| 2005 |
ARID2 (BAF200) is a specificity subunit of the PBAF chromatin-remodeling complex (SWI/SNF family) required for selective transcriptional activation of interferon-responsive genes; PBAF and BAF regulate expression of distinct gene sets, and this selectivity requires BAF200 but not the previously described PBAF-specificity subunit BAF180. |
Biochemical complex purification, in vivo gene expression studies comparing PBAF vs BAF complex activity on interferon-responsive gene promoters |
Genes & development |
High |
15985610
|
| 2014 |
BAF200 (ARID2) is required for heart morphogenesis and coronary artery development in vivo; BAF200 mutant mice are embryonic lethal with thin myocardium, ventricular septum defect, common atrioventricular valve, double outlet right ventricle, and reduced intramyocardial coronary arteries, indicating a role in migration and differentiation of subepicardial venous cells into arterial endothelial cells. |
BAF200 mutant mouse generation (conditional knockout), histology, embryonic phenotype analysis |
PloS one |
High |
25299188
|
| 2016 |
ARID2 suppresses hepatoma cell proliferation and tumor growth by physically interacting with E2F1 and decreasing E2F1/RNA Pol II binding to the promoters of CCND1 (cyclin D1) and CCNE1 (cyclin E1), thereby repressing their transcription and retarding G1/S cell cycle progression. |
Co-immunoprecipitation (physical interaction with E2F1), ChIP assay (E2F1/RNA Pol II binding to CCND1/CCNE1 promoters), gain/loss-of-function proliferation assays, mouse xenograft tumor growth |
Oncotarget |
Medium |
27351279
|
| 2017 |
ARID2 is required for nucleotide excision repair (NER): ARID2 knockout in HCC cells attenuates NER at UV-induced and chemically induced DNA damage sites because XPG (xeroderma pigmentosum group G protein) cannot accumulate without ARID2, resulting in susceptibility to carcinogens and increased somatic mutation burden. |
CRISPR/Cas9 ARID2 knockout, gene expression profiling, UV irradiation sensitivity assays, XPG recruitment assay, large-scale public dataset validation |
Journal of hepatology |
High |
28238438
|
| 2017 |
Baf200 (ARID2) facilitates homologous recombination-dependent DNA double-strand break (DSB) repair by recruiting Rad51 to DSBs; Baf200 and Rad51 are present in the same complex mediated by C-terminal sequences in both proteins. Baf200 also forms at least two distinct PBAF complexes: one canonical form containing BRG1, and another containing Baf180 but not BRG1. |
Cytological and biochemical approaches (co-immunoprecipitation, homology-directed repair assays, Rad51 recruitment assays, cell survival after DNA damage) |
The Journal of biological chemistry |
High |
28381560
|
| 2018 |
Baf200 (ARID2) is required for fetal hematopoietic stem cell (HSC) expansion and erythropoiesis; Tie2-Cre-mediated loss causes perinatal death from defective erythropoiesis; conditional knockout HSCs show impaired long-term reconstitution potential in transplantation assays; loss of Baf200 in MLL-AF9-driven leukemia accelerates tumor burden, indicating a tumor suppressor role in hematopoiesis. |
Tie2-Cre, Vav-iCre, Mx1-Cre conditional knockouts, fetal liver/bone marrow transplantation, RNA-seq, cell cycle/apoptosis assays, MLL-AF9 leukemia mouse model |
Journal of hematology & oncology |
High |
29482581
|
| 2019 |
HBV core protein (HBc) physically interacts with BAF200 (ARID2) C-terminus, disrupting PBAF complex stability; this interaction suppresses IFITM1 transcription, where basal IFITM1 expression depends on BAF200 rather than the JAK-STAT1 pathway. HBc-mediated PBAF disruption thus inhibits IFNα-induced IFITM1 expression, contributing to HBV immune evasion. |
Yeast two-hybrid (initial identification), co-immunoprecipitation in 293T, HepG2, HepG2-NTCP cells, IFITM1 luciferase/expression assays, HBV replication assays |
Viruses |
Medium |
31075894
|
| 2020 |
