Ask about this productRelated genes to: BCAS2 antibody
- Gene:
- BCAS2 NIH gene
- Name:
- BCAS2 pre-mRNA processing factor
- Previous symbol:
- -
- Synonyms:
- DAM1, SPF27, Snt309
- Chromosome:
- 1p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2000-01-31
- Date modifiied:
- 2019-01-25
Related products to: BCAS2 antibody
Related articles to: BCAS2 antibody
- Gα is a critical mediator of cell and tissue responses to G-coupled receptor stimulation. Canonically, active Gα regulates PLCβ and RhoGEFs. To identify novel Gα signaling partners, we performed a proximity labeling proteomic screen in HEK293A cells using TurboID-tagged Gα. Top Gα enriched proteins included known Gα interactors (PLCβs, RhoGEFs, and GRK2), supporting the validity of this approach. Also highly enriched were several nuclear proteins including SMARCD3, a component of the SWI/SNF chromatin remodeling complex, and BCAS2, a component of the spliceosome. Luciferase complementation experiments show that Gα selectively interacts with BCAS2 and SMARCD3 in an activation-dependent manner, and pulldown experiments with purified components demonstrate direct interaction of Gα and SMARCD3. We also show that a small but significant portion of Gα is present in the nucleus, and this is increased following GPCR activation or introduction of an activating mutation. Proximity ligation assays indicate that Gα engages SMARCD3 in the nucleus. These data suggest that Gα engages downstream targets in the nucleus and could therefore directly regulate nuclear processes. - Source: PubMed
Publication date: 2026/02/25
Loomis JosephChandan NaincyBurroughs MichaelAbraham SajiZhang RongxiCao YiyiBrody Matthew JTall Gregory GSmrcka Alan V - Growing oocytes accumulate maternal mRNA to support subsequent meiotic maturation and maternal-to-zygotic transition. However, the regulatory mechanisms governing the fate of these maternal mRNAs remain largely unknown. Here, we identified heterogeneous nuclear ribonucleoprotein M (hnRNPM) as a critical regulator of pre-mRNA alternative splicing during mouse oocyte development. Genetic ablation of hnRNPM leads to severe cytoplasmic defects, meiotic arrest, and complete female infertility. Using SCAN-seq, we uncovered novel transcript isoforms and systematically characterized hnRNPM-regulated alternative splicing events. Furthermore, LACE-seq revealed hnRNPM-binding sites at single-nucleotide resolution in oocytes, linking its RNA-binding activity to splicing fidelity. Additionally, hnRNPM interacts with BCAS2, a known splicing factor critical for oocyte development, and modulates its binding to pre-mRNA loci to precisely control the alternative splicing. Overall, our study not only uncover an essential role of hnRNPM in mammalian oocyte development and female fertility but also unveils a critical regulatory network governing alternative splicing during oocyte development. - Source: PubMed
Publication date: 2026/02/12
Zhou ShuminLiu DalinGan ShimingYu ZiqiSu RuibaoZhou HaoZhang JiaqiXu HaoranZhao YifanZhang HuaDeng ZuoqiWu XuanLuo ChunhaiLiu YunlongYuan ShuiqiaoFan Heng-YuSun Fei - The incidence of prostate cancer continues to increase, making it the second most common malignant tumor among men worldwide. Immunotherapy has emerged as a key therapeutic strategy for treating tumors. Numerous studies have established that the efficacy of tumor immunotherapy is closely associated with the tumor microenvironment and T cell subsets. However, the specific functions of certain T cell subsets in prostate cancer remain incompletely characterized. Therefore, this study aimed to systematically investigate the distribution patterns of T cell subsets within the tumor microenvironment of prostate cancer patients and their correlations with clinicopathological parameters. Therefore, we investigated the impact of T cells on the tumor microenvironment of prostate cancer at the single-cell level. We employed a variety of analytical methods to reveal the functions of T cells, including cell interaction analysis, time-series analysis, enrichment analysis, immune infiltration analysis, and other analytical approaches. By integrating bulk RNA-seq data, we constructed and validated a prognostic risk model based on T cell marker genes. Finally, we utilized the ssGSEA and ESTIMATE algorithms to explore the relationship between the prognostic risk model and