| 2000 |
p270/ARID1A is an integral subunit of human SWI/SNF complexes and contains a non-sequence-specific DNA-binding ARID domain, establishing it as a human counterpart of yeast SWI1. |
Co-purification from mammalian cells, biochemical fractionation, ARID domain characterization, DNA binding assay |
Molecular and cellular biology |
High |
10757798
|
| 1998 |
p270/ARID1A is an integral member of the human SWI/SNF chromatin remodeling complex, co-purifying with SWI/SNF components. |
Co-immunoprecipitation, biochemical purification, antibody cross-reactivity analysis |
Molecular and cellular biology |
High |
9584200
|
| 2005 |
p270/ARID1A is required for cell cycle arrest on differentiation induction; its depletion prevents up-regulation of p21 and down-regulation of cyclins/E2F-responsive products, demonstrating functional distinctness from ARID1B-containing complexes. |
siRNA knockdown, BrdU incorporation (DNA synthesis assay), Western blotting for p21 and cyclins |
Cancer research |
High |
16230384
|
| 2008 |
BAF250a/ARID1A is required for ES cell pluripotency and self-renewal; its ablation promotes differentiation into primitive endoderm-like cells and blocks mesodermal layer formation in early mouse embryos. |
Conditional knockout mouse model, ES cell culture, DNA microarray, immunostaining, embryoid body differentiation assays |
Proceedings of the National Academy of Sciences of the United States of America |
High |
18448678
|
| 2009 |
ARID1A/BAF250A physically interacts with the tumor suppressor HIC1 in a BRG1-dependent manner and is recruited to the E2F1 promoter in a repressive SWI/SNF complex; ARID1A does not interact with BRM. |
Yeast two-hybrid screen, co-immunoprecipitation in WI38 fibroblasts and BRG1-/- SW13 cells, sequential ChIP (ChIP-reChIP) |
Biochemical and biophysical research communications |
Medium |
19486893
|
| 2010 |
BAF250/ARID1 (predominantly ARID1B isoform studies, but functional context applies to ARID1A) assembles with Elongin C, Cullin 2, and Roc1 into an E3 ubiquitin ligase that monoubiquitinates histone H2B at lysine 120 in vitro; Drosophila osa (BAF250 ortholog) or BAF250 RNAi depletion reduced global H2Bub. |
Immunopurification from mammalian cells, in vitro ubiquitination assay, RNAi in Drosophila and human cells |
Molecular and cellular biology |
Medium |
20086098
|
| 2012 |
BAF250a/ARID1A regulates cardiac progenitor cell differentiation; conditional ablation in mouse second heart field causes trabeculation defects, ventricular septal defect, and embryonic lethality. Mechanistically, BAF250a binds to target gene promoters (Mef2c, Nkx2.5, Bmp10) and recruits BRG1 to modulate chromatin accessibility. |
Conditional knockout mouse, ES cell cardiomyocyte differentiation model, ChIP, DNase I hypersensitivity assay |
The Journal of biological chemistry |
High |
22621927
|
| 2013 |
BAF250a/ARID1A deletion disrupts replication timing at specific chromosomal domains in ES cells, and BAF250a-deficient fibroblasts reprogrammed to pluripotency fail to reprogram replication timing in these same domains. |
Conditional knockout ES cells, Repli-seq (replication timing), esBAF ChIP |
Epigenetics & chromatin |
Medium |
24330833
|
| 2014 |
Baf250a/ARID1A in the sinoatrial node activates Tbx3 expression and, together with Tbx3 and HDAC3, represses Nkx2.5; disruption of this pathway switches on contractile cardiomyocyte programming in the SAN, causing sick sinus disease. |
SAN-specific conditional knockout mouse, gene expression time-series analysis, ChIP, functional cardiac assays |
Cell research |
High |
25145359
|
| 2015 |
ARID1A is recruited to DNA double-strand breaks via interaction with the ATR kinase; it facilitates processing of DSBs to single-strand ends and sustains DNA damage signaling. ARID1A deficiency sensitizes cancer cells to PARP inhibitors. |