ARID2 suppresses HCC metastasis and epithelial-mesenchymal transition (EMT) by recruiting DNMT1 to the Snail promoter, increasing promoter methylation and inhibiting Snail transcription. ARID2 mutants with disrupted C2H2 domain lose this metastasis suppressor function. |
ARID2 KO in HCC mouse models, in vitro migration/invasion assays, in vivo metastasis assays, ChIP assay (DNMT1 recruitment to Snail promoter), bisulfite sequencing (promoter methylation), domain mutant functional analysis |
Proceedings of the National Academy of Sciences of the United States of America |
High |
32071245
|
| 2020 |
ARID2 is a pomalidomide-induced neosubstrate of the CRL4CRBN E3 ubiquitin ligase complex; pomalidomide induces ARID2 degradation in multiple myeloma cells, and BRD7 (another PBAF subunit) is critical for this pomalidomide-induced ARID2 degradation. ARID2 regulates transcription of pomalidomide target genes including MYC. |
Proteomics, co-immunoprecipitation, BRD7 knockdown, pomalidomide treatment with protein degradation assays, MYC expression assays, proliferation assays |
Nature chemical biology |
High |
32958952
|
| 2020 |
ARID2 deficiency leads to STAT1 upregulation, which subsequently causes increased expression of T-cell-attracting chemokines CXCL9, CXCL10, and CCL5, sensitizing melanoma to anti-PD-L1 immune checkpoint inhibitors with increased CD8+ T cell infiltration. |
ARID2 knockout in melanoma cells, in vivo anti-PD-L1 treatment, flow cytometry (CD8+ T cell infiltration), gene expression analysis |
The Journal of investigative dermatology |
Medium |
33333124
|
| 2020 |
Loss of Arid2 in HSCs impairs lymphoid lineage differentiation in a cell-autonomous manner; Arid2 knockout enriches myeloid-biased MPP signatures while depleting lymphoid-biased MPPs, and upregulates inflammatory pathways including TLR receptors and downstream signaling genes. |
Conditional Arid2 knockout mouse, bone marrow transplantation, RNA-seq, in vitro lymphocyte growth assays with LPS stimulation |
Experimental hematology |
Medium |
33346030
|
| 2021 |
ARID2 deficiency promotes lung adenocarcinoma progression; through ChIP-seq and RNA-seq integration, Hspa1a was identified as upregulated by Arid2 loss, and HSPA1A knockdown specifically inhibits malignant progression of Arid2-deficient but not Arid2-wild-type lung cancers in cell lines and animal models. |
Kras-based genetically engineered mouse models, ARID2 KO, ChIP-seq, RNA-seq, HSPA1A knockdown, HSPA1A inhibitor treatment, in vivo tumor models |
National science review |
High |
34858604
|
| 2022 |
ARID2 mitigates hepatic steatosis by repressing JAK2-STAT5-PPARγ signaling; ARID2 promotes ubiquitination and degradation of JAK2 via NEDD4L (an E3 ligase for JAK2). Mechanistically, ARID2 recruits CARM1 to increase H3R17me2a at the NEDD4L promoter, activating NEDD4L transcription. |
Liver-specific Arid2 KO mouse (including HFD model), ChIP assay (CARM1 and H3R17me2a at NEDD4L promoter), ubiquitination assays, JAK2 inhibitor (Fedratinib) rescue, co-immunoprecipitation |
Cell death and differentiation |
High |
36396719
|
| 2022 |
BRD4 inhibition (JQ1) induces synthetic lethality in ARID2-deficient HCC cells by exacerbating DNA double-strand breaks; both ARID2 and BRD4 synergistically maintain transcriptional enhancer-promoter loops for BRCA1, RAD51, and 53BP1, and loss of both impairs their expression, preventing DSB repair. |
High-throughput drug screening, JQ1 treatment in ARID2-depleted HCC cells, DNA damage assays (DSB measurement), HR and NHEJ repair pathway assays, chromatin conformation capture, gene expression assays for BRCA1/RAD51/53BP1 |
Oncogene |
Medium |
35017665
|
| 2022 |
USP2 (ubiquitin-specific protease 2) physically interacts with ARID2 and reduces ARID2 protein degradation via the ubiquitination pathway; USP2 inhibits lung cancer cell invasion and migration by stabilizing ARID2 protein. |
IP-Mass Spectrometry, co-immunoprecipitation, immunofluorescent colocalization, CHX chase assay, ubiquitination assay, transwell/wound healing migration assay |
