Ignet

Gene Information

Gene symbol: HDAC5

Gene name: histone deacetylase 5

HGNC ID: 14068

Synonyms: KIAA0600, NY-CO-9, FLJ90614

Related Genes

#	Gene Symbol	Number of hits
1	AGT	1 hits
2	CREBBP	1 hits
3	EP300	1 hits
4	HDAC1	1 hits
5	HDAC4	1 hits
6	HDAC9	1 hits
7	INS	1 hits
8	MAPK1	1 hits
9	MAPK14	1 hits
10	MYEF2	1 hits
11	NCOR1	1 hits
12	NCOR2	1 hits
13	PPARG	1 hits
14	PPARGC1A	1 hits
15	PRKAA1	1 hits
16	PRKAA2	1 hits
17	SLC2A4	1 hits

Related Sentences

#	PMID	Sentence
1	10640275	Transcriptional repression mediated by corepressors N-CoR and SMRT is a critical function of nuclear hormone receptors, and is dysregulated in human myeloid leukemias.
2	10640275	Surprisingly, however, numerous biochemical studies have not detected N-CoR or SMRT in mSin3- and HDAC1-containing complexes.
3	10640275	Here we show that these RDs are nonredundant, and that one RD, which is conserved in N-CoR and SMRT, represses transcription by interacting directly with class II HDAC4 and HDAC5.
4	10640275	Endogenous N-CoR and SMRT each associate with HDAC4 in a complex that does not contain mSin3A or HDAC1.
5	15111488	Overexpression of GLUT4 in skeletal muscle enhances whole-body insulin action.
6	15111488	Exercise increases GLUT4 gene and protein expression, and a binding site for the myocyte enhancer factor 2 (MEF-2) is required on the GLUT4 promoter for this response.
7	15111488	In various cell systems, MEF-2 regulation is a balance between transcriptional repression by histone deacetylases (HDACs) and transcriptional activation by the nuclear factor of activated T-cells (NFAT), peroxisome proliferator-activated receptor-gamma coactivator 1 (PGC-1), and the p38 mitogen-activated protein kinase.
8	15111488	After exercise, HDAC5 was dissociated from MEF-2 and exported from the nucleus, whereas nuclear PGC-1 was associated with MEF-2.
9	15111488	Exercise increased total and nuclear p38 phosphorylation and association with MEF-2, without changes in total or nuclear p38 protein abundance.
10	15111488	This result was associated with p38 sequence-specific phosphorylation of MEF-2 and an increase in GLUT4 mRNA.
11	15111488	From these data, it appears that HDAC5, PGC-1, and p38 regulate MEF-2 and could be potential targets for modulating GLUT4 expression.
12	15111488	Overexpression of GLUT4 in skeletal muscle enhances whole-body insulin action.
13	15111488	Exercise increases GLUT4 gene and protein expression, and a binding site for the myocyte enhancer factor 2 (MEF-2) is required on the GLUT4 promoter for this response.
14	15111488	In various cell systems, MEF-2 regulation is a balance between transcriptional repression by histone deacetylases (HDACs) and transcriptional activation by the nuclear factor of activated T-cells (NFAT), peroxisome proliferator-activated receptor-gamma coactivator 1 (PGC-1), and the p38 mitogen-activated protein kinase.
15	15111488	After exercise, HDAC5 was dissociated from MEF-2 and exported from the nucleus, whereas nuclear PGC-1 was associated with MEF-2.
16	15111488	Exercise increased total and nuclear p38 phosphorylation and association with MEF-2, without changes in total or nuclear p38 protein abundance.
17	15111488	This result was associated with p38 sequence-specific phosphorylation of MEF-2 and an increase in GLUT4 mRNA.
18	15111488	From these data, it appears that HDAC5, PGC-1, and p38 regulate MEF-2 and could be potential targets for modulating GLUT4 expression.
19	16620308	Glucose transporter isoform 4 gene expression is increased immediately following a single bout of exercise, and the GLUT-4 enhancer factor (GEF) and myocyte enhancer factor 2 (MEF2) transcription factors are required for this response.
