Human Polyclonal CD79A Ab
- Known as:
- Human Polyclonal CD79A Antibody
- Catalog number:
- a0331
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ABclonal
- Gene target:
- Human Polyclonal CD79A
Related genes to: Human Polyclonal CD79A Ab
- Gene:
- CD79A NIH gene
- Name:
- CD79a molecule
- Previous symbol:
- IGA
- Synonyms:
- MB-1
- Chromosome:
- 19q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-07-31
- Date modifiied:
- 2019-04-23
Related products to: Human Polyclonal CD79A Ab
Related articles to: Human Polyclonal CD79A Ab
- Although diabetic peripheral neuropathy (DPN) is a serious complication of diabetes, its molecular causes are still unclear. The aim of this study was therefore to further investigate the pathogenesis of diabetes through whole transcriptome sequencing. - Source: PubMed
Publication date: 2026/06/13
Yan QiZhang MingXu Li-JuanMa JingWang JingWang Xian-MinMa Li - Neonatal leukemia is a rare and aggressive hematologic malignancy, accounting for less than 1% of pediatric leukemias. Mixed phenotype acute leukemia (MPAL) is particularly uncommon in this age group and poses significant diagnostic and therapeutic challenges. Hyperleukocytosis and leukostasis are life-threatening complications requiring urgent intervention. - Source: PubMed
Publication date: 2026/05/29
Bustamante-Ordoñez Marina AMacavilca-Toribio Michele AArenas-Vasquez Judith RRoman-Lazarte VictorZavaleta-Corvera CarlosSamanez-Obeso Ángel - To test, under a pre-planned clinical framework, whether simple multiparametric MRI biomarkers show candidate associations with selected molecular alterations in primary central nervous system lymphoma (PCNSL), with a focus on non-invasive enrichment for CD79B status and the MCD-like phenotype of potential relevance to Bruton tyrosine kinase (BTK) inhibitor stratification. - Source: PubMed
Publication date: 2026/05/29
García-Hidalgo ClementeGarcía Kempf Audena MaríaGaldo Galián DavidConsentino Hernández José AntonioCayuela Espí José Vicente - Lung cancer (LC), particularly lung adenocarcinoma, is a leading cause of cancer-related mortality, while systemic sclerosis-associated interstitial lung disease (SSc-ILD) is a chronic fibrotic autoimmune disorder. Growing evidence suggests shared molecular mechanisms between these conditions, although their genetic overlap remains insufficiently characterized. In this study, integrative bioinformatics approaches were applied to identify common differentially expressed genes (DEGs) and regulatory networks linking LC and SSc-ILD. Comparative transcriptomic analysis revealed 72 shared DEGs, including 10 hub genes: , , and (upregulated), and , , , , , , and (downregulated). Regulatory network analysis identified key miRNAs (hsa-miR-34a-5p, hsa-miR-126-3p, hsa-miR-335-5p) and central transcription factors (FOS, JUN, NFKB1). Pathway enrichment highlighted interleukin-10 signaling as a critical shared pathway, implicating immune regulation and extracellular matrix remodeling. Molecular docking suggested a potential interaction between doxycycline and MMP7 (binding affinity -6.4 kcal/mol), while X-ray diffraction and Rietveld refinement confirmed its crystalline purity. Additionally, doxycycline demonstrated antibacterial activity against via minimum inhibitory concentration assays. Overall, these findings provide preliminary insights into shared molecular features between LC and SSc-ILD and suggest doxycycline as a potential repurposed candidate warranting further experimental and clinical validation. - Source: PubMed
Publication date: 2026/05/27
Dasgupta SanjuktaGhosh MoupiyaSadhukhan SukhenduSet Srijit - Differentiation therapy holds significant potential for the treatment of multiple myeloma (MM). We previously identified that the aminopeptidase N (APN) inhibitor Bestatin promotes MM cell differentiation. Herein, we elucidate the underlying molecular mechanisms of this process. Utilizing MM1.S, U266, and RPMI-8226 cell lines, a combination of CCK-8 assays, flow cytometry, Wright-Giemsa staining, Western blotting, qRT-PCR, ELISA, APN enzymatic activity analysis, SA-β-gal staining, and bioinformatic analyses revealed elevated APN expression across all cell types. Bestatin treatment induced MM cell differentiation in a concentration-dependent manner, which was accompanied by the upregulation of the differentiation marker CD49e, increased immunoglobulin light chain secretion, elevated cellular senescence, and a concomitant suppression of cell proliferation and APN enzymatic activity. Mechanistically, Bestatin exerts its effects by downregulating the CD79B/BTK signaling pathway, thereby activating the downstream transcription factor STAT3. Consistent with this axis, direct inhibition of CD79B/BTK alone was sufficient to induce differentiation, while blockade of STAT3 completely abrogated the differentiation-promoting effect of Bestatin. The APN-neutralizing antibody (WM15) yielded consistent results with Bestatin, further validating this regulatory axis. Furthermore, both the CD79B/BTK inhibitor Ibrutinib and the STAT3 agonist GCDA potentiated the cytotoxicity of the clinical MM drug Ixazomib. Bestatin itself synergized with Ixazomib and enhanced the anti-proliferative effect of IL-6. In summary, our findings establish that the APN inhibitor Bestatin induces MM cell differentiation via the CD79B/BTK-STAT3 signaling axis. Targeting this pathway represents a promising strategy to enhance the efficacy of Ixazomib, providing a compelling rationale for novel combination therapies in MM. - Source: PubMed
Publication date: 2026/05/21
Wang XiaokeFang ChunyanLi ShanyuZeng HuakaiLiu JunyiDuan XinweiZhang XiaoyiJiang WenyanWang Xuejian