BioMed research international |
Medium |
36567903
|
| 2016 |
ARID2 represses CD44 promoter activity and protein expression in hepatocellular carcinoma cells; overexpression of ARID2 inhibits cell invasion and metastasis in vitro and tumor growth in vivo in nude mice, mediated at least in part through transcriptional repression of CD44. |
Luciferase reporter assay (CD44 promoter), Western blot, adenoviral ARID2 overexpression, cell migration assay, subcutaneous tumor xenograft in nude mice |
Zhonghua gan zang bing za zhi |
Medium |
27095763
|
| 2017 |
HBx (HBV X protein) suppresses ARID2 transcription through ATOH1-binding elements in the ARID2 promoter region (nt-1040/nt-601); ectopic ATOH1 expression or mutation of ATOH1 binding sites partially abolishes HBx-triggered ARID2 repression, and ARID2 abrogates HBx-enhanced HCC cell migration and proliferation. |
Promoter deletion/luciferase assays, site-directed mutagenesis of ATOH1 binding sites, ectopic ATOH1 expression, Western blot, cell migration assays |
Cancer science |
Medium |
28498550
|
| 2020 |
ARID2 haploinsufficiency is associated with enhanced RAS-MAPK (ERK1/2) activity; this is mediated through reduced IFITM1 expression, which normally interacts with caveolin-1 (CAV-1) to inhibit ERK activation. ARID2 KO in HeLa cells increases ERK1 and ERK2 phosphorylation; patient iPSCs show impaired neuronal differentiation with enhanced RAS-MAPK activity. |
Transient ARID2 knockout via shRNA (ERK phosphorylation), patient-derived iPSC differentiation assays, Arid2 haploinsufficient mice (CRISPR/Cas9), IFITM1/CAV-1 expression analysis |
Journal of medical genetics |
Medium |
33051312
|
| 2018 |
NMR backbone resonance assignment of the ARID domain of human BAF200 (ARID2) was completed, providing secondary structure information; the ARID domain has the potential to bind DNA sequences with high affinity, though the exact DNA binding specificities within the PBAF context were not yet established. |
NMR spectroscopy (backbone 1H, 13C, 15N chemical shift assignment) |
Biomolecular NMR assignments |
Low |
30535613
|
| 2024 |
PBAF (defined by ARID2) occupies repressive chromatin regions co-bound by PRC2, and ARID2 loss disrupts PBAF complex formation, impairing REST transcription factor binding to its target loci. This leads to upregulation of synaptic/neuronal transcripts normally silenced by REST, a gene signature conserved in melanoma patients with ARID2 mutations. |
Comprehensive epigenomic profiling (ChIP-seq for SWI/SNF complexes), ARID2 knockout in melanoma cells and melanocytes, time-resolved chromatin accessibility assays, REST occupancy assays |
bioRxivpreprint |
Medium |
|
| 2024 |
ARID2 knockout in TFE3-rearranged renal cell carcinoma (TFE3-RCC) enhances ERBB3 expression; ChIP assay demonstrated that PRCC-TFE3 directly binds and upregulates ERBB3, and ARID2 KO further enhances this effect. ARID2-KO TFE3-RCC cells show increased MAPK and ERBB3 signaling activation and heightened sensitivity to ERBB3 inhibitor AZD8931. |
In vitro and in vivo ARID2 KO experiments, transcriptomic analysis, ChIP assay (PRCC-TFE3 binding to ERBB3), ERBB3 inhibitor sensitivity assays, migration/proliferation assays |
Current issues in molecular biology |
Medium |
39727945
|
| 2025 |
Arid2 is required for normal B cell differentiation in vivo; Mb1-Cre-mediated deletion causes marked reduction of splenic and circulating Follicular B cells through impaired differentiation (not proliferation or survival). Arid2 loss disrupts stage-specific gene expression programs in pro-B, pre-B, and Follicular B cells, with cumulative downregulation of B cell receptor signaling pathways, and functionally impairs germinal center expansion and IgG antibody production. |
Conditional KO mice (Mb1-Cre, CD19-Cre), flow cytometry, RNA-seq of isolated B cell populations, immunization assays, bone marrow transplantation |
bioRxivpreprint |
Medium |
41256460
|