20	16620308	These studies find possible roles for histone deacetylase 5 (HDAC5), adenosine monophosphate-activated protein kinase (AMPK), peroxisome proliferator-activated receptor gamma coactivator 1alpha (PGC-1alpha) and p38 mitogen-activated protein kinase (MAPK) in regulating MEF2 through a series of complex interactions potentially involving MEF2 repression, coactivation and phosphorylation. 4.
21	17823368	Angiotensin II stimulates protein kinase D-dependent histone deacetylase 5 phosphorylation and nuclear export leading to vascular smooth muscle cell hypertrophy.
22	18184930	AMP-activated protein kinase regulates GLUT4 transcription by phosphorylating histone deacetylase 5.
23	19793100	It has been shown that HDAC4 and 5 co-operatively regulate a number of genes involved in various aspects of metabolism.
24	19793100	The HDACs are also regulated by ubiquitin-mediated proteasomal degradation, although the exact mediators of this process have not been identified. 5.
25	19793100	Together, these data show that HDAC4 and 5 are critical regulators of metabolic gene expression and that understanding their regulation could provide a number of points of intervention for therapies designed to treat metabolic diseases, such as insulin resistance, obesity and Type 2 diabetes.
26	19793100	It has been shown that HDAC4 and 5 co-operatively regulate a number of genes involved in various aspects of metabolism.
27	19793100	The HDACs are also regulated by ubiquitin-mediated proteasomal degradation, although the exact mediators of this process have not been identified. 5.
28	19793100	Together, these data show that HDAC4 and 5 are critical regulators of metabolic gene expression and that understanding their regulation could provide a number of points of intervention for therapies designed to treat metabolic diseases, such as insulin resistance, obesity and Type 2 diabetes.
29	21953612	Specific control of pancreatic endocrine β- and δ-cell mass by class IIa histone deacetylases HDAC4, HDAC5, and HDAC9.
30	23235480	Involvement of p300/CBP and epigenetic histone acetylation in TGF-β1-mediated gene transcription in mesangial cells.
31	23235480	Transforming growth factor-β1 (TGF-β1)-induced expression of plasminogen activator inhibitor-1 (PAI-1) and p21 in renal mesangial cells (MCs) plays a major role in glomerulosclerosis and hypertrophy, key events in the pathogenesis of diabetic nephropathy.
32	23235480	We evaluated the roles of histone acetylation, specific HATs, and HDACs in TGF-β1-induced gene expression in rat mesangial cells (RMCs) and in glomeruli from diabetic mice.
33	23235480	Overexpression of HATs CREB binding protein (CBP) or p300, but not p300/CBP-activating factor, significantly enhanced TGF-β1-induced PAI-1 and p21 mRNA levels as well as transactivation of their promoters in RMCs.
34	23235480	Conversely, they were significantly attenuated by HAT domain mutants of CBP and p300 or overexpression of HDAC-1 and HDAC-5.
35	23235480	Chromatin immunoprecipitation assays showed that TGF-β1 treatment led to a time-dependent enrichment of histone H3-lysine9/14-acetylation (H3K9/14Ac) and p300/CBP occupancies around Smad and Sp1 binding sites at the PAI-1 and p21 promoters.
36	23235480	TGF-β1 also enhanced the interaction of p300 with Smad2/3 and Sp1 and increased Smad2/3 acetylation.
37	23235480	High glucose-treated RMCs exhibited increased PAI-1 and p21 levels, and promoter H3K9/14Ac, which were blocked by TGF-β1 antibodies.
38	23235480	Furthermore, increased PAI-1 and p21 expression was associated with elevated promoter H3K9/14Ac levels in glomeruli from diabetic mice.
39	23235480	Thus TGF-β1-induced PAI-1 and p21 expression involves interaction of p300/CBP with Smads and Sp1, and increased promoter access via p300/CBP-induced H3K9/14Ac.