A1/182 BAP31
- Known as:
- A1/182 BAP31
- Catalog number:
- mc-066
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- A1/182 BAP31
Related genes to: A1/182 BAP31
- 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
- Gene:
- NELFB NIH gene
- Name:
- negative elongation factor complex member B
- Previous symbol:
- COBRA1
- Synonyms:
- KIAA1182, NELF-B
- Chromosome:
- 9q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 2008-02-21
- Date modifiied:
- 2016-10-05
Related products to: A1/182 BAP31
182
182 kDa tankyrase-1-binding protein,Homo sapiens,Human,KIAA1741,TAB182,TNKS1BP1182 kDa tankyrase-1-binding protein,Kiaa1741,Mouse,Mus musculus,Tab182,Tnks1bp12_oxaspiro[4.7]dodecane 2_oxaspiro[4.7]dodecan4_Isoquinolineboronicacid 4_Isoquinolineboronicac7,8,15,16,23,24_hexaoxatrispiro[5.2.5.2. 7,8,15,16,23,24_hexaoxA1/182 BAP31ABCD1 AntibodyABCD1 Antibody.AdvanceSTEM Growth Supplement HyCloneAMPKbeta1 (Ab-182) Antibody (OAEC00689)Analysis Tool Software for L-182, RayBioAnalysis Tool Software for L-182, RayBioAnthraxPAAnti- BCAP31 BAP31 Antibody Related articles to: A1/182 BAP31
- 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 - 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. - Source: PubMed
Publication date: 2026/02/17
Fan HongjieWu YiwenPeng YuanyuanWang LingzhiTu ShengkePeng HuiYang JingLi XiaolanShi ZiweiLi MinSong Kui - Gaining insights into the molecular features associated with T cell exhaustion (TEX) can offer fresh perspectives on predicting treatment responses, and we aim to investigate TEX-related tumor associated macrophages (TAM) subset to deeply understand underlying mechanisms of immune exhaustion. - Source: PubMed
Publication date: 2025/12/22
Li ShanZhu JianjunHuang XiangJi FengmingLi JinrongYao ZhigangTang HaoyuLiu LingYan BingZhanghuang Chenghao - Head and neck cancer (HNC) continues to pose a significant global health challenge, highlighting the urgent need for discovering new therapeutic targets. Recent studies highlight the role of solute carrier (SLC) proteins in cancer progression. This study investigates the expression and potential role of SLC10A3 in HNC, aiming to determine its clinical significance and therapeutic relevance. Publicly available datasets, including The Cancer Genome Atlas (TCGA), Clinical Proteomics Tumor Analysis Consortium (CPTAC), and Gene Expression Omnibus (GEO), were analyzed to assess SLC10A3 expression in head and neck squamous cell carcinoma (HNSCC). The prognostic relevance of SLC10A3 was assessed using Kaplan-Meier (KM) survival and Receiver Operating Characteristic (ROC) curve analysis. Correlation analysis within TCGA, CPTAC, and GEO datasets identified genes associated with SLC10A3 expression. Protein-protein docking studies were performed to predict potential interactions between SLC10A3 and identified protein coding genes. SLC10A3 was found to be significantly upregulated in HNSCC tumor samples compared to normal tissues across TCGA and CPTAC datasets. Increased SLC10A3 expression correlated with poor survival outcomes in TCGA-HNSCC patients. Correlation analysis identified 26 genes positively associated with SLC10A3, where BCAP31, IRAK1, and UBL4A showed consistent correlation across TCGA, CPTAC, and GEO datasets. Computational protein interaction modeling using docking and AI/ML-based Evolutionary Scale Modelling (ESM) framework revealed significant binding affinities between SLC10A3 and identified protein-coding genes, suggesting potential functional interactions. These findings establish SLC10A3 as a promising therapeutic target in HNC. Its consistent upregulation, association with poor prognosis, and potential interactions with key regulatory proteins highlight its relevance for future therapeutic strategies. - Source: PubMed
Publication date: 2025/11/17
Bintee BinteeBanerjee RuchiraHegde MangalaManteghi NafisehBhuyan PlabitaLongkumar ImliwatiAhmed Gazi NaseemBaruah Munindra NarayanAhn Kwang SeokKunnumakkara Ajaikumar B