CD42b
- Known as:
- CD42b
- Catalog number:
- 11-367-C100
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- CD42b
Related genes to: CD42b
- Gene:
- GP1BA NIH gene
- Name:
- glycoprotein Ib platelet subunit alpha
- Previous symbol:
- GP1B
- Synonyms:
- CD42b, GPIbalpha
- Chromosome:
- 17p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-09-10
- Date modifiied:
- 2019-04-23
Related products to: CD42b
Related articles to: CD42b
- Myelodysplastic neoplasms (MDS) are clonal hematopoietic disorders defined by ineffective hematopoiesis, cytopenias, and variable risk of progression to acute myeloid leukemia. Although genomic and epigenomic studies have provided insight into disease pathogenesis, reliable biomarkers for diagnosis and prognosis remain limited. Proteomics offers an important advantage because it reflects the functional protein state and captures post-translational modifications, making it highly relevant for risk assessment and therapy guidance. Recent studies have identified several groups of candidate biomarkers. Kinases and signal transduction proteins such as CAMK1D, PRKCZ, KIT, MAST4, PAK6, PTK7, and NTRK1 are dysregulated in MDS and associated with poor outcomes, immune evasion, and aberrant stem cell signaling. Oncofetal proteins like IGF2BP3 and signaling regulators such as RBP4 further highlight proteomic signatures linked to chemoresistance and subtype specificity. In the transplant setting, immune regulators including CSK, FGR, CRTAM, GP1BA, UBE2N, and STAT1 may serve as predictors of graft rejection and relapse. Cytoskeletal and extracellular matrix proteins such as CEP55, Talin-1, Kindlin-3, Vinculin, THBS1, LRG1, SPARC, SAA1, Clusterin, and PRDM16 underscore the role of bone marrow microenvironmental remodeling and adhesion defects in disease progression. Finally, metabolic enzymes such as LDHA reflect altered energy metabolism and correlate with more aggressive disease biology. Collectively, these proteomic candidates illustrate the complex interplay of signaling, immune regulation, bone microenvironment, and metabolism in MDS. Their validation in clinical cohorts could enable early detection, refined risk stratification, and new therapeutic avenues, positioning proteomics as a central tool in the future management of MDS. - Source: PubMed
Novak RuđerMandac Smoljanović IngaGrgurević Lovorka - Chronic Chagas cardiomyopathy (CCC) remains a major cause of heart failure (HF)-related mortality in Latin America and is increasingly recognized as a global health concern. Prognostic models developed in non-Chagas populations often perform poorly in CCC, highlighting the need for etiology-specific risk stratification. - Source: PubMed
Publication date: 2026/06/08
Patané José S LGiugni Fernando RRosa Rogério SMarcondes-Braga Fabiana GMansur Alfredo JPereira Alexandre CKrieger Jose E - Bernard-Soulier syndrome (BSS), a rare inherited platelet disorder, is characterized by macrothrombocytopenia, typically with mild to moderate thrombocytopenia, and abnormal expression of the GPIb-IX-V complex on the platelet surface. BSS is caused by missense, nonsense, and frameshift mutations in the GP1BA, GP1BB, and GP9 genes. This study aimed to characterize the mutations associated with BSS in Iranian patients. - Source: PubMed
Publication date: 2026/05/23
Ghodratnia ElnazTabibian ShadiBarati MahmoodSafa Majid - Genome-wide association studies (GWASs) have identified common genetic risk loci for ischemic stroke (IS), primarily in European populations older than 55 years. We aimed to identify common and rare risk variants associated with early-onset IS (ages 18-54) in Taiwan. - Source: PubMed
Publication date: 2026/06/01
Wang Yin-ChengLiu Kai-MingGan Yu-LingChi Nai-FangLu Liang-SueiChou Che-YuWang Liang-YunChang Li-HsinHou Ming-ChihFu Yun-ChingChiou Jeng-FongWu Ming-ShiangYang Shun-FaPang See-TongWang Jaw-YuanTsai Yi-TingHuang Chih-YangChiu Kuan-MingChen MingChiang Fu-TienWang Chih-HungYao Wei-JenLee Sing-LianHuang Chi-HungLiu Yo-TsenWang Shuu-JiunKo Wen-YaChen Chien-HsiunLee I-Hui - : Pancreatic adenocarcinoma (PAAD) is a highly aggressive malignancy with limited treatment options and a poor prognosis. Extracellular vesicles (EVs), which play a central role in intercellular communication, have emerged as promising non-invasive biomarkers for both diagnosis and prognosis. This study aimed to identify EV-related genes, construct a more accurate prognostic model using data from multiple databases, and explore the functional roles of key genes in PAAD. : Four publicly available datasets, PAAD_ExoRbase, TcgaTargetGtex-PAAD, GSE62452_GPL6244, and GSE78229_GPL6244, were analyzed, leading to the identification of 40 differentially expressed EV-related genes. Using the Least Absolute Shrinkage and Selection Operator (LASSO) Cox regression, five prognostic genes, , , , , and , were selected to construct a nomogram model for predicting patient outcomes. Single-cell analysis showed that these five genes were expressed in T-proliferative, malignant, and ductal cells. Analyses of immune cell infiltration and immune checkpoints further supported the model's prognostic performance. The regulatory role of the key gene was validated in an in-house cohort and confirmed through in vitro experiments and RNA sequencing. Furthermore, analyses of conditioned medium, EV isolation and characterization, and endothelial tube formation assays demonstrated that EVs derived from CFPAC-1 cells carrying enhanced PAAD angiogenesis through VEGF/VEGFR signaling. - Source: PubMed
Publication date: 2026/05/01
Ma TianyinGongye XiangdongDongzhi CairangMa ShuxianChai YiboGuo Wing-WaWang QikunTian Ming