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anti-Human ARID1A Antibodies:
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Human Polyclonal ARID1A Primary Antibody for ICC, IF - ABIN4281563
Bolander, Agnarsdóttir, Strömberg, Ponten, Hesselius, Uhlen, Bergqvist: The protein expression of TRP-1 and galectin-1 in cutaneous malignant melanomas. in Cancer genomics & proteomics 2009
Show all 21 Pubmed References
Human Polyclonal ARID1A Primary Antibody for WB - ABIN188644
Wurster, Precht, Pazin: NF-κB and BRG1 bind a distal regulatory element in the IL-3/GM-CSF locus. in Molecular immunology 2011
Show all 2 Pubmed References
ARID1A alterations may characterize cholangiolocellular carcinoma with ductal plate malformation-pattern
The elevated immune activity in ARID1A-mutated gastrointestinal (GI) cancers was associated with the higher tumor mutation burden and lower tumor aneuploidy level. ARID1A-mutated GI cancers more highly expressed PD-L1 than ARID1A-wildtype GI cancers. ARID1A mutation could be a useful biomarker for identifying GI cancer patients responsive to immunotherapy.
Data indicate the role of AT rich interactive domain 1A (SWI- like) (ARID1A) in maintaining mitotic integrity and the lack of genomic instability in ARID1A-mutated cancers.
ARID1A may serve as a tumour suppressor in osteosarcoma progression.
Depletion of ARID1A represses RNA polymerase II (RNAPII) transcription but results in modest changes to accessibility.
Study utilizes human endometrial epithelial cells to elucidate the consequences of ARID1A loss and PIK3CAH1047R in vitro and discover a mechanism by which ARID1A and PIK3CA mutations result in a partial epithelial-to-mesenchymal transition phenotype capable of collective invasion into the uterine myometrium.
Loss of ARID1A is tightly associated with high PD-L1 expression in GC.
We demonstrate here that ARID1A-L is critical for ES maintenance and supports oncogenic transformation. We further report a novel feed-forward cycle in which EWS-FLI1 leads to preferential splicing of ARID1A-L, promoting ES growth, and ARID1A-L reciprocally promotes EWS-FLI1 protein stability.
ARID1A loss by immunohistochemistry is uncommon in small intestinal adenocarcinomas.
The pharmaceutical inhibition with p38MAPK-specific inhibitor SCIO-469 revealed that p38MAPK-related signalling axis regulates ARID1A expression and thereby modulates paclitaxel sensitivity in triple-negative breast cancer triple-negative breast cancer (TNBC)
In the 33 cases included in poor prognosis group, TP53 was most mutated gene (p = 0.011) and exclusively present in these cases. Similarly, ARID1A was exclusive of this group (p = 0.024). TP53 and ARID1A are mutually exclusive in this study. Statistical analysis showed mutations in TP53 and ARID1A genes and amplification of MET gene as independent predictors of poor prognosis
study revealed significant associations of two variants rs6598860 and rs4589135 in ARID1A with overweight/obesity. We also identified association of rs3804562 in KAT2B gene with body mass index
ARID1A Gene Driver Mutations are associated with Lung Adenocarcinomas.
Results suggest that ARID1A mutation in endometrial cancer helped cell proliferation and inhibited cell apoptosis and also caused cell cycle arrest at the G2/M phase.
ARID1A loss in premalignant EH is an accurate and almost perfectly specific prognostic marker for coexistent cancer.
Data show that AT-rich interaction domain 1A (ARID1A) knockdown in ovarian cancer cells reduced their apoptosis rate, led to multiple drug resistance (MDR) and transcriptionally activates the expression of multidrug resistance-associated protein 2 (MRP2).
The expression levels of ARID1A and PIK3CA in gastric cancer were significantly associated with the depth of invasion of gastric cancer.
High Beclin-1 and ARIDIA expression are strongly associated with poor prognosis in ICC patients, and thus Beclin-1 and ARID1A should be simultaneously considered as potential prognostic biomarkers for ICC patients.
The ARID1A and PIK3CA were the most frequently mutated genes. Specifically, ARID1A mutations and PIK3CA mutations were detected in 77.8% and 66.7% of ovarian clear cell carcinoma patients, respectively. Mutations in other genes, including MLH1 (6.3%) and CREBBP (6.3%), were detected in the Taiwanese population.
these results suggest ARID1A deficiency contributes to impaired MMR and mutator phenotype in cancer, and may cooperate with immune checkpoint blockade therapy.
Study shows that monoallelic loss of Arid1a in the mouse endometrial epithelium is sufficient for vaginal bleeding when combined with Pik3ca activation. Pik3ca activation partially rescues the mesenchymal phenotypes driven by Arid1a loss through antagonism of Arid1a target gene expression, resulting in partial epithelial-to-mesenchymal transition and invasion.
this study demonstrates that hepatocyte-specific inactivation of Arid1a reduced fatty acid oxidation, and aggravated diet-induced steatosis and insulin resistance in mice.
ARID1A-containing SWI/SNF complex (ARID1A-SWI/SNF) operates as an inhibitor of the pro-oncogenic transcriptional coactivators YAP and TAZ
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
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)