SIRT1
Basic information
Region (hg38): 10:67884656-67918390
Links
Phenotypes
GenCC
Source:
ClinVar
This is a list of variants' phenotypes submitted to
Variants pathogenicity by type
Statistics on ClinVar variants can assist in determining whether a specific variant type in the SIRT1 gene is commonly pathogenic or not.
In the table, we include only reliable ClinVar variants with their consequences to MANE Select, Mane Plus Clinical transcripts, or transcripts with TSL equals 1. Click the count to view the source variants.
Warning: slight differences between displayed counts and the number of variants in ClinVar may occur, primarily due to (1) the application of a different transcript and/or consequence by our variant effect predictor or (2) differences in clinical significance: we classify Benign/Likely benign variants as Likely benign and Pathogenic/Likely pathogenic variants as Likely pathogenic.
Variant type | Pathogenic | Likely pathogenic | VUS | Likely benign | Benign | Sum |
---|---|---|---|---|---|---|
synonymous | 23 | 27 | ||||
missense | 68 | 78 | ||||
nonsense | 2 | |||||
start loss | 0 | |||||
frameshift | 1 | |||||
inframe indel | 10 | |||||
splice donor/acceptor (+/-2bp) | 0 | |||||
splice region | 1 | 1 | ||||
non coding | 7 | |||||
Total | 0 | 0 | 80 | 38 | 7 |
Variants in SIRT1
This is a list of pathogenic ClinVar variants found in the SIRT1 region.
You can filter this list by clicking the number of variants in the Variants pathogenicity by type table.
Position | Type | Phenotype | Significance | ClinVar |
---|---|---|---|---|
10-67884727-G-A | Likely benign (Dec 28, 2021) | |||
10-67884732-A-G | Uncertain significance (Nov 24, 2022) | |||
10-67884736-G-A | Likely benign (Aug 02, 2023) | |||
10-67884744-C-T | Uncertain significance (Sep 11, 2023) | |||
10-67884745-C-A | Likely benign (Jan 24, 2024) | |||
10-67884747-T-C | Uncertain significance (Nov 06, 2023) | |||
10-67884761-T-C | SIRT1-related disorder | Uncertain significance (Dec 04, 2023) | ||
10-67884763-C-T | Likely benign (Jan 14, 2023) | |||
10-67884765-C-T | Uncertain significance (Feb 18, 2023) | |||
10-67884768-C-A | Uncertain significance (Nov 28, 2023) | |||
10-67884769-G-A | Benign/Likely benign (Jan 12, 2024) | |||
10-67884774-C-T | not specified | Uncertain significance (Apr 07, 2023) | ||
10-67884777-G-C | not specified | Likely benign (Apr 07, 2023) | ||
10-67884780-C-A | not specified | Uncertain significance (Oct 29, 2021) | ||
10-67884780-C-G | not specified | Uncertain significance (Sep 30, 2021) | ||
10-67884783-A-G | not specified | Uncertain significance (Oct 06, 2021) | ||
10-67884790-G-A | Likely benign (Dec 07, 2023) | |||
10-67884797-T-G | not specified | Uncertain significance (Jul 14, 2021) | ||
10-67884798-C-T | Uncertain significance (Dec 30, 2021) | |||
10-67884809-G-A | not specified | Uncertain significance (Jan 26, 2022) | ||
10-67884830-C-G | Uncertain significance (Dec 20, 2022) | |||
10-67884831-C-T | SIRT1-related disorder | Benign (Jan 13, 2024) | ||
10-67884852-T-A | not specified | Uncertain significance (Oct 05, 2023) | ||
10-67884863-C-T | not specified | Uncertain significance (Oct 30, 2023) | ||
10-67884864-C-T | Uncertain significance (Nov 04, 2022) |
GnomAD
Source:
Gene | Type | Bio Type | Transcript | Coding Exons | Length |
---|---|---|---|---|---|
SIRT1 | protein_coding | protein_coding | ENST00000212015 | 9 | 33721 |
pLI Probability LOF Intolerant | pRec Probability LOF Recessive | Individuals with no LOFs | Individuals with Homozygous LOFs | Individuals with Heterozygous LOFs | Defined | p |
---|---|---|---|---|---|---|
0.0873 | 0.913 | 125733 | 0 | 15 | 125748 | 0.0000596 |
Z-Score | Observed | Expected | Observed/Expected | Mutation Rate | Total Possible in Transcript | |
