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)
- 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 - Genome-wide association studies have identified numerous loci associated with nonsyndromic cleft lip with/without cleft palate (nsCL/P). However, the causal genes within these loci remain to be systematically investigated. Through a multiomics screening strategy, we identified 20 candidate genes, with ARID3B emerging as the most significant risk gene for nsCL/P. Focusing on the ARID3B locus, we found a casual variant at rs1821848 that diminished the binding affinity of NR2C2, resulting in the upregulation of ARID3B. Notably, we observed the formation of ARID3B granules through liquid-liquid phase separation (LLPS) both in vivo and in vitro. This ARID3B-mediated LLPS could essentially recruit coactivators SMAD2/3 and establish enhancer activity necessary for initiating the gene profile related to nsCL/P. Ultimately, disrupting the LLPS of arid3b effectively rescued migration, apoptosis, and phenotype deficits in zebrafish models. This study systematically revealed biological functions of both rs1821848 and ARID3B during nsCL/P development. - Source: PubMed
Publication date: 2025/09/30
Li XiaofengLi DandanLou ShuLin JunyanGao YueVona BarbaraMi CongboWang LinMa LanDu MulongPan Yongchu - Ovarian cancer (OC) is one of the most common and lethal solid malignancies among women, with its incidence steadily rising. Despite substantial advancements in OC research, its pathogenesis remains largely elusive. Recent studies indicate that the regulator of G protein signaling 3 (RGS3) is implicated in tumorigenesis, however, its specific role in OC development has not been extensively investigated. Herein, this research elucidated that the overexpression of RGS3 in OC correlates with adverse clinical pathological features and tumor progression. Furthermore, we demonstrated that silencing RGS3 promotes apoptosis, effectively inhibiting tumor growth and metastasis. Additionally, our findings reveal that RGS3 enhances oncogenic activity by participating in the regulation of the transforming growth factor-beta (TGF-β) pathway and corresponding epithelial-mesenchymal transition (EMT). The in-depth mechanism lies in the RGS3 facilitating the phosphorylation of SMAD2/3 by directly interacting with AT-rich interactive domain-containing protein 3B (ARID3B), which ultimately drives OC cell proliferation and metastasis. Therefore, our results position RGS3 as a significant prognostic biomarker and tumor-promoting factor in OC, underscoring the pivotal role of the RGS3/TGF-β/EMT signaling pathway in the pathogenesis of this malignancy. - Source: PubMed
Publication date: 2025/06/02
Wang ZizhaoSun HuatingZhu ShunpengWang FangLi QuanZhou Jinhua - Self-limited delayed puberty (SLDP) is the most common cause of delayed puberty and exhibits high heritability, although few causal genes have been identified. This study aims to identify potential candidate genes associated with SLDP. - Source: PubMed
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