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Validated All-in-One™ qPCR Primer for ARID1A(NM_006015.5) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
This gene encodes a member of the SWI/SNF family, whose members have helicase and ATPase activities and are thought to regulate transcription of certain genes by altering the chromatin structure around those genes. The encoded protein is part of the large ATP-dependent chromatin remodeling complex SNF/SWI, which is required for transcriptional activation of genes normally repressed by chromatin. It possesses at least two conserved domains that could be important for its function. First, it has a DNA-binding domain that can specifically bind an AT-rich DNA sequence known to be recognized by a SNF/SWI complex at the beta-globin locus.
Gene References into function
- largest subunits of SWI/SNF participate in promoting transcriptional activation by the steroid hormone receptors
- BAF250 chromatin-remodeling complexes contain a mixed-lineage leukemia chromosomal translocation partner.
- ARID1B is associated with SWI/SNF-related complexes and indicates that ARID1A and ARID1B, similar to the ATPase subunits BRG1 and hBRM, are alternative, mutually exclusive subunits of the complexes
- Levels of ARID1A are frequently deficient in renal cell carcinoma samples.
- The noncatalytic subunits of mammalian SWI/SNF complexes include p270/ARID1A. p270-containing complexes are functionally distinct from ARID1B-containing complexes and a deficiency of p270 is suggested to play a causative role in carcinogenesis.
- The subset of SWI/SNF complexes containing ARID1A have an associated histone deacetylase (HDAC) activity.
- in the primary breast carcinoma, transforming ARID1A sequence was an antisense cDNA, and was the product of a genomic rearrangement; identified a lung adenocarcinoma cell line with a highly localized homozygous genomic deletion in the 5' end of ARID1A