---|---|---|---|---|---|---|
Missense | 1.79 | 243 | 336 | 0.724 | 0.0000161 | 4861 |
Missense in Polyphen | 63 | 127.11 | 0.49564 | 1635 | ||
Synonymous | -0.978 | 130 | 117 | 1.12 | 0.00000574 | 1466 |
Loss of Function | 3.47 | 7 | 26.1 | 0.268 | 0.00000133 | 378 |
LoF frequencies by population
Ethnicity | Sum of pLOFs | p |
---|---|---|
African & African-American | 0.000185 | 0.000185 |
Ashkenazi Jewish | 0.00 | 0.00 |
East Asian | 0.0000544 | 0.0000544 |
Finnish | 0.0000925 | 0.0000924 |
European (Non-Finnish) | 0.0000623 | 0.0000527 |
Middle Eastern | 0.0000544 | 0.0000544 |
South Asian | 0.000196 | 0.0000980 |
Other | 0.00 | 0.00 |
dbNSFP
Source:
- Function
- FUNCTION: NAD-dependent protein deacetylase that links transcriptional regulation directly to intracellular energetics and participates in the coordination of several separated cellular functions such as cell cycle, response to DNA damage, metobolism, apoptosis and autophagy. Can modulate chromatin function through deacetylation of histones and can promote alterations in the methylation of histones and DNA, leading to transcriptional repression. Deacetylates a broad range of transcription factors and coregulators, thereby regulating target gene expression positively and negatively. Serves as a sensor of the cytosolic ratio of NAD(+)/NADH which is altered by glucose deprivation and metabolic changes associated with caloric restriction. Is essential in skeletal muscle cell differentiation and in response to low nutrients mediates the inhibitory effect on skeletal myoblast differentiation which also involves 5'-AMP-activated protein kinase (AMPK) and nicotinamide phosphoribosyltransferase (NAMPT). Component of the eNoSC (energy-dependent nucleolar silencing) complex, a complex that mediates silencing of rDNA in response to intracellular energy status and acts by recruiting histone-modifying enzymes. The eNoSC complex is able to sense the energy status of cell: upon glucose starvation, elevation of NAD(+)/NADP(+) ratio activates SIRT1, leading to histone H3 deacetylation followed by dimethylation of H3 at 'Lys-9' (H3K9me2) by SUV39H1 and the formation of silent chromatin in the rDNA locus. Deacetylates 'Lys-266' of SUV39H1, leading to its activation. Inhibits skeletal muscle differentiation by deacetylating PCAF and MYOD1. Deacetylates H2A and 'Lys-26' of HIST1H1E. Deacetylates 'Lys-16' of histone H4 (in vitro). Involved in NR0B2/SHP corepression function through chromatin remodeling: Recruited to LRH1 target gene promoters by NR0B2/SHP thereby stimulating histone H3 and H4 deacetylation leading to transcriptional repression. Proposed to contribute to genomic integrity via positive regulation of telomere length; however, reports on localization to pericentromeric heterochromatin are conflicting. Proposed to play a role in constitutive heterochromatin (CH) formation and/or maintenance through regulation of the available pool of nuclear SUV39H1. Upon oxidative/metabolic stress decreases SUV39H1 degradation by inhibiting SUV39H1 polyubiquitination by MDM2. This increase in SUV39H1 levels enhances SUV39H1 turnover in CH, which in turn seems to accelerate renewal of the heterochromatin which correlates with greater genomic integrity during stress response. Deacetylates 'Lys-382' of p53/TP53 and impairs its ability to induce transcription-dependent proapoptotic program and modulate cell senescence. Deacetylates TAF1B and thereby represses rDNA transcription by the RNA polymerase I. Deacetylates MYC, promotes the association of MYC with MAX and decreases MYC stability leading to compromised transformational capability. Deacetylates FOXO3 in response to oxidative stress thereby increasing its ability to induce cell cycle arrest and resistance to oxidative stress but inhibiting