Co-immunoprecipitation (ARID1A-ATR interaction), laser-induced DSB recruitment (live imaging), siRNA knockdown, in vitro and in vivo PARP inhibitor sensitivity assays |
Cancer discovery |
High |
26069190
|
| 2017 |
ARID1A has context-dependent oncogenic and tumor suppressor functions in hepatocellular carcinoma. ARID1A gain-of-function promotes tumor initiation via increased CYP450-mediated oxidative stress, while ARID1A loss within established tumors decreases chromatin accessibility and reduces transcription of genes associated with migration, invasion, and metastasis. |
Liver-specific conditional KO and overexpression mouse models, ATAC-seq, RNA-seq, tumorigenesis assays |
Cancer cell |
High |
29136504
|
| 2018 |
ARID1A is a transcriptional repressor at ER cis-regulatory elements; it recruits HDAC1 to enhancers in a FOXA1-dependent, ER-independent manner. ARID1A loss results in decreased HDAC1 binding, increased H4K acetylation, and subsequent BRD4-driven transcription and proliferation. |
Genome-wide CRISPR screen, ChIP-seq, ATAC-seq, HDAC1 Co-IP, H4K acetylation Western blotting |
Nature genetics |
High |
31913353
|
| 2018 |
ARID1A loss suppresses pancreatic neoplasia partly through regulation of MYC activity and protein synthesis; ARID1A knockdown in human pancreatic ductal epithelial cells increases MYC expression, which is abolished by MYC knockdown. ChIP-seq showed increased H3K27ac at enhancers/promoters upon Arid1a loss. |
Conditional Arid1a KO mouse, siRNA/CRISPR knockdown in human cells, RNA-seq, ChIP-seq for H3K27ac |
Gut |
High |
30315093
|
| 2019 |
ARID1A loss increases susceptibility to hepatic steatosis and insulin resistance; mechanistically, Arid1a deficiency impairs fatty acid oxidation by downregulating PPARα and altering the epigenetic landscape of metabolism genes. |
Hepatocyte-specific Arid1a KO mouse, GTT/ITT, ChIP, ATAC-seq, RNA-seq |
EBioMedicine |
High |
30879920
|
| 2020 |
ARID1A inactivation causes resistance to ER degraders by facilitating a switch from ER-dependent luminal to ER-independent basal-like cells; this is mediated by loss of ARID1A-dependent SWI/SNF targeting to luminal lineage-determining TF (ER, FOXA1, GATA3) sites. ARID1A also regulates genome-wide ER-FOXA1 chromatin interactions. |
Epigenome CRISPR KO screen, ChIP-seq, ATAC-seq, patient sample analysis |
Nature genetics |
High |
31932695
|
| 2020 |
ARID1A interacts with EZH2 via its carboxyl terminus and antagonizes EZH2-mediated suppression of IFN-responsive gene chromatin accessibility; ARID1A loss limits chromatin accessibility to IFN-responsive genes and impairs IFN gene expression. |
Co-immunoprecipitation (ARID1A-EZH2 interaction), ATAC-seq, IFN reporter assays, murine cancer models |
The Journal of clinical investigation |
High |
32027624
|
| 2020 |
ARID1A deficiency in the endometrium leads to loss of TGF-β tumor suppressive function; ARID1A-deficiency/TGF-β axis inactivation promotes migration and invasion of PTEN-deleted endometrial tumor cells. |
Conditional KO mouse models (Arid1a, Pten), transcriptome analysis, functional migration/invasion assays, systems biology approach |
Nature communications |
High |
32483112
|
| 2020 |
The E3 ligase TRIM32 and deubiquitinase USP11 control ARID1A protein stability via the ubiquitin-proteasome system in squamous cell carcinoma; TRIM32 stabilizes ARID1A while USP11 promotes its degradation. SDC2 is a downstream target of the TRIM32/USP11-ARID1A axis. |
siRNA knockdown, co-immunoprecipitation, ubiquitination assay, proliferation/invasion assays |
Cell reports |
Medium |
31914402
|
| 2021 |
ARID1A loss leads to DNA replication stress associated with R-loops and transcription-replication conflicts; ARID1A-deficient cells show reduced TOP2A binding at R-loop sites. |
ARID1A KO human cell lines, R-loop immunofluorescence (S9.6 antibody), DRIP-seq, replication dynamics analysis |
PLoS genetics |
High |
33826602
|
| 2021 |
