstream targets.
16	20501654	Using transgenic mice containing VEGF-LacZ bicistronic transcripts, we found that inhibition of glomerular miR-93 by peptide-conjugated morpholino oligomers elicited increased expression of VEGF.
17	20501654	Our findings also indicate that high glucose decreases miR-93 expression by down-regulating the promoter of the host MCM7 gene.
18	20501654	Taken together, our findings provide new insights into the role of miR-93 in VEGF signaling pathway and offer a potentially novel target in preventing the progression of diabetic nephropathy.
19	20501654	Identification of microRNA-93 as a novel regulator of vascular endothelial growth factor in hyperglycemic conditions.
20	20501654	Here, we provide evidence that microRNA-93 (miR-93) regulates VEGF expression in experimental models of diabetes both in vitro and in vivo.
21	20501654	We identified VEGF-A as a putative target of miR-93 in the kidney with a perfect complementarity between miR-93 and the 3'-untranslated region of vegfa in several species.
22	20501654	We showed that forced expression of miR-93 in cells abrogated VEGF protein secretion.
23	20501654	Conversely, anti-miR-93 inhibitors increased VEGF release.
24	20501654	Transfection of miR-93 also prevented the effect of high glucose on VEGF downstream targets.
25	20501654	Using transgenic mice containing VEGF-LacZ bicistronic transcripts, we found that inhibition of glomerular miR-93 by peptide-conjugated morpholino oligomers elicited increased expression of VEGF.
26	20501654	Our findings also indicate that high glucose decreases miR-93 expression by down-regulating the promoter of the host MCM7 gene.
27	20501654	Taken together, our findings provide new insights into the role of miR-93 in VEGF signaling pathway and offer a potentially novel target in preventing the progression of diabetic nephropathy.
28	20501654	Identification of microRNA-93 as a novel regulator of vascular endothelial growth factor in hyperglycemic conditions.
29	20501654	Here, we provide evidence that microRNA-93 (miR-93) regulates VEGF expression in experimental models of diabetes both in vitro and in vivo.
30	20501654	We identified VEGF-A as a putative target of miR-93 in the kidney with a perfect complementarity between miR-93 and the 3'-untranslated region of vegfa in several species.
31	20501654	We showed that forced expression of miR-93 in cells abrogated VEGF protein secretion.
32	20501654	Conversely, anti-miR-93 inhibitors increased VEGF release.
33	20501654	Transfection of miR-93 also prevented the effect of high glucose on VEGF downstream targets.
34	20501654	Using transgenic mice containing VEGF-LacZ bicistronic transcripts, we found that inhibition of glomerular miR-93 by peptide-conjugated morpholino oligomers elicited increased expression of VEGF.
35	20501654	Our findings also indicate that high glucose decreases miR-93 expression by down-regulating the promoter of the host MCM7 gene.
36	20501654	Taken together, our findings provide new insights into the role of miR-93 in VEGF signaling pathway and offer a potentially novel target in preventing the progression of diabetic nephropathy.
37	20501654	Identification of microRNA-93 as a novel regulator of vascular endothelial growth factor in hyperglycemic conditions.
38	20501654	Here, we provide evidence that microRNA-93 (miR-93) regulates VEGF expression in experimental models of diabetes both in vitro and in vivo.
39	20501654	We identified VEGF-A as a putative target of miR-93 in the kidney with a perfect complementarity between miR-93 and the 3'-untranslated region of vegfa in several species.
40	20501654	We showed that forced expression of miR-93 in cells abrogated VEGF protein secretion.
41	20501654	Conversely, anti-miR-93 inhibitors increased VEGF release.
42	20501654	Transfection of miR-93 also prevented the effect of high glucose on VEGF downstream targets.
43	20501654	Using transgenic mice containing VEGF-LacZ bicistronic transcripts, we found that inhibition of glomerular miR-93 by peptide-conjugated morpholino oligomers elicited increased expression of VEGF.
44	20501654	Our findings also indicate that high glucose decreases miR-93 expression by down-regulating the promoter of the host MCM7 gene.
45	20501654	Taken together, our findings provide new insights into the role of miR-93 in VEGF signaling pathway and offer a potentially novel target in preventing the progression of diabetic nephropathy.
46	20501654	Identification of microRNA-93 as a novel regulator of vascular endothelial growth factor in hyperglycemic conditions.
47	20501654	Here, we provide evidence that microRNA-93 (miR-93) regulates VEGF expression in experimental models of diabetes both in vitro and in vivo.
48	20501654	We identified VEGF-A as a putative target of miR-93 in the kidney with a perfect complementarity between miR-93 and the 3'-untranslated region of vegfa in several species.
49	20501654	We showed that forced expression of miR-93 in cells abrogated VEGF protein secretion.
50	20501654	Conversely, anti-miR-93 inhibitors increased VEGF release.
51	20501654	Transfection of miR-93 also prevented the effect of high glucose on VEGF downstream targets.
52	20501654	Using transgenic mice containing VEGF-LacZ bicistronic transcripts, we found that inhibition of glomerular miR-93 by peptide-conjugated morpholino oligomers elicited increased expression of VEGF.