FOXO3-mediated induction of apoptosis transcriptional activity; also leading to FOXO3 ubiquitination and protesomal degradation. Appears to have a similar effect on MLLT7/FOXO4 in regulation of transcriptional activity and apoptosis. Deacetylates DNMT1; thereby impairs DNMT1 methyltransferase-independent transcription repressor activity, modulates DNMT1 cell cycle regulatory function and DNMT1-mediated gene silencing. Deacetylates RELA/NF-kappa-B p65 thereby inhibiting its transactivating potential and augments apoptosis in response to TNF-alpha. Deacetylates HIF1A, KAT5/TIP60, RB1 and HIC1. Deacetylates FOXO1 resulting in its nuclear retention and enhancement of its transcriptional activity leading to increased gluconeogenesis in liver. Inhibits E2F1 transcriptional activity and apoptotic function, possibly by deacetylation. Involved in HES1- and HEY2-mediated transcriptional repression. In cooperation with MYCN seems to be involved in transcriptional repression of DUSP6/MAPK3 leading to MYCN stabilization by phosphorylation at 'Ser-62'. Deacetylates MEF2D. Required for antagonist-mediated transcription suppression of AR-dependent genes which may be linked to local deacetylation of histone H3. Represses HNF1A- mediated transcription. Required for the repression of ESRRG by CREBZF. Modulates AP-1 transcription factor activity. Deacetylates NR1H3 AND NR1H2 and deacetylation of NR1H3 at 'Lys-434' positively regulates transcription of NR1H3:RXR target genes, promotes NR1H3 proteosomal degradation and results in cholesterol efflux; a promoter clearing mechanism after reach round of transcription is proposed. Involved in lipid metabolism. Implicated in regulation of adipogenesis and fat mobilization in white adipocytes by repression of PPARG which probably involves association with NCOR1 and SMRT/NCOR2. Deacetylates ACSS2 leading to its activation, and HMGCS1. Involved in liver and muscle metabolism. Through deacteylation and activation of PPARGC1A is required to activate fatty acid oxidation in skeletel muscle under low-glucose conditions and is involved in glucose homeostasis. Involved in regulation of PPARA and fatty acid beta-oxidation in liver. Involved in positive regulation of insulin secretion in pancreatic beta cells in response to glucose; the function seems to imply transcriptional repression of UCP2. Proposed to deacetylate IRS2 thereby facilitating its insulin-induced tyrosine phosphorylation. Deacetylates SREBF1 isoform SREBP-1C thereby decreasing its stability and transactivation in lipogenic gene expression. Involved in DNA damage response by repressing genes which are involved in DNA repair, such as XPC and TP73, deacetylating XRCC6/Ku70, and faciliting recruitment of additional factors to sites of damaged DNA, such as SIRT1-deacetylated NBN can recruit ATM to initiate DNA repair and SIRT1-deacetylated XPA interacts with RPA2. Also involved in DNA repair of DNA double-strand breaks by homologous recombination and specifically single-strand annealing independently of XRCC6/Ku70 and NBN. Transcriptional suppression of XPC probably involves an E2F4:RBL2 suppressor complex and protein kinase B (AKT) signaling. Transcriptional suppression of TP73 probably involves E2F4 and PCAF. Deacetylates WRN thereby regulating its helicase and exonuclease activities and regulates WRN nuclear translocation in response to DNA damage. Deacetylates APEX1 at 'Lys-6' and 'Lys-7' and stimulates cellular AP endonuclease activity by promoting the association of APEX1 to XRCC1. Increases p53/TP53-mediated transcription-independent apoptosis by blocking nuclear translocation of cytoplasmic p53/TP53 and probably redirecting it to mitochondria. Deacetylates XRCC6/Ku70 at 'Lys-539' and 'Lys-542' causing it to sequester BAX