Ask about this productRelated genes to: BCAP31 antibody
- Gene:
- BCAP31 NIH gene
- Name:
- B cell receptor associated protein 31
- Previous symbol:
- -
- Synonyms:
- DXS1357E, BAP31, 6C6-Ag, CDM
- Chromosome:
- Xq28
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-22
- Date modifiied:
- 2017-12-06
Related products to: BCAP31 antibody
Related articles to: BCAP31 antibody
- Colorectal cancer (CRC) is one of the most common malignancies worldwide. Early and accurate diagnosis remains a clinical priority, yet current biopsy techniques are invasive, spatially limited, and may not capture the molecular heterogeneity of tumors. We evaluated the feasibility and diagnostic potential of electroporation-based biopsy (e-biopsy) as a minimally invasive technique for proteomic sampling of colorectal cancer tissues. We conducted a multicenter, multinational study involving 19 patients undergoing surgical resection for CRC. Paired tumor and adjacent normal tissues were sampled ex vivo using e-biopsy. Proteins extracted from each sample were analyzed via LC-MS/MS. Bioinformatics pipelines, including differential expression, PCA, and pathway analysis, were used to identify CRC-specific signatures. E-biopsy consistently retrieved more proteins from tumor tissues than from adjacent healthy tissues (mean: 1300 vs. 800). Of the 3246 proteins identified, 54% were significantly upregulated in tumor tissues. Notably, proteins such as DLAT, LETM1, RBBP4, PPIB, and BCAP31 emerged as potential CRC biomarkers. Functional analyses revealed dysregulation in RNA processing, immune response, and metabolic pathways, consistent with known CRC biology. The integrated workflow, spanning tissue collection, electroporation, protein isolation, and mass spectrometry analysis across four institutions in two countries, was successfully executed, demonstrating the feasibility of multi-institutional implementation of the e-biopsy protocol while preserving tissue integrity throughout. E-biopsy enables rapid, reproducible, and minimally invasive molecular sampling of CRC tissue. This study demonstrates its potential to complement standard histopathology, aid in early diagnosis, and support molecularly guided treatment strategies in colorectal oncology. - Source: PubMed
Saulis GintautasVitkin EdwardSaule RitaWise JuliaGulbinas AntanasDambrauskas ŽilvinasIvanauskienė SandraŽilinskas JustasPoskiene LinaGolberg Alexander - Aging involves the progressive decline of cellular function, yet the key molecular regulators that determine aging require further identification. Building on our previous finding that the intracellular domain of CD44 (CD44ICD) is a critical aging regulator, we performed an interactome screen to identify its functional partners. This approach revealed BCAP31 and POLR1E as two previously unrecognized modulators of senescence. Depletion of their respective orthologs in Caenorhabditis elegans (C. elegans) shortened lifespan and accelerated age-related functional decline. In human vascular endothelial cells, knockdown of BCAP31 or POLR1E induced premature cellular senescence, whereas their overexpression countered it. Importantly, the protein levels of both BCAP31 and POLR1E decreased during physiological aging across species, including in senescent endothelial cells, aged nematodes, and tissues from old mice, with BCAP31 reduction being particularly pronounced in the cardiovascular system. Our findings establish BCAP31 and POLR1E as evolutionarily conserved components of a CD44-associated network that protects against cellular senescence and organismal aging, highlighting new potential targets for mitigating age-related vascular decline. - Source: PubMed
Li MengyuGuo ZhenyuanJiang YuweiZhao LianghaoZhang YuxiangMeng LingxinNi ChengzhiChen ZhiqiangZhang Lu - Hemizygous variants in B-cell receptor-associated protein 31 () can cause deafness, dystonia, and cerebral hypomyelination syndrome, which typically presents in infancy. - Source: PubMed
