ARID1A

Source: Wikipedia, the free encyclopedia.
ARID1A
Gene ontology
Molecular function
Cellular component
Biological process
Sources:Amigo / QuickGO
Ensembl
UniProt
RefSeq (mRNA)

NM_139135
NM_006015
NM_018450

NM_001080819
NM_001363070

RefSeq (protein)

NP_006006
NP_624361

Location (UCSC)Chr 1: 26.69 – 26.78 MbChr 4: 133.68 – 133.76 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

AT-rich interactive domain-containing protein 1A is a protein that in humans is encoded by the ARID1A gene.[5][6][7]

Function

ARID1A is a member of the

beta-globin locus. Second, the C-terminus of the protein can stimulate glucocorticoid receptor-dependent transcriptional activation. The protein encoded by this gene confers specificity to the SWI/SNF complex and recruits the complex to its targets through either protein-DNA or protein-protein interactions.[8] Two transcript variants encoding different isoforms have been found for this gene.[7]

Clinical significance

Gene encoding for ARID1A is the most frequently mutated SWI/SNF subunit across cancers.

In
mTOR inhibitors. These findings provide a rationale for why tumors accumulate ARID1A mutations.[16][17]

Research

Lack of this gene/protein seems to protect rats from some types of liver damage.[18]

Interactions

ARID1A has been shown to

interact with SMARCB1[19][20] and SMARCA4.[20][21]

References

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000117713Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000007880Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. PMID 9630625
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  7. ^ a b "Entrez Gene: ARID1A AT rich interactive domain 1A (SWI-like)".
  8. PMID 37788668
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  18. ^ "Tissue Regeneration Promoted through Gene Suppression". Genetic Engineering & Biotechnology News. March 2016.
  19. PMID 11734557
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  20. ^ .
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Further reading

External links

This article incorporates text from the United States National Library of Medicine, which is in the public domain.

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