SWI/SNF represses glutaminase (GLS1), and ARID1A inactivation upregulates GLS1, increasing glutamine utilization through the TCA cycle to support aspartate synthesis; this creates a metabolic dependency exploitable with GLS1 inhibition. |
ARID1A KO cell lines, ChIP, metabolic flux analysis, orthotopic and PDX mouse models, genetic OCCC mouse model |
Nature cancer |
High |
34085048
|
| 2021 |
ARID1A loss promotes pancreatic neoplasia in a compartment-specific manner; in acinar cells, postnatal Arid1a silencing with oncogenic KrasG12D induces rapid irreversible reprogramming to mucinous PDAC precursor lesions, while embryonic Arid1a silencing preserves acinar identity. |
Inducible/reversible shRNA in KrasG12D mouse pancreas, lineage tracing, histological analysis |
eLife |
High |
30014851
|
| 2021 |
ARID1A promotes both NHEJ and HR DNA DSB repair; it accumulates at DSBs and recruits RAD21 and CTCF to regulate chromatin loop formation; simultaneously facilitates transcription silencing at DSBs by recruiting HDAC1 and RSF1 to control chromatin accessibility and evict RNAPII. |
ChIP-seq, ATAC-seq, proximity ligation, NHEJ/HR reporter assays, ARID1A KO cells |
Nucleic acids research |
High |
38587186
|
| 2021 |
ARID1A loss in HCC activates mTOR signaling (increased pS6) and SOX9 nuclear expression; mTORC1 physically interacts with ARID1A and promotes its ubiquitination and proteasomal degradation, driving YAP-dependent transcription and liver tumor development. |
Co-immunoprecipitation (mTORC1-ARID1A), ubiquitination assay, in vitro/in vivo tumor models, ChIP for YAP targets |
Cancer research |
High |
34429326
|
| 2022 |
Inflammatory signaling activates IKKβ to phosphorylate ARID1A, leading to its β-TRCP-mediated degradation; ARID1A downregulation silences the A20 deubiquitinase enhancer, unleashing NF-κB signaling and CXCR2 ligand-mediated PMN-MDSC chemotaxis. |
Co-immunoprecipitation, phosphorylation assay, ChIP for A20 enhancer, prostate-specific conditional KO mouse, MDSC neutralization experiment |
Nature communications |
High |
36435834
|
| 2021 |
TP53 and ARID1A mutations drive shared and distinct tumorigenic programs; ARID1A normally directly represses p53 pathway genes including ATF3 in vivo, and p53 pathway is activated following ARID1A loss in the endometrial epithelium. |
Conditional KO mouse models (Arid1a, TP53, PIK3CA), ChIP-seq, RNA-seq, functional invasion assays |
PLoS genetics |
High |
34941867
|
| 2022 |
ARID1A loss in biliary cells suppresses TGF-β-Smad4 tumor suppressor pathway, enabling a biliary proliferative response; an ARID1A-TGF-β-Smad4 axis limits biliary epithelial response to oncogenic insults. |
Hepatocyte/biliary lineage-specific KO mouse models, cultured cells, proliferation/senescence assays, chromatin structure analysis, SMAD4 pathway analysis |
Cell reports |
High |
36044839
|
| 2022 |
ARID1A deficiency in HCC upregulates USP9X and PRKAA2 (AMPKα2) by losing ARID1A-HDAC1 repressive complex at the USP9X promoter (via ARID1A C-terminal DUF3518 domain recruiting HDAC1), enabling survival under glucose starvation. |
CRISPR KO, mass spectrometry, Co-IP, GST pulldown, ChIP, luciferase reporter assay |
Cellular and molecular gastroenterology and hepatology |
High |
35390516
|
| 2021 |
ARID1A interacts with and directly binds the transcriptional coactivators YAP and TAZ, sequestering them from their DNA-binding partner TEAD, thereby suppressing postnatal cardiomyocyte proliferation and promoting maturation. |
Conditional Arid1a KO in cardiomyocytes, ARID1A-YAP/TAZ direct binding assay, genome-wide transcriptome and epigenome (ATAC-seq, ChIP-seq) |
Nature communications |
High |
37543677
|
| 2021 |
ARID1A physically interacts with progesterone receptor-A (PGR-A) but not PGR-B in mouse and human endometrium; uterine Arid1a KO mice are infertile due to loss of epithelial PGR signaling. |
Co-immunoprecipitation, proximity ligation assay (PLA), uterine-specific Arid1a KO mouse, immunostaining |
