Ask about this productRelated genes to: ARID3A antibody
- Gene:
- ARID3A NIH gene
- Name:
- AT-rich interaction domain 3A
- Previous symbol:
- DRIL1
- Synonyms:
- BRIGHT
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-08-22
- Date modifiied:
- 2015-11-17
Related products to: ARID3A antibody
Related articles to: ARID3A antibody
- : B-cell receptor (BCR) signalling is implicated in Burkitt lymphoma (BL) lymphomagenesis, although its activation may differ across biological and epidemiological settings. While surface IgM is the predominant immunoglobulin isotype of BCR in BL, cases expressing IgA transcripts or lacking detectable surface immunoglobulin (sIg) expression have been reported, suggesting a more complex pattern of sIg expression than previously recognized. This study aimed to evaluate sIg heavy-chain expression by immunohistochemistry in a relatively large series of BL cases from endemic and sporadic settings and to investigate the mutational landscape of surface immunoglobulin-undetectable (sIg-UND) cases. : sIg heavy-chain expression was assessed by immunohistochemistry in 55 formalin-fixed paraffin-embedded BL samples. Targeted next-generation sequencing was performed on four sIg-UND cases using an Illumina capture-based custom panel covering 74 lymphoma-related genes. and hotspot mutations were additionally assessed by real-time PCR. : Overall, 41/55 cases showed IgM expression, including 31 IgM-positive and 10 IgM+/UND cases, whereas 8/55 cases showed IgA expression (IgA+/UND). IgA-expressing cases were significantly enriched at mucosal sites, particularly the oral cavity and gastrointestinal tract, consistent with the relevance of these anatomical sites to mucosal IgA production. Six cases lacked detectable sIg expression, showing negativity for all tested immunoglobulin heavy chains in more than 90% of neoplastic cells. Four sIg-UND cases were available for sequencing. These cases harbored mutations affecting genes commonly altered in BL, together with alterations in genes less commonly represented in recurrent BL series, such as , , , , , , and . : Our study provides a systematic immunohistochemical characterization of surface immunoglobulin heavy-chain expression in a relatively large series of endemic and sporadic BL. We identified a subset of IgA-expressing BL cases enriched at mucosal sites, whereas rarer cases lacked detectable surface immunoglobulin expression. The mutational profile of sIg-UND cases highlights alterations affecting genes involved in epigenetic regulation, chromatin organization, and B-cell differentiation, which may contribute to the biological heterogeneity of these cases. No or hotspot mutations were detected in the four sequenced sIg-UND cases, as assessed by targeted NGS and real-time PCR. Further functional studies are needed to clarify the biological and clinical significance of sIg-UND BL cases and to determine the functional relevance of the identified alterations. - Source: PubMed
Publication date: 2026/07/30
Siciliano Maria ChiaraLori CosimoVannucchi MargheritaAmato TeresaBertolazzi GiorgioGuazzo RaffaellaNoel OnyangoOnyuma TimothyGranai MassimoBoccacci RobertoGrace KirakaPeter OyiroOnsongo SimonGeorgina MagomaWedaga Sakeah PatienceFoster KwawuMildred HagembeJoshua NyagolFischer AnjaBellan CristianaSiebert ReinerLeoncini LorenzoLazzi Stefano - Numbers of ARID3a ( AT - R ich Interaction D omain 3a ) -expressing B lymphocytes from patients with systemic lupus erythematosus (SLE) are associated with increased disease activity. Normally, ARID3a-expressing circulating naïve B cells are rare, but in SLE naïve B cells dramatically increase ARID3a expression. We found that stimulation of B lymphocytes from healthy individuals with a cocktail of cytokines and agonists induced ARID3a in a subset of activated naïve B cells and in IgD CD27 double negative B cells previously associated with autoimmunity. Single cell RNA-seq of isolated naïve B cells from ten SLE patients, with varying frequencies of ARID3a-expressing cells, revealed that ARID3a-associated genes included activation markers. Moreover, our data revealed the unexpected co-expression of the scavenger receptor CD68 with ARID3a, at both the transcript and protein level, in activated subsets of naïve B cells. Inhibition of ARID3a in stimulated B cell cultures blocked naïve B cell activation and CD68 expression. Together, these data identify ARID3a and CD68 as markers of naïve B cell precursors associated with autoimmunity in SLE. - Source: PubMed
Publication date: 2026/07/16