53	20501654	Our findings also indicate that high glucose decreases miR-93 expression by down-regulating the promoter of the host MCM7 gene.
54	20501654	Taken together, our findings provide new insights into the role of miR-93 in VEGF signaling pathway and offer a potentially novel target in preventing the progression of diabetic nephropathy.
55	20501654	Identification of microRNA-93 as a novel regulator of vascular endothelial growth factor in hyperglycemic conditions.
56	20501654	Here, we provide evidence that microRNA-93 (miR-93) regulates VEGF expression in experimental models of diabetes both in vitro and in vivo.
57	20501654	We identified VEGF-A as a putative target of miR-93 in the kidney with a perfect complementarity between miR-93 and the 3'-untranslated region of vegfa in several species.
58	20501654	We showed that forced expression of miR-93 in cells abrogated VEGF protein secretion.
59	20501654	Conversely, anti-miR-93 inhibitors increased VEGF release.
60	20501654	Transfection of miR-93 also prevented the effect of high glucose on VEGF downstream targets.
61	20501654	Using transgenic mice containing VEGF-LacZ bicistronic transcripts, we found that inhibition of glomerular miR-93 by peptide-conjugated morpholino oligomers elicited increased expression of VEGF.
62	20501654	Our findings also indicate that high glucose decreases miR-93 expression by down-regulating the promoter of the host MCM7 gene.
63	20501654	Taken together, our findings provide new insights into the role of miR-93 in VEGF signaling pathway and offer a potentially novel target in preventing the progression of diabetic nephropathy.
64	20501654	Identification of microRNA-93 as a novel regulator of vascular endothelial growth factor in hyperglycemic conditions.
65	20501654	Here, we provide evidence that microRNA-93 (miR-93) regulates VEGF expression in experimental models of diabetes both in vitro and in vivo.
66	20501654	We identified VEGF-A as a putative target of miR-93 in the kidney with a perfect complementarity between miR-93 and the 3'-untranslated region of vegfa in several species.
67	20501654	We showed that forced expression of miR-93 in cells abrogated VEGF protein secretion.
68	20501654	Conversely, anti-miR-93 inhibitors increased VEGF release.
69	20501654	Transfection of miR-93 also prevented the effect of high glucose on VEGF downstream targets.
70	20501654	Using transgenic mice containing VEGF-LacZ bicistronic transcripts, we found that inhibition of glomerular miR-93 by peptide-conjugated morpholino oligomers elicited increased expression of VEGF.
71	20501654	Our findings also indicate that high glucose decreases miR-93 expression by down-regulating the promoter of the host MCM7 gene.
72	20501654	Taken together, our findings provide new insights into the role of miR-93 in VEGF signaling pathway and offer a potentially novel target in preventing the progression of diabetic nephropathy.
73	20501654	Identification of microRNA-93 as a novel regulator of vascular endothelial growth factor in hyperglycemic conditions.
74	20501654	Here, we provide evidence that microRNA-93 (miR-93) regulates VEGF expression in experimental models of diabetes both in vitro and in vivo.
75	20501654	We identified VEGF-A as a putative target of miR-93 in the kidney with a perfect complementarity between miR-93 and the 3'-untranslated region of vegfa in several species.
76	20501654	We showed that forced expression of miR-93 in cells abrogated VEGF protein secretion.
77	20501654	Conversely, anti-miR-93 inhibitors increased VEGF release.
78	20501654	Transfection of miR-93 also prevented the effect of high glucose on VEGF downstream targets.
79	20501654	Using transgenic mice containing VEGF-LacZ bicistronic transcripts, we found that inhibition of glomerular miR-93 by peptide-conjugated morpholino oligomers elicited increased expression of VEGF.
80	20501654	Our findings also indicate that high glucose decreases miR-93 expression by down-regulating the promoter of the host MCM7 gene.
81	20501654	Taken together, our findings provide new insights into the role of miR-93 in VEGF signaling pathway and offer a potentially novel target in preventing the progression of diabetic nephropathy.
82	23493574	miRNA-93 inhibits GLUT4 and is overexpressed in adipose tissue of polycystic ovary syndrome patients and women with insulin resistance.
83	23493574	In AT, analysis of the IRS/PI3-K/AKT pathway signaling components identified only GLUT4 expression to be significantly lower in PCOS patients and in control subjects with IR.
84	23493574	We examined the role of miRNAs, particularly in the regulation of GLUT4, the insulin-sensitive glucose transporter, in the AT of PCOS and matched control subjects.
85	23493574	GLUT4 is a highly predicted target for miR-93, while miR-133 and miR-223 have been demonstrated to regulate GLUT4 expression in cardiomyocytes.
86	23493574	Expression of miR-93 revealed a strong correlation between the homeostasis model assessment of IR in vivo values and GLUT4 and miR-93 but not miR-133 and -223 expression in human AT.