Publication date: 2026/06/10
Ishiguro MayuFunayama ManabuPark Daniel HHatano TakuNakazato TomokoLuo YueOsawa MonamiLi YuanzheYoshino HiroyoHattori NobutakaKanai Kazuaki - Brucella outer membrane protein 10 (OMP10) plays a critical role in host–pathogen interactions, yet its molecular mechanisms in modulating inflammatory and apoptotic pathways remain unclear. Here, we combined in vivo transcriptional profiling with computational analyses to investigate OMP10 function. Oral delivery of OMP10-expressing Lactococcus lactis in mice induced significant upregulation of BCAP31, CASP8, and IL1B, indicating engagement of ER stress, apoptotic, and NF-κB–mediated inflammatory responses. Protein–protein interaction network analysis across STRING confidence thresholds (0.4, 0.7, 0.9) highlighted CASP8 and IL1B as central hubs, with BCAP31 and PACS2 as key intermediates. Sequence-based docking and molecular dynamics simulations identified stable, energetically favorable interactions between OMP10 and BCAP31, PACS2, and TNFSF10, consistent with modulation of ER–MAM signaling and caspase-8 priming. Functional enrichment linked these interactions to unfolded protein response, CASP8 activation, and IL-1β production. Collectively, these results reveal OMP10 as a multifunctional Brucella effector that orchestrates ER stress–inflammation–apoptosis crosstalk and suggest that targeting the OMP10–BCAP31 axis could inform novel therapeutic or vaccine strategies against brucellosis. - Source: PubMed
Publication date: 2026/04/24
Khonsari Yasamin NasiriHabibi RezaAlami FatemehMustafa Rana MahmoudVarkiani Mahsa ManafiBanimahdidehkordi ArmitaFekri MehrshadAsl Hossein BakhtarMoosavi MonaHeidari-Soureshjani Ehsan - OBJECTIVE: Extramedullary disease (EMD) in multiple myeloma (MM) is associated with poor prognosis and presents considerable treatment challenges. However, the underlying molecular mechanisms remain incompletely understood. This study aimed to identify prognostic biomarkers through bioinformatics analysis and investigate the mechanisms governing proliferation and metastasis in MM. METHODS: Differentially expressed genes (DEGs) between MM and control samples were identified from datasets GSE146649 and GSE24870 through differential expression analysis. Prognostic biomarkers associated with MM were subsequently screened using weighted gene co-expression network analysis (WGCNA), support vector machine recursive feature elimination (SVM-RFE), and gene set enrichment analysis (GSEA). The biological effects and underlying mechanisms of growth differentiation factor 15 (GDF15) in MM were further evaluated using enzyme-linked immunosorbent assay (ELISA), CCK-8 assay, flow cytometry, cell adhesion assay, transwell migration assay, Western blotting, and co-immunoprecipitation (Co-IP). RESULTS: Four prognostic biomarkers—BIRC3, PRDX1, BCAP31, and GDF15 were identified as being involved in MM proliferation and metatasis. GDF15 was selected as the key gene for further investigation. Serum GDF15 levels were significantly elevated in MM patients with EMD compared to those without EMD and healthy controls. Inhibition of GFRAL, the specific receptor for GDF15, reversed the activation of the PI3K/Akt/NF-κB signaling pathway and attenuated upregulation of CXC chemokine receptors 4 (CXCR4) and matrix metalloproteinases 9 (MMP9). Treatment with uprosertib, a Akt inhibitor, abrogated the GDF15-induced increases in CXCR4 and MMP9 expression. CONCLUSION: Upregulation of GDF15 is positively correlated with MM progression. Moreover, GDF15 enhances the migratory and invasive capacities of MM cells via the PI3K/Akt/NF-κB signaling pathway, mediated by CXCR4 and MMP9. Thus, GDF15 may represent a potential therapeutic target for EMD in multiple myeloma. - Source: PubMed
Publication date: 2026/02/17
Fan HongjieWu YiwenPeng YuanyuanWang LingzhiTu ShengkePeng HuiYang JingLi XiaolanShi ZiweiLi MinSong Kui