away from mitochondria thereby inhibiting stress-induced apoptosis. Is involved in autophagy, presumably by deacetylating ATG5, ATG7 and MAP1LC3B/ATG8. Deacetylates AKT1 which leads to enhanced binding of AKT1 and PDK1 to PIP3 and promotes their activation. Proposed to play role in regulation of STK11/LBK1- dependent AMPK signaling pathways implicated in cellular senescence which seems to involve the regulation of the acetylation status of STK11/LBK1. Can deacetylate STK11/LBK1 and thereby increase its activity, cytoplasmic localization and association with STRAD; however, the relevance of such activity in normal cells is unclear. In endothelial cells is shown to inhibit STK11/LBK1 activity and to promote its degradation. Deacetylates SMAD7 at 'Lys-64' and 'Lys-70' thereby promoting its degradation. Deacetylates CIITA and augments its MHC class II transactivation and contributes to its stability. Deacteylates MECOM/EVI1. Deacetylates PML at 'Lys-487' and this deacetylation promotes PML control of PER2 nuclear localization. During the neurogenic transition, repress selective NOTCH1-target genes through histone deacetylation in a BCL6-dependent manner and leading to neuronal differentiation. Regulates the circadian expression of several core clock genes, including ARNTL/BMAL1, RORC, PER2 and CRY1 and plays a critical role in maintaining a controlled rhythmicity in histone acetylation, thereby contributing to circadian chromatin remodeling. Deacetylates ARNTL/BMAL1 and histones at the circadian gene promoters in order to facilitate repression by inhibitory components of the circadian oscillator. Deacetylates PER2, facilitating its ubiquitination and degradation by the proteosome. Protects cardiomyocytes against palmitate-induced apoptosis (PubMed:11672523, PubMed:12006491, PubMed:14976264, PubMed:14980222, PubMed:15126506, PubMed:15152190, PubMed:15205477, PubMed:15469825, PubMed:15692560, PubMed:16079181, PubMed:16166628, PubMed:16892051, PubMed:16998810, PubMed:17283066, PubMed:17334224, PubMed:17505061, PubMed:17612497, PubMed:17620057, PubMed:17936707, PubMed:18203716, PubMed:18296641, PubMed:18662546, PubMed:18687677, PubMed:19188449, PubMed:19220062, PubMed:19364925, PubMed:19690166, PubMed:19934257, PubMed:20097625, PubMed:20100829, PubMed:20203304, PubMed:20375098, PubMed:20620956, PubMed:20670893, PubMed:20817729, PubMed:21149730, PubMed:21245319, PubMed:21471201, PubMed:21504832, PubMed:21555002, PubMed:21698133, PubMed:21701047, PubMed:21775285, PubMed:21807113, PubMed:21841822, PubMed:21890893, PubMed:21909281, PubMed:21947282, PubMed:22274616). Deacetylates XBP1 isoform 2; deacetylation decreases protein stability of XBP1 isoform 2 and inhibits its transcriptional activity (PubMed:20955178). Involved in the CCAR2- mediated regulation of PCK1 and NR1D1 (PubMed:24415752). Deacetylates CTNB1 at 'Lys-49' (PubMed:24824780). In POMC (pro- opiomelanocortin) neurons, required for leptin-induced activation of PI3K signaling (By similarity). {ECO:0000250|UniProtKB:Q923E4, ECO:0000269|PubMed:11672523, ECO:0000269|PubMed:12006491, ECO:0000269|PubMed:14976264, ECO:0000269|PubMed:14980222, ECO:0000269|PubMed:15126506, ECO:0000269|PubMed:15152190, ECO:0000269|PubMed:15205477, ECO:0000269|PubMed:15469825, ECO:0000269|PubMed:15692560, ECO:0000269|PubMed:16079181, ECO:0000269|PubMed:16166628, ECO:0000269|PubMed:16892051, ECO:0000269|PubMed:16998810, ECO:0000269|PubMed:17283066, ECO:0000269|PubMed:17290224, ECO:0000269|PubMed:17334224, ECO:0000269|PubMed:17505061, ECO:0000269|PubMed:17612497, ECO:0000269|PubMed:17620057, ECO:0000269|PubMed:17936707, ECO:0000269|PubMed:18203716, ECO:0000269|PubMed:18296641, ECO:0000269|PubMed:18662546, ECO:0000269|PubMed:18687677, ECO:0000269|PubMed:19188449, ECO:0000269|PubMed:19220062, ECO:0000269|PubMed:19364925, ECO:0000269|PubMed:19690166, ECO:0000269|PubMed:19934257, ECO:0000269|PubMed:20097625, ECO:0000269|PubMed:20100829, ECO:0000269|PubMed:20203304, ECO:0000269|PubMed:20375098, ECO:0000269|PubMed:20620956, ECO:0000269|PubMed:20670893, ECO:0000269|PubMed:20817729, ECO:0000269|PubMed:20955178, ECO:0000269|PubMed:21149730, ECO:0000269|PubMed:21245319, ECO:0000269|PubMed:21471201, ECO:0000269|PubMed:21504832, ECO:0000269|PubMed:21555002, ECO:0000269|PubMed:21698133, ECO:0000269|PubMed:21701047, ECO:0000269|PubMed:21775285, ECO:0000269|PubMed:21807113, ECO:0000269|PubMed:21841822, ECO:0000269|PubMed:21890893, ECO:0000269|PubMed:21909281, ECO:0000269|PubMed:21947282, ECO:0000269|PubMed:22274616, ECO:0000269|PubMed:24415752, ECO:0000269|PubMed:24824780}.; FUNCTION: (Microbial infection) In case of HIV-1 infection, interacts with and deacetylates the viral Tat protein. The viral Tat protein inhibits SIRT1 deacetylation activity toward RELA/NF- kappa-B p65, thereby potentiates its transcriptional activity and SIRT1 is proposed to contribute to T-cell hyperactivation during infection. {ECO:0000269|PubMed:18329615}.;
- Pathway
- Longevity regulating pathway - multiple species - Homo sapiens (human);FoxO signaling pathway - Homo sapiens (human);AMPK signaling pathway - Homo sapiens (human);Glucagon signaling pathway - Homo sapiens (human);Longevity regulating pathway - Homo sapiens (human);Amphetamine addiction - Homo sapiens (human);MicroRNAs in cancer - Homo sapiens (human);Cellular senescence - Homo sapiens (human);Metformin Pathway, Pharmacodynamic;IGF-Ncore;TGF-Ncore;Androgen receptor signaling pathway;Energy Metabolism;Sterol Regulatory Element-Binding Proteins (SREBP) signalling;SREBF and miR33 in cholesterol and lipid homeostasis;Melatonin metabolism and effects;NAD metabolism, sirtuins and aging;NAD+ metabolism;NAD+ biosynthetic pathways;Simplified Interaction Map Between LOXL4 and Oxidative Stress Pathway;Somatroph axis (GH) and its relationship to dietary restriction and aging;Caloric restriction and aging;SIRT1 negatively regulates rRNA expression;Negative epigenetic regulation of rRNA expression;Epigenetic regulation of gene expression;Gene expression (Transcription);Regulation of HSF1-mediated heat shock response;Cellular responses to stress;HIF-2-alpha transcription factor network;p73 transcription factor network;AndrogenReceptor;regulation of transcriptional activity by pml;Cellular responses to external stimuli;Cellular response to heat stress;Regulation of Androgen receptor activity;Signaling events mediated by HDAC Class III;FoxO family signaling;Regulation of retinoblastoma protein;E2F transcription factor network
(Consensus)
Recessive Scores
- pRec
- 0.622
Intolerance Scores
- loftool
- 0.571
- rvis_EVS
- 0.2
- rvis_percentile_EVS
- 67.19
Haploinsufficiency Scores
- pHI
- 0.922
- hipred
- Y
- hipred_score
- 0.783
- ghis
- 0.465
Essentials
- essential_gene_CRISPR
- N
- essential_gene_CRISPR2
- N
- essential_gene_gene_trap
- H
- gene_indispensability_pred
- E
- gene_indispensability_score
- 0.991
Gene Damage Prediction
All | Recessive | Dominant | |
---|---|---|---|
Mendelian | Medium | Medium | Medium |
Primary Immunodeficiency | Medium | Medium | Medium |
Cancer | Medium | Medium | Medium |
Mouse Genome Informatics
- Gene name
- Sirt1
- Phenotype
