ITGB3 (phospho-Tyr785) Antibody
- Known as:
- ITGB3 (phosphorilated-Tyr785) Antibody
- Catalog number:
- abx000303
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- ITGB3 (phospho-Tyr785) Antibody
Related genes to: ITGB3 (phospho-Tyr785) 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 (phospho-Tyr785) Antibody
Related articles to: ITGB3 (phospho-Tyr785) Antibody
- Neonatal hypoxic-ischemic brain damage (HIBD) is characterized by severe endothelial injury, inflammation, and apoptosis, which together contribute to irreversible neurodevelopmental deficits. In this study, we developed a biomimetic magnetic nanovesicle platform (IDR-MNC@RMVs) loaded with the host defense peptide IDR-1018 as a targeted therapeutic strategy for neonatal HIBD. Under external magnetic guidance, IDR-MNC@RMVs preferentially accumulated in ischemic brain regions, where they markedly reduced neuronal and vascular injury, attenuated brain atrophy, and improved neurological recovery in neonatal mice. Mechanistically, integrated analyses using single-cell RNA sequencing, transcriptomics, and functional assays showed that IDR-MNC@RMVs enhanced endothelial survival and angiogenic activity through activation of the ITGB3/VEGFA signaling axis. In vitro, IDR-MNC@RMVs protected hypoxia-injured human brain microvascular endothelial cells by restoring proliferation and migration while reducing apoptosis, whereas these protective effects were largely abolished after ITGB3 knockdown. In vivo, histological analyses further indicated reduced inflammatory injury and improved vascular preservation after treatment. Collectively, these findings identify IDR-MNC@RMVs as a promising nanotherapeutic strategy that promotes vascular repair and tissue recovery after neonatal hypoxic-ischemic injury. This work highlights the potential of combining biomimetic nanotechnology with peptide-based therapy for neonatal brain injury. - Source: PubMed
Publication date: 2026/06/02
Zhao JingLiang DaoxinXiong MaotingDeng JiahongHu LihongJiang LinYang Can - Marrow senescence contributes to overall organismal aging and involves functional alterations in both the mesenchymal and hematopoietic compartments of bone marrow. Although matrix remodeling-associated 7 () has been demonstrated to modulate mesenchymal function and megakaryocyte differentiation in mice, this study aimed to investigate the potential role of in marrow senescence. Single-cell RNA sequencing was performed on bone marrow cells from young and aged wild-type and -knockout mice. Comparative analysis of 2-month-old and 2-year-old mice revealed that aging significantly altered the cellular proportions within the bone marrow niche, and deficiency markedly increased Macro1 macrophages in aged mice, likely driven by the dysregulation of the axis. deficiency altered Mid1 expression and the macrophage migration inhibitory factor (), , and Von Willebrand factor signaling pairs (), all of which are closely associated with cell status in the bone marrow microenvironment. In summary, these findings underscore 's role in cellular profile shifts during bone marrow aging, offering novel insights into how coordinates hematopoietic and immune homeostasis in the bone marrow. - Source: PubMed
Publication date: 2026/05/28
Qin YuzhenZhao ZiyanChen YihanZheng YudanMa KunpengLin DandanLiu XinWang Yiqiang - Glanzmann Thrombasthenia (GT) is characterized by absent platelet aggregation in response to all agonists except ristocetin and is caused by recessive inactivating variants in ITGA2B or ITGB3. While GT patients typically are described as having normal platelet counts, autosomal dominant activating variants in ITGA2B or ITGB3 cause macrothrombocytopenia. Interestingly, in our cohort of 16 GT patients, eight consistently exhibited platelet counts at the lower end of the normal range. We studied the role of integrin αIIbβ3 in platelet formation using megakaryocytes (MKs) derived from genetically modified immortalized megakaryocyte cell lines (imMKCLs), focusing on two modifications of ITGB3: ITGB3-/- (inactivating) and ITGB3WT/D673_E713del (activating). In static differentiation cultures, ITGB3-/- and ITGB3WT/D673_E713del imMKCLs exhibited normal MK differentiation but reduced proplatelet formation. Platelet production was also impaired in a 3D silk-based bone marrow system and in shaking cultures, confirming a quantitative role for ITGB3 in platelet production, independent of the type of variant. While TRAP-activated in vitro-generated platelets lacking αIIbβ3 failed to bind the activation-dependent PAC-1 antibody, ITGB3WT/D673_E713del platelets bound PAC-1 prior to activation mimicking the patient's phenotype. Transcriptome profiling and metabolomic analyses of integrin αIIbβ3 deficient MKs revealed impaired serine metabolism and downregulation of SLC3A2 (CD98hc), an amino acid transporter chaperon known to interact with the β3 subunit. Flow cytometry confirmed decreased CD98hc in mutant MKs, while re-expression of wild-type ITGB3 in ITGB3-/- MKs restored αIIbβ3 and CD98hc expression, normalized proplatelet formation, and enhanced serine uptake. These results uncover a previously unrecognized role of integrin αIIbβ3 in coupling serine metabolism to platelet biogenesis. - Source: PubMed
Publication date: 2026/05/29
Ramaekers KatoTran MyLunghi MarcoHermans AmyThys ChantalDe Wispelaere KoenraadTurro ErnestVan Geet Christel Van GeetVan Thillo QuentinPeerlinck KathelijneEto KojiNurden Alan TBalduini AlessandraDi Buduo Christian AndreaLabarque VeerleFreson Kathleen - Colorectal cancer (CRC) is a highly aggressive and heterogeneous malignancy with a poor prognosis. Mitochondria and programmed cell death (PCD) play crucial roles in CRC tumorigenesis and cancer progression. However, the prognostic significance of mitochondrial programmed cell death (MPCD) remains unclear. This study aims to investigate prognostic value of MPCD-related genes. - Source: PubMed
Publication date: 2026/05/25
Jiang SanyaJin Yongjun - Variants in integrin β3 (Itgb3) are associated with autism spectrum disorder and intellectual disability. Itgb3 deletion in mice leads to aberrant development of excitatory pyramidal neurons in the cerebral cortex and hippocampus, as well as aberrant social and repetitive behaviors. However, its expression pattern in the developing brain has not been well studied. Due to its functional importance in the developing forebrain, we hypothesized that Itgb3 expression would be developmentally regulated and localized to cortical and hippocampal pyramidal neurons in the mouse brain. We found that Itgb3 mRNA is strongly expressed throughout the forebrain, especially in layer 5 of cerebral cortex and CA3 of hippocampus. In mouse cortical layer 5 and in hippocampal CA3, Itgb3 mRNA expression is high at postnatal day 6-7 and is downregulated in cortex by postnatal day 20-21. It is expressed preferentially in glutamatergic excitatory pyramidal neurons. Peak Itgb3 expression therefore coincides with the timeframe for peak dendritic formation and synaptogenesis in cortical and hippocampal glutamatergic excitatory pyramidal neurons. - Source: PubMed
Publication date: 2026/05/23
Cook Hollyn NVinson Elizabeth CKalinowski Anna RRodriguez Hilda VDenzler Collin JVidal George S