Ignet

Gene Information

Gene symbol: HIC1

Gene name: hypermethylated in cancer 1

HGNC ID: 4909

Synonyms: ZBTB29, ZNF901

Related Genes

#	Gene Symbol	Number of hits
1	CIITA	1 hits
2	PTEN	1 hits
3	SIRT1	1 hits
4	TNS1	1 hits

Related Sentences

#	PMID	Sentence
1	20129651	Relationship between down-regulation of HIC1 and PTEN genes and dysfunction of pancreatic islet cells in diabetic rats.
2	20129651	The aim of the study was to investigate the protein expression of hypermethylated in cancer 1 (HIC1 ) and phosphatase and tensin homologue (PTEN) genes and to study their mRNA expressions in normal and diabetic pancreatic islet cells in rats in order to try and identify the functions of these genes in the development and advancement of diabetes.
3	20129651	The expressions of HIC1, PTEN and mTOR genes were examined in the pancreatic islets of 20 normal male Wistar rats and 47 diabetic male Wistar rats by immunohistochemistry, Western blot, RT-PCR and real-time RT-PCR.
4	20129651	Results showed that expressions of HIC1 and PTEN in protein and mRNA levels were lower in pancreatic islets of diabetic rats than in normal rats.
5	20129651	The down-regulation of HIC1 and PTEN and up-regulation of mTOR in protein and mRNA level are positively correlated with functional impairment of islet cells in diabetic rats.
6	20129651	From this study we conclude that HIC1, PTEN and mTOR cannot be recognized as the key influencing factors promoting pancreatic islet cells apoptosis of diabetic rats; however, lower expressions of HIC1 and PTEN and higher expression of mTOR may affect the function of the pancreatic islet cells in diabetic rats.
7	20129651	Relationship between down-regulation of HIC1 and PTEN genes and dysfunction of pancreatic islet cells in diabetic rats.
8	20129651	The aim of the study was to investigate the protein expression of hypermethylated in cancer 1 (HIC1 ) and phosphatase and tensin homologue (PTEN) genes and to study their mRNA expressions in normal and diabetic pancreatic islet cells in rats in order to try and identify the functions of these genes in the development and advancement of diabetes.
9	20129651	The expressions of HIC1, PTEN and mTOR genes were examined in the pancreatic islets of 20 normal male Wistar rats and 47 diabetic male Wistar rats by immunohistochemistry, Western blot, RT-PCR and real-time RT-PCR.
10	20129651	Results showed that expressions of HIC1 and PTEN in protein and mRNA levels were lower in pancreatic islets of diabetic rats than in normal rats.
11	20129651	The down-regulation of HIC1 and PTEN and up-regulation of mTOR in protein and mRNA level are positively correlated with functional impairment of islet cells in diabetic rats.
12	20129651	From this study we conclude that HIC1, PTEN and mTOR cannot be recognized as the key influencing factors promoting pancreatic islet cells apoptosis of diabetic rats; however, lower expressions of HIC1 and PTEN and higher expression of mTOR may affect the function of the pancreatic islet cells in diabetic rats.
13	20129651	Relationship between down-regulation of HIC1 and PTEN genes and dysfunction of pancreatic islet cells in diabetic rats.
14	20129651	The aim of the study was to investigate the protein expression of hypermethylated in cancer 1 (HIC1 ) and phosphatase and tensin homologue (PTEN) genes and to study their mRNA expressions in normal and diabetic pancreatic islet cells in rats in order to try and identify the functions of these genes in the development and advancement of diabetes.
15	20129651	The expressions of HIC1, PTEN and mTOR genes were examined in the pancreatic islets of 20 normal male Wistar rats and 47 diabetic male Wistar rats by immunohistochemistry, Western blot, RT-PCR and real-time RT-PCR.
16	20129651	Results showed that expressions of HIC1 and PTEN in protein and mRNA levels were lower in pancreatic islets of diabetic rats than in normal rats.
17	20129651	The down-regulation of HIC1 and PTEN and up-regulation of mTOR in protein and mRNA level are positively correlated with functional impairment of islet cells in diabetic rats.
18	20129651	From this study we conclude that HIC1, PTEN and mTOR cannot be recognized as the key influencing factors promoting pancreatic islet cells apoptosis of diabetic rats; however, lower expressions of HIC1 and PTEN and higher expression of mTOR may affect the function of the pancreatic islet cells in diabetic rats.
19	20129651	Relationship between down-regulation of HIC1 and PTEN genes and dysfunction of pancreatic islet cells in diabetic rats.
20	20129651	The aim of the study was to investigate the protein expression of hypermethylated in cancer 1 (HIC1 ) and phosphatase and tensin homologue (PTEN) genes and to study their mRNA expressions in normal and diabetic pancreatic islet cells in rats in order to try and identify the functions of these genes in the development and advancement of diabetes.
21	20129651	The expressions of HIC1, PTEN and mTOR genes were examined in the pancreatic islets of 20 normal male Wistar rats and 47 diabetic male Wistar rats by immunohistochemistry, Western blot, RT-PCR and real-time RT-PCR.
22	20129651	Results showed that expressions of HIC1 and PTEN in protein and mRNA levels were lower in pancreatic islets of diabetic rats than in normal rats.
23	20129651	The down-regulation of HIC1 and PTEN and up-regulation of mTOR in protein and mRNA level are positively correlated with functional impairment of islet cells in diabetic rats.
24	20129651	From this study we conclude that HIC1, PTEN and mTOR cannot be recognized as the key influencing factors promoting pancreatic islet cells apoptosis of diabetic rats; however, lower expressions of HIC1 and PTEN and higher expression of mTOR may affect the function of the pancreatic islet cells in diabetic rats.