Garton JoshuaHocker JamesGarman LoriZhong HuaZimmerman KurtGuthridge Joel MJames Judith AWebb Carol F - 2-cell like cells (2CLC) are a transiently cycling population of cells with totipotent-associated features. Although CTCF depletion induces 2CLC conversion in mouse ESC, whether this reprogramming is a consequence of disrupted higher-order chromatin organization or of CTCF-specific functions remained unclear. Here, we show that depletion of the cohesin release factor WAPL in ESC also promotes 2CLC reprogramming, which is increased by CTCF co-depletion. Single-cell RNA-seq/ATAC-seq analyses in CTCF/WAPL-depleted ESC revealed that chromatin accessibility precedes 2C-associated gene expression. Moreover, we identified ARID3A as a transcription factor that regulates the extent of 2CLC conversion following WAPL/CTCF depletion. Although WAPL or CTCF depletion induces distinct transcriptional changes in human ESC, these do not resemble transcriptional programs of early human embryogenesis, suggesting limited evolutionary conservation. Finally, we demonstrate that 2CLC conversion mediated by alterations in chromatin organization depends on the DPPA2/DUX axis and correlates with nucleolar integrity. Together, these findings establish a mechanistic link between higher-order chromatin organization and totipotency-like cell identity in mice. - Source: PubMed
Publication date: 2026/07/09
Carey Grace IVega-Sendino MariaTillo DesireeHoelscher Sarah CKhan AmirTaukulis IanOlbrich TeresaSaykali BecharaTran Andy DSoni BhavyaLee Fong AnnaMikolaj MelissaHarned AdamNarayan KedarKruhlak Michael JKelly MichaelLiu Ning Qingde Wit ElzoRuiz Sergio - AT-rich interaction domain 3A (ARID3A) is a tumor regulator that modifies the PTEN and Akt pathway. The present study aimed to investigate the effect of ARID3A knockdown on ferroptosis and the interaction between ARID3A and the PTEN/Akt pathway in breast cancer. Firstly, MCF-7 and MDA-MB-231 cell lines were cultured. Negative control small interfering RNA (siNC) and ARID3A small interfering RNA (siARID3A) were transfected into the cells. Subsequently, siNC, PTEN small interfering RNA (siPTEN) and siARID3A were transfected into the cells alone or in combination. Comprehensive ferroptosis-associated indices were assessed. siARID3A transfection decreased cell viability, mitochondrial membrane potential (MMP) and glutathione peroxidase 4 (GPX4) expression, but increased the levels of malondialdehyde, reactive oxygen species (ROS) and ferrous iron (Fe), suggesting that siARID3A transfection promoted ferroptosis. Furthermore, siARID3A transfection upregulated PTEN expression and downregulated phosphorylated (p)-Akt levels, while siPTEN transfection elevated p-Akt levels and attenuated the effect of siARID3A transfection on p-Akt levels, indicating that siARID3A transfection modified the PTEN-mediated Akt pathway. In addition, siPTEN transfection increased cell viability, MMP and GPX4 expression, while decreasing ROS and Fe levels. siPTEN transfection weakened the effect of siARID3A transfection on the majority of the aforementioned ferroptosis-associated indices, suggesting that PTEN was implicated in the function of ARID3A in ferroptosis. Overall, ARID3A knockdown promoted ferroptosis partly through modulation of the PTEN/Akt pathway in breast cancer. Despite this, further verification is still needed in future studies. - Source: PubMed
Publication date: 2026/06/29
Shi PengfeiYi YanZhang MaojieLiu YongjunJiang MingZhang Jiaming - Ferroptosis, a unique modality of regulated cell death, has become an emerging strategy for tumor therapy. Multiple cellular pathways, including redox homeostasis, iron handling, epigenetic regulation, and metabolic changes, could mediate ferroptosis. Here, we demonstrate that high expression of iron-responsive element binding protein (IRP1)/A + T rich interaction domain protein 3a (ARID3A) inhibits ferroptosis and enhances chemoresistance of pancreatic cancer cells via handling the promoter region of a ferroptosis gene, cytoglobin (CYGB). Mechanistically, the high level of iron leads to nuclear translocation of IRP1 and ARID3A, thereby mediating ARID3A binding to the promoter region of CYGB and down-regulation of chromatin accessibility. The decrease of CYGB expression results in pancreatic cancer cell resistance to ferroptosis, which makes them more resistant to chemotherapy. Clinically, high expression of IRP1 and ARID3A associates with unsatisfactory chemotherapeutic response and poor survival of patients with pancreatic cancer. Our study highlights the role of IRP1/ARID3A complex as a chemotherapy target and its potential in the combined application of ferroptosis drugs. - Source: PubMed
Publication date: 2025/09/24
Li ZeruQin ChengZhao BangboLi TianyuZhao YutongHuang LiruiShi HaoyuXie YipingYan YutongZhang XiangyuWang Weibin