Entity Details

Primary name HMGA2_HUMAN
Entity type UniProt
Source Source Link

Details

AccessionP52926
EntryNameHMGA2_HUMAN
FullNameHigh mobility group protein HMGI-C
TaxID9606
Evidenceevidence at protein level
Length109
SequenceStatuscomplete
DateCreated1996-10-01
DateModified2021-06-02

Ontological Relatives

GenesHMGA2

GO terms

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GOName
GO:0000122 negative regulation of transcription by RNA polymerase II
GO:0000228 nuclear chromosome
GO:0000976 transcription cis-regulatory region binding
GO:0001837 epithelial to mesenchymal transition
GO:0002062 chondrocyte differentiation
GO:0003131 mesodermal-endodermal cell signaling
GO:0003680 minor groove of adenine-thymine-rich DNA binding
GO:0003712 transcription coregulator activity
GO:0003714 transcription corepressor activity
GO:0003906 DNA-(apurinic or apyrimidinic site) endonuclease activity
GO:0005634 nucleus
GO:0005654 nucleoplasm
GO:0006284 base-excision repair
GO:0006325 chromatin organization
GO:0006355 regulation of transcription, DNA-templated
GO:0007095 mitotic G2 DNA damage checkpoint signaling
GO:0007275 multicellular organism development
GO:0008134 transcription factor binding
GO:0008301 DNA binding, bending
GO:0009615 response to virus
GO:0010564 regulation of cell cycle process
GO:0010628 positive regulation of gene expression
GO:0030261 chromosome condensation
GO:0031052 chromosome breakage
GO:0031492 nucleosomal DNA binding
GO:0031507 heterochromatin assembly
GO:0032993 protein-DNA complex
GO:0035497 cAMP response element binding
GO:0035500 MH2 domain binding
GO:0035501 MH1 domain binding
GO:0035978 histone H2A-S139 phosphorylation
GO:0035985 senescence-associated heterochromatin focus
GO:0035986 senescence-associated heterochromatin focus assembly
GO:0035987 endodermal cell differentiation
GO:0035988 chondrocyte proliferation
GO:0040008 regulation of growth
GO:0042769 DNA damage response, detection of DNA damage
GO:0043065 positive regulation of apoptotic process
GO:0043066 negative regulation of apoptotic process
GO:0043392 negative regulation of DNA binding
GO:0043922 negative regulation by host of viral transcription
GO:0045444 fat cell differentiation
GO:0045766 positive regulation of angiogenesis
GO:0045869 negative regulation of single stranded viral RNA replication via double stranded DNA intermediate
GO:0045892 negative regulation of transcription, DNA-templated
GO:0045893 positive regulation of transcription, DNA-templated
GO:0045944 positive regulation of transcription by RNA polymerase II
GO:0046332 SMAD binding
GO:0048333 mesodermal cell differentiation
GO:0048762 mesenchymal cell differentiation
GO:0048863 stem cell differentiation
GO:0051301 cell division
GO:0051575 5'-deoxyribose-5-phosphate lyase activity
GO:0070742 C2H2 zinc finger domain binding
GO:0071141 SMAD protein complex
GO:0071864 positive regulation of cell proliferation in bone marrow
GO:0071902 positive regulation of protein serine/threonine kinase activity
GO:0090402 oncogene-induced cell senescence
GO:2000036 regulation of stem cell population maintenance
GO:2000648 positive regulation of stem cell proliferation
GO:2000685 positive regulation of cellular response to X-ray
GO:2000773 negative regulation of cellular senescence
GO:2000774 positive regulation of cellular senescence
GO:2001022 positive regulation of response to DNA damage stimulus
GO:2001033 negative regulation of double-strand break repair via nonhomologous end joining
GO:2001038 regulation of cellular response to drug

Subcellular Location

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Subcellular Location
Nucleus

Domains

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DomainNameCategoryType
IPR000116 High mobility group protein HMGAFamilyFamily
IPR000637 HMG-I/HMG-Y, DNA-binding, conserved siteSiteConserved site
IPR017956 AT hook, DNA-binding motifSiteConserved site

Diseases

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Disease IDSourceNameDescription
618908 OMIMSilver-Russell syndrome 5 (SRS5)A form of Silver-Russell syndrome, a clinically heterogeneous condition characterized by severe intrauterine growth retardation, poor postnatal growth, craniofacial features such as a triangular shaped face and a broad forehead, body asymmetry, and a variety of minor malformations. The phenotypic expression changes during childhood and adolescence, with the facial features and asymmetry usually becoming more subtle with age. SRS5 inheritance is autosomal dominant. The disease is caused by variants affecting the gene represented in this entry.