25	20129651	Relationship between down-regulation of HIC1 and PTEN genes and dysfunction of pancreatic islet cells in diabetic rats.
26	20129651	The aim of the study was to investigate the protein expression of hypermethylated in cancer 1 (HIC1 ) and phosphatase and tensin homologue (PTEN) genes and to study their mRNA expressions in normal and diabetic pancreatic islet cells in rats in order to try and identify the functions of these genes in the development and advancement of diabetes.
27	20129651	The expressions of HIC1, PTEN and mTOR genes were examined in the pancreatic islets of 20 normal male Wistar rats and 47 diabetic male Wistar rats by immunohistochemistry, Western blot, RT-PCR and real-time RT-PCR.
28	20129651	Results showed that expressions of HIC1 and PTEN in protein and mRNA levels were lower in pancreatic islets of diabetic rats than in normal rats.
29	20129651	The down-regulation of HIC1 and PTEN and up-regulation of mTOR in protein and mRNA level are positively correlated with functional impairment of islet cells in diabetic rats.
30	20129651	From this study we conclude that HIC1, PTEN and mTOR cannot be recognized as the key influencing factors promoting pancreatic islet cells apoptosis of diabetic rats; however, lower expressions of HIC1 and PTEN and higher expression of mTOR may affect the function of the pancreatic islet cells in diabetic rats.
31	20129651	Relationship between down-regulation of HIC1 and PTEN genes and dysfunction of pancreatic islet cells in diabetic rats.
32	20129651	The aim of the study was to investigate the protein expression of hypermethylated in cancer 1 (HIC1 ) and phosphatase and tensin homologue (PTEN) genes and to study their mRNA expressions in normal and diabetic pancreatic islet cells in rats in order to try and identify the functions of these genes in the development and advancement of diabetes.
33	20129651	The expressions of HIC1, PTEN and mTOR genes were examined in the pancreatic islets of 20 normal male Wistar rats and 47 diabetic male Wistar rats by immunohistochemistry, Western blot, RT-PCR and real-time RT-PCR.
34	20129651	Results showed that expressions of HIC1 and PTEN in protein and mRNA levels were lower in pancreatic islets of diabetic rats than in normal rats.
35	20129651	The down-regulation of HIC1 and PTEN and up-regulation of mTOR in protein and mRNA level are positively correlated with functional impairment of islet cells in diabetic rats.
36	20129651	From this study we conclude that HIC1, PTEN and mTOR cannot be recognized as the key influencing factors promoting pancreatic islet cells apoptosis of diabetic rats; however, lower expressions of HIC1 and PTEN and higher expression of mTOR may affect the function of the pancreatic islet cells in diabetic rats.
37	22064865	Interferon gamma (IFN-γ) disrupts energy expenditure and metabolic homeostasis by suppressing SIRT1 transcription.
38	22064865	Further analysis reveals that IFN-γ requires class II transactivator (CIITA) to repress SIRT1 transcription.
39	22064865	CIITA, once induced by IFN-γ, is recruited to the SIRT1 promoter by hypermethylated in cancer 1 (HIC1) and promotes down-regulation of SIRT1 transcription via active deacetylation of core histones surrounding the SIRT1 proximal promoter.
40	22064865	Silencing CIITA or HIC1 restores SIRT1 activity and expression of metabolic genes in skeletal muscle cells challenged with IFN-γ.
41	22064865	Therefore, our data delineate an IFN-γ/HIC1/CIITA axis that contributes to metabolic dysfunction by suppressing SIRT1 transcription in skeletal muscle cells and as such shed new light on the development of novel therapeutic strategies against type 2 diabetes.
42	22064865	Interferon gamma (IFN-γ) disrupts energy expenditure and metabolic homeostasis by suppressing SIRT1 transcription.
43	22064865	Further analysis reveals that IFN-γ requires class II transactivator (CIITA) to repress SIRT1 transcription.
44	22064865	CIITA, once induced by IFN-γ, is recruited to the SIRT1 promoter by hypermethylated in cancer 1 (HIC1) and promotes down-regulation of SIRT1 transcription via active deacetylation of core histones surrounding the SIRT1 proximal promoter.
45	22064865	Silencing CIITA or HIC1 restores SIRT1 activity and expression of metabolic genes in skeletal muscle cells challenged with IFN-γ.
46	22064865	Therefore, our data delineate an IFN-γ/HIC1/CIITA axis that contributes to metabolic dysfunction by suppressing SIRT1 transcription in skeletal muscle cells and as such shed new light on the development of novel therapeutic strategies against type 2 diabetes.
47	22064865	Interferon gamma (IFN-γ) disrupts energy expenditure and metabolic homeostasis by suppressing SIRT1 transcription.
48	22064865	Further analysis reveals that IFN-γ requires class II transactivator (CIITA) to repress SIRT1 transcription.
49	22064865	CIITA, once induced by IFN-γ, is recruited to the SIRT1 promoter by hypermethylated in cancer 1 (HIC1) and promotes down-regulation of SIRT1 transcription via active deacetylation of core histones surrounding the SIRT1 proximal promoter.
50	22064865	Silencing CIITA or HIC1 restores SIRT1 activity and expression of metabolic genes in skeletal muscle cells challenged with IFN-γ.
51	22064865	Therefore, our data delineate an IFN-γ/HIC1/CIITA axis that contributes to metabolic dysfunction by suppressing SIRT1 transcription in skeletal muscle cells and as such shed new light on the development of novel therapeutic strategies against type 2 diabetes.