ARID3B antibody - N-terminal region (ARP34275_T100)
- Known as:
- ARID3B (anti-) - N-terminal region (ARP34275_T100)
- Catalog number:
- arp34275_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- ARID3B antibody - N-terminal region (ARP34275_T100)
Related genes to: ARID3B antibody - N-terminal region (ARP34275_T100)
- Gene:
- ARID3B NIH gene
- Name:
- AT-rich interaction domain 3B
- Previous symbol:
- -
- Synonyms:
- BDP, DRIL2
- Chromosome:
- 15q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-28
- Date modifiied:
- 2016-10-05
Related products to: ARID3B antibody - N-terminal region (ARP34275_T100)
Related articles to: ARID3B antibody - N-terminal region (ARP34275_T100)
- Liquid-liquid phase separation (LLPS) of ARID3B is critical in nonsyndromic cleft lip/palate pathogenesis. Here, we present a protocol to visualize ARID3B LLPS. We describe steps for regenerating LLPS with purified protein in vitro and detecting ARID3B condensates in mammalian cells. This protocol enables analysis of ARID3B phase separation dynamics and the study of other transcription factors that undergo LLPS. For complete details on the use and execution of this protocol, please refer to Li et al.. - Source: PubMed
Publication date: 2026/07/02
Han WenyuLi XiaofengLin JunyanPan Yongchu - To investigate the association between serum folate and Primary biliary cholangitis (PBC) progression through clinical, transcriptomic, and protein-level analyses. - Source: PubMed
Publication date: 2026/06/03
Yan YujieMu QieLi BonanSun YuqingYang HongHuang ZhiqinYu BaofengZhang LiHuang Huifang - Microsatellite-stable/proficient mismatch repair (MSS/pMMR) colorectal cancer (CRC) is characterized by a cold tumor microenvironment, with limited CD8⁺ T cell infiltration and poor responsiveness to immune checkpoint inhibitors (ICIs). Here, using an in vivo CRISPR/Cas9 screen in a CMT93 cell-derived murine tumor model, we identify Arid3b as a key negative regulator of CD8⁺ T cell infiltration and antitumor activity. Genetic ablation of Arid3b in CD8⁺ T cells significantly enhances their intratumoral accumulation and promotes robust tumor control. Mechanistically, Arid3b deficiency upregulates Runx3, driving a tissue-resident memory-like phenotype and effector function. Notably, the benefits conferred by Arid3b deficiency are abrogated upon Runx3 deletion, indicating a RUNX3-dependent mechanism. Together, targeting ARID3B could offer a promising strategy to reshape the tumor microenvironment and sensitize MSS CRC to immunotherapy. - Source: PubMed
Publication date: 2026/05/15
Wang ShuoHou SenLuo CeZhang HaoruiJin YitengZhang RuiZhao YanpingXiong XiaoyuGuo RuiWang ChaoBao YudiWen LiangPan DengYe YingjiangZeng ZexianGao Zhidong - Transcription factors that control stem cell programs are central drivers of cancer progression, metastasis, and therapy resistance. ARID3B, a DNA-binding protein overexpressed across multiple tumor types, expands the cancer stem cell population by regulating these pathways. Yet, how ARID3B is regulated remains largely unknown. Here, we uncover phosphorylation at Serine 89 as a critical switch controlling ARID3B localization and function. We used site-directed mutagenesis to generate phospho-dead (S89A) and phospho-mimetic (S89D) ARID3B constructs, and we generated a phospho-specific antibody for S89. With these tools, we showed that phosphorylation confines ARID3B to the nucleus in ovarian cancer and glioblastoma cells, as well as in human tissues, while unphosphorylated ARID3B can localize to the nucleus, cytoplasm, and membrane. Functionally, S89D mirrors wild-type ARID3B in regulating key transcriptional programs, whereas S89A diverges, consistent with altered subcellular localization. Chromatin immunoprecipitation confirms that direct gene regulation is enhanced in WT ARID3B and S89D compared to cells expressing S89A. Collectively, these findings reveal phosphorylation as a previously unrecognized molecular switch that dictates ARID3B's localization and transcriptional activity, providing novel insights into cancer stem cell regulation and identifying a potential targetable vulnerability in aggressive tumors. - Source: PubMed
Publication date: 2026/03/30
Landeros-Rodriguez MicneyaAiliani KrishnaDahl RichardCowden Dahl Karen D - This investigation sought to explore the possible role of mmu_circ_0000684 and its homolog hsa_circ_0067098 in the evolution of ischemia-reperfusion-induced acute kidney injury (AKI), with an emphasis on their viability as therapeutic targets. - Source: PubMed
Publication date: 2025/11/29
Yang BenZheng QiangPu YanHu YingyingZhang Dongshan