Biochemical and biophysical research communications |
Medium |
33706098
|
| 2023 |
ARID1A loss represses expression of the glycolytic gene PKM, shifting glucose metabolism from aerobic glycolysis to dependence on TCA cycle and oxidative phosphorylation; ARID1A-deficient HCC cells show synthetic lethality with TCA cycle/cuproptosis-related gene inhibition. |
CRISPR-Cas9 synthetic lethality screen in ARID1A-deficient HCC cells, metabolic flux analysis, xenograft models, ChIP for PKM |
Cell reports. Medicine |
High |
37939712
|
| 2023 |
ARID1A loss reduces chromatin accessibility and expression of rate-limiting mevalonate pathway enzymes (HMGCR, HMGCS1), creating a synthetic lethality with mevalonate pathway inhibitors and inducing immunomodulating pyroptosis. |
ATAC-seq, RNA-seq, orthotopic and genetic OCCC mouse models, immune checkpoint blockade combination experiments |
Cancer cell |
High |
36963401
|
| 2024 |
ARID1A recognizes R-loops with high affinity in an ATM-dependent manner, recruits METTL3 and METTL14 to drive m6A methylation of R-loop RNA, which then facilitates RNase H1 recruitment to resolve R-loops and promote DNA end resection at DSBs. |
Co-immunoprecipitation, m6A-seq, R-loop immunofluorescence, RNase H1 recruitment assays, ARID1A/METTL3/METTL14 KO cells, DSB end resection assay |
Cell reports |
High |
38358891
|
| 2024 |
ARID1A orchestrates SWI/SNF-mediated sequential binding of PU.1 and NF-kB at key genes for cytokine and CD40 signaling in B cells during germinal center response; ARID1A loss tilts GC cell fate toward immature IgM+CD80-PD-L2- memory B cells. |
Conditional Arid1a KO mouse, ChIP-seq, ATAC-seq, scRNA-seq, BCL2 oncogene cooperation model |
Cancer cell |
High |
38458187
|
| 2024 |
ARID1A is required for IRF4 expression and physically associates with IRF4 protein on chromatin in multiple myeloma; Arid1a deletion in activated B cells disrupts IRF4-dependent transcriptional networks and blocks plasma cell differentiation. |
Conditional Arid1a KO in activated B cells, multi-omics (functional genomics screen, spatial proteomics, global chromatin mapping), Co-IP of ARID1A-IRF4 |
Cancer cell |
High |
38906156
|
| 2024 |
ARID1A harbors a prion-like domain (PrLD) that drives liquid-liquid phase separation (LLPS) to form nuclear condensates at EWS/FLI1 target enhancers, inducing long-range chromatin architectural changes and activating oncogenic target genes in Ewing's sarcoma. |
Phase separation assay, live-cell imaging of condensates, genome-wide chromatin conformation (Hi-C), ChIP-seq, ATAC-seq, PrLD mutagenesis, patient sample analysis |
Nature communications |
High |
39095374
|
| 2023 |
ARID1A loss decreases PgR (progesterone receptor) transcription by reducing SWI/SNF (ARID1A and BRG1) and H3K27ac occupancy at the PgR enhancer region in endometrial cells. |
ChIP-seq in isogenic ARID1A-/- and ARID1A+/+ endometrial cells, conditional Arid1a/Pten KO mouse model, immunohistochemistry in human samples |
Modern pathology |
High |
36853791
|
| 2020 |
BAF250a/ARID1A regulates the physical interaction between OCT4 and β-CATENIN at promoters of key mesodermal lineage genes (MESP1, EOMES) during cardiac lineage differentiation from human ESCs; ARID1A deletion reduces OCT4-BRG1 interaction in mesoderm. |
Co-immunoprecipitation (OCT4-β-CATENIN interaction), ChIP at MESP1/EOMES/CCND2/CCND3 promoters, ARID1A KO in human ESCs, differentiation assays |
Frontiers in cell and developmental biology |
Medium |
32039194
|
| 2018 |
The ARID domain of BAF250a has non-sequence-specific DNA binding; a conserved valine at position 1067, when mutated to glycine, destabilizes the ARID domain and abolishes DNA binding. The C-terminal BAF250_C region adopts an ARM-repeat fold. |
Comparative sequence analysis, computational modeling, in vitro mutagenesis of V1067G, structural stability and DNA binding affinity assays |
PloS one |
Medium |
30307988
|