immunotherapy. After quality control, 16,999 cells from the single-cell data were retained for downstream analysis. Our study focused on T cells, revealing the communication between various cell types and T cells. Pseudotime analysis showed that different T cell marker genes exhibited differential expression at various time points, corresponding to distinct biological processes. Enrichment analysis indicated that T cell marker genes were enriched in several immune-related pathways. From our analysis, BCAS2, EIF2S2, RIOK3, and ATP6V1E1 were ultimately identified as prognostic markers. Immune infiltration analysis revealed that high-risk patients had lower immune scores, stromal scores, and ESTIMATE scores and greater tumor purity compared to low-risk patients. We analyzed the mechanisms involving T cells in prostate cancer from multiple perspectives, constructed a prognostic model, and conducted immune infiltration analysis. Our findings contribute to the understanding of prostate cancer and its prognosis, providing valuable insights for future research and prognostic assessments in prostate cancer. - Source: PubMed
Publication date: 2025/12/31
Wang ZhiduXing YanShang DongmeiJin Xuefei - In children, hyper-IgM syndrome type 1 (HIGM1) is a type of severe antibody disorder, the pathogenesis of which remains unclear. The antibody diversity is partially determined by the alternative splicing (AS) in the germline, which is mainly regulated by RNA-binding proteins, including Breast cancer amplified sequence 2 (Bcas2). However, the effect of Bcas2 on AS and antibody production in activated B cells, the main immune cell type in the germline, remains unknown. To fill this gap, we created a conditional knockout (cKO, B cell-specific AID-Cre ) mouse model and performed integrated mechanistic analysis on alternative splicing (AS) and CSR in B cells through the RNA-sequencing approach, cross-linking immunoprecipitation and sequencing (CLIP-seq) analysis, and interactome proteomics. The results demonstrate that cKO significantly decreased CSR in activated B cells without inhibiting the B cell development. Mechanistically, Bcas2 interacts with SRSF7 at a conservative circular domain, forming a complex to regulate the AS of genes involved in the post-switch transcription, thereby causing broad-spectrum changes in antibody production. Importantly, we identified GAAGAA as the binding motif of Bcas2 to RNAs and revealed its essential role in the regulation of Bcas2-dependent AS and CSR. In addition, we detected a mutation of at the 3'UTR of gene in children with HIGM1 and observed similar patterns of AS events and CSR in the patient that were discovered in the cKO B cells. Combined, our study elucidates the mechanism by which Bcas2-mediated AS affects CSR, offering potential insights into the clinical implications of Bcas2 in HIGM1. - Source: PubMed
Publication date: 2025/02/16
Chen YuSun SiyuanLu ChenxuLi YixuanFang BingTang XiangfengLi XuepengYu WeiruLei YumeiSun LongjieZhang MingSun JiazengLiu PingLuo YongtingZhao XingwangZhan JingLiu LibingLiu RongHuang JiaqiangYi ZiweiYu YifeiXiao WeihanDing ZhengLi LeiSu DanRen FazhengCao ChangchangWang RanShi WenbiaoChen Juan - Breast carcinoma amplified sequence 2 (BCAS2), a core component of the hPrP19 complex, plays crucial roles in various physiological and pathological processes. However, whether BCAS2 has functions other than being a key RNA-splicing regulator within the nucleus remains unknown. Here, we show that BCAS2 is essential for primitive hematopoiesis in zebrafish and mouse embryos. The activation of Wnt/β-catenin signaling, which is required for hematopoietic progenitor differentiation, is significantly decreased upon depletion of in zebrafish embryos and mouse embryonic fibroblasts. Interestingly, BCAS2 deficiency has no obvious impact on the splicing efficiency of β-catenin pre-mRNA, while significantly attenuating β-catenin nuclear accumulation. Moreover, we find that BCAS2 directly binds to β-catenin via its coiled-coil domains, thereby sequestering β-catenin within the nucleus. Thus, our results uncover a previously unknown function of BCAS2 in promoting Wnt signaling by enhancing β-catenin nuclear retention during primitive hematopoiesis. - Source: PubMed
Publication date: 2025/06/13
Ning GuozhuLin YuMa HaixiaZhang JiaqiYang LipingLiu ZhengyuLi LeiHe XinyuWang Qiang