87	23493574	Overexpression of miR-93 resulted in downregulation of GLUT4 gene expression in adipocytes through direct targeting of the GLUT4 3'UTR, while inhibition of miR-93 activity led to increased GLUT4 expression.
88	23493574	These results point to a novel mechanism for regulating insulin-stimulated glucose uptake via miR-93 and demonstrate upregulated miR-93 expression in all PCOS, and in non-PCOS women with IR, possibly accounting for the IR of the syndrome.
89	23493574	miRNA-93 inhibits GLUT4 and is overexpressed in adipose tissue of polycystic ovary syndrome patients and women with insulin resistance.
90	23493574	In AT, analysis of the IRS/PI3-K/AKT pathway signaling components identified only GLUT4 expression to be significantly lower in PCOS patients and in control subjects with IR.
91	23493574	We examined the role of miRNAs, particularly in the regulation of GLUT4, the insulin-sensitive glucose transporter, in the AT of PCOS and matched control subjects.
92	23493574	GLUT4 is a highly predicted target for miR-93, while miR-133 and miR-223 have been demonstrated to regulate GLUT4 expression in cardiomyocytes.
93	23493574	Expression of miR-93 revealed a strong correlation between the homeostasis model assessment of IR in vivo values and GLUT4 and miR-93 but not miR-133 and -223 expression in human AT.
94	23493574	Overexpression of miR-93 resulted in downregulation of GLUT4 gene expression in adipocytes through direct targeting of the GLUT4 3'UTR, while inhibition of miR-93 activity led to increased GLUT4 expression.
95	23493574	These results point to a novel mechanism for regulating insulin-stimulated glucose uptake via miR-93 and demonstrate upregulated miR-93 expression in all PCOS, and in non-PCOS women with IR, possibly accounting for the IR of the syndrome.
96	23493574	miRNA-93 inhibits GLUT4 and is overexpressed in adipose tissue of polycystic ovary syndrome patients and women with insulin resistance.
97	23493574	In AT, analysis of the IRS/PI3-K/AKT pathway signaling components identified only GLUT4 expression to be significantly lower in PCOS patients and in control subjects with IR.
98	23493574	We examined the role of miRNAs, particularly in the regulation of GLUT4, the insulin-sensitive glucose transporter, in the AT of PCOS and matched control subjects.
99	23493574	GLUT4 is a highly predicted target for miR-93, while miR-133 and miR-223 have been demonstrated to regulate GLUT4 expression in cardiomyocytes.
100	23493574	Expression of miR-93 revealed a strong correlation between the homeostasis model assessment of IR in vivo values and GLUT4 and miR-93 but not miR-133 and -223 expression in human AT.
101	23493574	Overexpression of miR-93 resulted in downregulation of GLUT4 gene expression in adipocytes through direct targeting of the GLUT4 3'UTR, while inhibition of miR-93 activity led to increased GLUT4 expression.
102	23493574	These results point to a novel mechanism for regulating insulin-stimulated glucose uptake via miR-93 and demonstrate upregulated miR-93 expression in all PCOS, and in non-PCOS women with IR, possibly accounting for the IR of the syndrome.
103	23493574	miRNA-93 inhibits GLUT4 and is overexpressed in adipose tissue of polycystic ovary syndrome patients and women with insulin resistance.
104	23493574	In AT, analysis of the IRS/PI3-K/AKT pathway signaling components identified only GLUT4 expression to be significantly lower in PCOS patients and in control subjects with IR.
105	23493574	We examined the role of miRNAs, particularly in the regulation of GLUT4, the insulin-sensitive glucose transporter, in the AT of PCOS and matched control subjects.
106	23493574	GLUT4 is a highly predicted target for miR-93, while miR-133 and miR-223 have been demonstrated to regulate GLUT4 expression in cardiomyocytes.
107	23493574	Expression of miR-93 revealed a strong correlation between the homeostasis model assessment of IR in vivo values and GLUT4 and miR-93 but not miR-133 and -223 expression in human AT.
108	23493574	Overexpression of miR-93 resulted in downregulation of GLUT4 gene expression in adipocytes through direct targeting of the GLUT4 3'UTR, while inhibition of miR-93 activity led to increased GLUT4 expression.
109	23493574	These results point to a novel mechanism for regulating insulin-stimulated glucose uptake via miR-93 and demonstrate upregulated miR-93 expression in all PCOS, and in non-PCOS women with IR, possibly accounting for the IR of the syndrome.
110	23954633	In addition, ectopic expression of miR-106b and miR-93 suppressed the mRNA level of Ucp1, a selective hallmark of brown adipocytes.
111	23954633	Taken together, our results identify miR-106b and miR-93 as negative regulators of brown adipocyte differentiation and the miR-106b-93 cluster may play an important role in regulating energy homeostasis.
112	23954633	In addition, ectopic expression of miR-106b and miR-93 suppressed the mRNA level of Ucp1, a selective hallmark of brown adipocytes.
113	23954633	Taken together, our results identify miR-106b and miR-93 as negative regulators of brown adipocyte differentiation and the miR-106b-93 cluster may play an important role in regulating energy homeostasis.