Ask about this productRelated genes to: ITGB3 antibody
- Gene:
- ITGB3 NIH gene
- Name:
- integrin subunit beta 3
- Previous symbol:
- GP3A
- Synonyms:
- CD61, GPIIIa
- Chromosome:
- 17q21.32
- Locus Type:
- gene with protein product
- Date approved:
- 1988-06-09
- Date modifiied:
- 2019-04-23
Related products to: ITGB3 antibody
Related articles to: ITGB3 antibody
- Viral infection involves co-evolution with hosts, yet the molecular determinants that constrain viral cross-species transmission remain poorly understood. Here, we established conspecific and heterospecific co-housing models for two closely related rat species, Rattus norvegicus (RN) and Rattus tanezumi (RT), both maintained in laboratory settings for over 10 generations, together with wild-caught RT individuals. Using meta-transcriptomic sequencing and population genomic analyses, we compared their RNA virus profiles and investigated the potential molecular constraints on cross-species viral transmission. From 63 rats, we characterized an extensive RNA virome comprising more than 600 viruses, including 7 zoonotic viruses, 29 viruses with cross-species transmission potential, and 335 novel viruses. Notably, the prevalence of Seoul orthohantavirus (SEOV) was significantly higher in RN than in RT. Population genomic analysis revealed that RN exhibited higher heterozygosity in Itgb3 (the gene encoding the SEOV receptor, β3-integrin) and Tlr7 (the gene encoding the receptor for viral ssRNA, Toll-like receptor 7) compared to RT. These genetic variations likely represent the molecular determinants responsible for the differential susceptibility to SEOV between the two species. Our findings clarify the diversity and prevalence of RNA viruses in closely related rodent species and highlight host genetic barriers that may influence zoonotic spillover risk. - Source: PubMed
Publication date: 2026/04/25
Li ZhimingZhang MingyuCao RuidongShi ChengminYang LeZhang JianxuZhang Yaohua - Glanzmann thrombasthenia (GT) is a rare inherited platelet function disorder caused by defects in the ITGA2B or ITGB3 genes encoding the αβ integrin. Repeated transfusions often lead to immunization against αβ and/or HLA antigens, compromising transfusion efficacy. - Source: PubMed
Publication date: 2026/04/21
Desprez Dominiqued'Oiron RoselineVoisin SophieFalaise CélineAlessi Marie-ChristineSaultier PaulLavigne GéraldineEssaydi ArnaudApithy Marie-JoelleDupuis ArnaudGoin ValérieHuguenin YoannFiore Mathieu - Endothelial-to-mesenchymal transition (EndMT) is a key contributor to cardiac fibrosis, yet the role and underlying mechanisms of endothelial integrin β3 (ITGB3) activation in EndMT remain poorly understood. This study aims to explore the involvement of a novel ITGB3- CaMKIIα (calcium-calmodulin-dependent protein kinase IIα)-CREB1 (cAMP-responsive element binding protein) signaling axis in EndMT and to demonstrate that targeting endothelial ITGB3 mitigates pressure overload-induced heart failure (HF) by reducing cardiac fibrosis. - Source: PubMed
Publication date: 2026/04/22
Wang MengwenDai LeiLi ZhiLuo LingyunLiu XiaoleiZhang YueqiZhong XiaodanWang LingyunZhang YingDong WeiYu DanWang HonghuiLai PingMadhusudhan ThatiZeng HesongWang Hongjie - Alkylating agents, particularly cyclophosphamide (CY), are known for their high toxicity, which can lead to iatrogenic premature ovarian insufficiency (POI) and infertility in young cancer survivors. Currently, effective prevention and treatment strategies remain limited. Given that chemotherapy induces cellular senescence, we investigated the therapeutic potential of dasatinib (D) and quercetin (Q), a senolytic combination known to eliminate senescent cells. Using a CY-induced murine model of ovarian injury, we found that CY treatment increased the accumulation of senescent cells in the ovaries. The resulting senescence-associated secretory phenotype (SASP) led to a deterioration of the ovarian microenvironment, characterized by increased follicular atresia and a decline in follicle quantity, ultimately culminating in POI. Our findings demonstrate that DQ therapy effectively mitigated CY-induced damage by clearing senescent cells and reducing SASP secretion. Clinically, DQ administration restored sex hormone levels and regularity of the estrous cycle, resulting in an overall increase in follicle numbers across all developmental stages. Furthermore, DQ treatment significantly normalized estrous cyclicity, restoring regular cycles in 60% of the CY+DQ mice compared to only ~15% in the CY-alone group (p<0.0001). RNA sequencing analysis revealed that DQ treatment upregulated Pagr1a, a gene associated with extraembryonic development, while downregulating genes involved in senescence induction (Itgb3, Wnt10b, Vegfa) and immune function (A2m, Ccl21d). These results suggest that senescent cells drive CY-induced ovarian damage and that DQ represents a promising therapeutic strategy for preserving the ovarian reserve and endocrine function in female cancer patients. - Source: PubMed
Publication date: 2026/04/21
Su HuinaMa RuiqiongSu DehuiTan ChengZhu YeYang Xin - Triple-negative breast cancer (TNBC), characterized by the absence of effective therapeutic targets, remains a major clinical challenge with poor prognosis. The identification of novel molecular targets is therefore crucial for developing effective treatment strategies. Eukaryotic elongation factor 2 kinase (eEF2K) is highly expressed in TNBC and known to promote tumor progression; however, the precise mechanisms underlying its oncogenic role remain elusive. In this study, we identified poly(rC)-binding protein 2 (PCBP2) as a previously unrecognized downstream substrate of eEF2K. Analysis of clinical TNBC specimens revealed a positive correlation between eEF2K and PCBP2 protein expression levels. Further studies demonstrated that site-specific phosphorylation of PCBP2 at serine 189 (Ser189) markedly promoted the malignant phenotype of TNBC cells. Mechanistically, eEF2K-mediated phosphorylation at Ser189 stabilized PCBP2 by preventing its ubiquitin-proteasome-dependent degradation. This phosphorylation-dependent stabilization, in turn, enabled PCBP2 to promote the mRNA stability of pro-oncogenic genes, including TNC, SOX5, and ITGB3, thereby driving TNBC progression. Collectively, these findings not only reveal PCBP2 as a critical downstream effector of eEF2K, but also highlight the eEF2K-PCBP2 signaling axis as a promising therapeutic target for TNBC. - Source: PubMed
Publication date: 2026/03/25
Cheng YueyingJiang TingZhu WenqianHe LinhaoChen ZonglingLi HangZhao RuigangJiang ShilongCheng Yan