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Human Polyclonal ARID1A Primary Antibody pour ICC, IF - ABIN4281563
Bolander, Agnarsdóttir, Strömberg, Ponten, Hesselius, Uhlen, Bergqvist: The protein expression of TRP-1 and galectin-1 in cutaneous malignant melanomas. dans Cancer genomics & proteomics 2009
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Human Polyclonal ARID1A Primary Antibody pour WB - ABIN188644
Wurster, Precht, Pazin: NF-κB and BRG1 bind a distal regulatory element in the IL-3/GM-CSF locus. dans Molecular immunology 2011
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Our data provide additional evidence that AT-rich interactive domain 1A might function as a tumor suppressor gene in pancreatic carcinogenesis.
Study identified a set of conserved and surface-exposed residues unique to the ARID when it co-occurs with the ARM repeat containing BAF250 complex in BAF250a. Several of these residues are found mutated in somatic cancers. Study predict that these residues in BAF250a may play important roles in mediating protein-DNA and protein-protein interactions in the BAF complex.
our findings characterize ARID1A as a key tumor-suppressor gene in breast cancer through cooperation with CEBPalpha, and loss-of-function mutations of ARID1A activates UCA1.
In addition, 6 other cancer-associated genes (BRAF, NRAS, HRAS, ERK1, ERK2 and PTEN) were also analyzed. In total, four somatic mutations were identified in three out of 101 ovarian endometriotic lesions (4%, 4/101), including a KRAS p.G12V, a PPP2R1A p.S256F and two ARID1A nonsense mutations (p.Q403* and p.G1926*); while no mutations were identified in the remaining 7 genes (BRAF, NRAS, HRAS, ERK1, ERK2, PTEN and PIK3CA)
BET inhibition may represent a novel treatment strategy for a subset of ARID1A mutated ovarian clear cell carcinomas.
ARID1a may be required for regulation of a subset of glucocorticoid responsive genes.
This study demonstrated that Hypoxia-Inducible Factor 1alpha and AT-Rich Interactive Domain-Containing Protein 1A Expression in Pituitary Adenomas.
Cells lacking ARID1A show enhanced AURKA transcription, which leads to the persistent activation of CDC25C, a key protein for G2/M transition and mitotic entry.
the correlation between the loss of ARID1A immunoreactivity and reduced ARID1B levels indicates that ARID1B could be an attractive target for anti-cancer therapy.
these data suggest that the combined treatment with PI3K inhibitor BKM120 and PARP inhibitor olaparib may be a promising therapeutic regimen for the treatment of gastric cancer, and ARID1A deficiency could serve as a potential predictive therapeutic biomarker.
Although Genome-Wide Association studies have not been carried out in the field of alcohol-related hepatocellular carcinoma (HCC), common single nucleotide polymorphisms conferring a small increase in the risk of liver cancer risk have been identified. Specific patterns of gene mutations including CTNNB1, TERT, ARID1A and SMARCA2 exist in alcohol-related HCC. [review]
The authors find that ARID1A has a dominant role in maintaining chromatin accessibility at enhancers, while the contribution of ARID1B is evident only in the context of ARID1A mutation.
ARID1A and human epidermal growth factor receptor-2 (Her-2) status were found to be independent prognostic factors of both overall survival (OS) and disease free survival (DFS).
ARID1A expression loss was associated with poor overall survival in Asians with gastric cancer. [meta-analysis]
the significant correlation was achieved between the negative ARID1A expression and the FIGO stage of endometrium-related gynecological cancers, but not the other characteristics.
This metaanalysis indicated that Gastric Cancer or Colorectal Cancer with ARID1A alteration might be a marker of poor prognosis. The ARID1A alteration of Gastric Cancer may result from different epigenetic factors.
Low ARID1A expression is associated with clear cell and endometrioid carcinoma of the ovary and the endometrium.
Loss of PTEN and ARID1A expression is highly specific for malignancy in effusion pathology
We propose a signaling cascade involving ARID1A, GADD45B and DUSP1 as mediators of the romidepsin effects in GCC cells.
head and neck squamous cell carcinoma patients with tumors having high level of miR-31 expression and high levels of Nanog/OCT4/Sox2/EpCAM expression, together with low level of ARID1A expression, were found to have the worst survival
Together, these results demonstrate Arid1a as a critical modulator of Kras-dependent changes in acinar cell identity, and underscore an unanticipated influence of timing and genetic context on the effects of SWI/SNF complex alterations in epithelial tumorigenesis.