- embryo phenotype; respiratory system phenotype; liver/biliary system phenotype; behavior/neurological phenotype (the observable actions or reactions of mammalian organisms that are manifested through development and lifespan); reproductive system phenotype; mortality/aging (the observable characteristics related to the ability of a mammalian organism to live and age that are manifested throughout development and life span); normal phenotype; cardiovascular system phenotype (the observable morphological and physiological characteristics of the mammalian heart, blood vessels, or circulatory system that are manifested through development and lifespan); hematopoietic system phenotype; neoplasm; hearing/vestibular/ear phenotype; nervous system phenotype (the observable morphological and physiological characteristics of the extensive, intricate network of electochemical structures in the body that is comprised of the brain, spinal cord, nerves, ganglia and parts of the receptor organs that are manifested through development and lifespan); limbs/digits/tail phenotype; digestive/alimentary phenotype; vision/eye phenotype; immune system phenotype; renal/urinary system phenotype; skeleton phenotype; integument phenotype (the observable morphological and physiological characteristics of the skin and its associated structures, such as the hair, nails, sweat glands, sebaceous glands and other secretory glands that are manifested through development and lifespan); growth/size/body region phenotype; endocrine/exocrine gland phenotype; adipose tissue phenotype (the observable morphological and physiological characteristics of mammalian fat tissue that are manifested through development and lifespan); craniofacial phenotype; cellular phenotype; homeostasis/metabolism phenotype;
Zebrafish Information Network
- Gene name
- sirt1
- Affected structure
- trunk vasculature
- Phenotype tag
- abnormal
- Phenotype quality
- spatial pattern
Gene ontology
- Biological process
- single strand break repair;negative regulation of transcription by RNA polymerase II;chromatin silencing at rDNA;pyrimidine dimer repair by nucleotide-excision repair;DNA synthesis involved in DNA repair;angiogenesis;ovulation from ovarian follicle;cellular glucose homeostasis;positive regulation of protein phosphorylation;positive regulation of endothelial cell proliferation;positive regulation of adaptive immune response;chromatin organization;chromatin silencing;establishment of chromatin silencing;maintenance of chromatin silencing;methylation-dependent chromatin silencing;rRNA processing;protein ADP-ribosylation;protein deacetylation;triglyceride mobilization;cellular response to DNA damage stimulus;response to oxidative stress;transforming growth factor beta receptor signaling pathway;spermatogenesis;regulation of mitotic cell cycle;muscle organ development;cell aging;positive regulation of cell population proliferation;cellular response to starvation;negative regulation of gene expression;positive regulation of cholesterol efflux;regulation of lipid storage;regulation of glucose metabolic process;macrophage cytokine production;positive regulation of phosphatidylinositol 3-kinase signaling;viral process;positive regulation of macroautophagy;protein ubiquitination;histone deacetylation;peptidyl-lysine acetylation;macrophage differentiation;negative regulation of cell growth;negative regulation of transforming growth factor beta receptor signaling pathway;negative regulation of prostaglandin biosynthetic process;protein destabilization;positive regulation of chromatin silencing;negative regulation of TOR signaling;regulation of endodeoxyribonuclease activity;negative regulation of NF-kappaB transcription factor activity;response to insulin;circadian regulation of gene expression;obsolete regulation of protein import into nucleus, translocation;leptin-mediated signaling pathway;regulation of smooth muscle cell apoptotic process;peptidyl-lysine deacetylation;cellular triglyceride homeostasis;regulation of peroxisome proliferator activated receptor signaling pathway;regulation of cell population proliferation;negative regulation of phosphorylation;response to hydrogen peroxide;behavioral