Deletion of Arid1a concomitant with Sox9 overexpression in Lgr5(+) ISCs restores self-renewal in Arid1a-deleted Lgr5(+) ISCs.
ARID1A regulates expression of SOX9, activation of the mTOR pathway, and differentiation of pancreatic ductal cells. ARID1A inhibits formation of pancreatic ductal adenocarcinomas from intraductal papillary mucinous neoplasms in mice with pancreatic expression of activated KRAS and is down-regulated in IPMN and PDAC tissues from patients.
Our results identified PIK3IP1 as a novel target of ARID1A and PGR in the murine uterus.
Mice with liver-specific homozygous or heterozygous Arid1a loss were resistant to tumor initiation while ARID1A overexpression accelerated initiation.
Loss of HDAC-mediated repression and gain of NF-kappaB activation underlie cytokine induction in ARID1A- and PIK3CA-mutation-driven ovarian cancer.
ARID1A mutation inactivates the apoptosis-promoting function of p53 by upregulating HDAC6, indicating that pharmacological inhibition of HDAC6 is a therapeutic strategy for ARID1A-mutated cancers.
ARID1A normally targets SWI/SNF complexes to enhancers.
Consistent with the latter, Arid1a reexpression in tumor cells led to increased p21 (Cdkn1a) expression and dramatic accumulation of cells in G2 phase of the cell cycle. These results also indicate a potential opportunity for therapeutic intervention in ARID1A-deficient human breast cancer subtypes that retain one intact copy of the gene and also maintain wild-type TRP53 activity
regulates embryo implantation and development of a functional placenta
The Arid1a loss reprograms chromatin to restrict promoter access by transcription factors such as C/ebpalpha, which enforces differentiation, and E2F4, which suppresses cell-cycle re-entry.
This study provides an alternative mechanism by which Arid1a deficiency contributes to hepatocellular carcinoma tumorigenesis.
ARID1A positively regulates Klf15 expression with PGR to inhibit epithelial proliferation at peri-implantation. Our results suggest that Arid1a has a critical role in modulating epithelial proliferation which is a critical requisite for fertility
Our results indicate that the Arid1a tumour suppressor gene has a key role in regulating ovarian endometrioid carcinoma differentiation
ARID1A and PIK3CA mutations cooperate to promote tumour growth through sustained IL-6 overproduction.
BAF250a mediates esBAF and polycomb recessive complex functions to establish the poised chromatin configuration in embryonic stem (ES) cells, which is essential for ES cell differentiation.
The Baf250a orchestrated a genetic program that repressed the expression of Nkx2.5 in the SAN through Tbx3 and HDAC3
Results demonstrate that inactivation of Arid1a alone is insufficient for tumor initiation but it requires additional genetic alteration(s) such as Pten deletion to drive tumorigenesis.
Loss of ARID1a-DNA binding led to a convergence of heart and vascular defects in mutant embryos, and the sum of defects culminated in ischemic arrest around midgestation.
Results thus identify BAF250a-mediated chromatin remodeling as an essential epigenetic mechanism mediating CPC differentiation.
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. Second, the C-terminus of the protein can stimulate glucocorticoid receptor-dependent transcriptional activation. It is thought that the protein encoded by this gene confers specificity to the SNF/SWI complex and may recruit the complex to its targets through either protein-DNA or protein-protein interactions. Two transcript variants encoding different isoforms have been found for this gene.
ARID domain-containing protein 1A
, AT-rich interactive domain-containing protein 1A
, BRG1-associated factor 250a
, OSA1 nuclear protein
, SWI-like protein
, SWI/SNF complex protein p270
, SWI/SNF-related, matrix-associated, actin-dependent regulator of chromatin subfamily F member 1
, brain protein 120
, chromatin remodeling factor p250
, osa homolog 1
, AT rich interactive domain 1A (Swi1 like)
, BRG1-associated factor 250
, SWI-SNF complex protein p270
, SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily f, member 1
, Swi1 like
, AT rich interactive domain 1A (SWI-like)
, AT-rich interactive domain-containing protein 1A-like
, AT rich interactive domain 1Aa (SWI-like)