response to starvation;cholesterol homeostasis;intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator;regulation of apoptotic process;positive regulation of apoptotic process;negative regulation of apoptotic process;negative regulation of I-kappaB kinase/NF-kappaB signaling;proteasome-mediated ubiquitin-dependent protein catabolic process;positive regulation of cysteine-type endopeptidase activity involved in apoptotic process;negative regulation of DNA-binding transcription factor activity;negative regulation of DNA damage response, signal transduction by p53 class mediator;positive regulation of blood vessel endothelial cell migration;response to leptin;positive regulation of MHC class II biosynthetic process;negative regulation of fat cell differentiation;positive regulation of DNA repair;positive regulation of angiogenesis;negative regulation of transcription, DNA-templated;positive regulation of transcription by RNA polymerase II;positive regulation of insulin receptor signaling pathway;white fat cell differentiation;negative regulation of helicase activity;positive regulation of smooth muscle cell differentiation;positive regulation of histone H3-K9 methylation;negative regulation of protein kinase B signaling;fatty acid homeostasis;negative regulation of androgen receptor signaling pathway;histone H3-K9 modification;cellular response to hydrogen peroxide;regulation of bile acid biosynthetic process;UV-damage excision repair;histone H3 deacetylation;cellular response to tumor necrosis factor;negative regulation of histone H3-K14 acetylation;cellular response to hypoxia;cellular response to ionizing radiation;regulation of protein serine/threonine kinase activity;regulation of brown fat cell differentiation;stress-induced premature senescence;regulation of cellular response to heat;negative regulation of histone H3-K9 trimethylation;negative regulation of neuron death;negative regulation of protein acetylation;negative regulation of intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator;negative regulation of oxidative stress-induced intrinsic apoptotic signaling pathway;positive regulation of endoplasmic reticulum stress-induced intrinsic apoptotic signaling pathway;positive regulation of adipose tissue development;histone H3-K9 deacetylation;cellular response to leukemia inhibitory factor;positive regulation of macrophage apoptotic process;negative regulation of cAMP-dependent protein kinase activity;positive regulation of cAMP-dependent protein kinase activity;negative regulation of histone H4-K16 acetylation;negative regulation of cellular response to testosterone stimulus;negative regulation of peptidyl-lysine acetylation;negative regulation of cellular senescence;positive regulation of cellular senescence
- Cellular component
- nuclear chromatin;nucleus;nuclear envelope;nuclear inner membrane;nucleoplasm;chromatin silencing complex;nuclear euchromatin;nuclear heterochromatin;nucleolus;cytoplasm;mitochondrion;cytosol;PML body;rDNA heterochromatin;ESC/E(Z) complex
- Molecular function
- RNA polymerase II distal enhancer sequence-specific DNA binding;p53 binding;transcription corepressor activity;NAD+ ADP-ribosyltransferase activity;histone deacetylase activity;protein binding;protein C-terminus binding;transcription factor binding;NAD-dependent histone deacetylase activity;deacetylase activity;enzyme binding;protein domain specific binding;protein deacetylase activity;NAD-dependent protein deacetylase activity;nuclear hormone receptor binding;histone binding;identical protein binding;HLH domain binding;bHLH transcription factor binding;metal ion binding;NAD-dependent histone deacetylase activity (H3-K9 specific);mitogen-activated protein kinase binding;NAD+ binding;keratin filament binding