Ask about this productRelated genes to: CD49f antibody
- Gene:
- ITGA6 NIH gene
- Name:
- integrin subunit alpha 6
- Previous symbol:
- -
- Synonyms:
- CD49f
- Chromosome:
- 2q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-08-06
- Date modifiied:
- 2015-12-15
Related products to: CD49f antibody
Related articles to: CD49f antibody
- High pathogenicity avian influenza (HPAI) poses a significant threat to poultry. Some chickens show resilience to HPAI, but the mechanisms involved are poorly understood. In this study, we aimed to identify the biological mechanisms associated with resilience to HPAIV infection in chickens. Chickens were inoculated with H7N1 HPAIV and classified as susceptible or resilient based on clinical signs, mortality, histopathological lesions, AIV antigen detection in tissues, and viral shedding. Blood transcriptomic analysis revealed that genes from resilient chickens are involved in the integrin-mediated signaling pathway (ITGA5, ITGA6, ITGB1), as well as in adaptive (BTK, TEC) and innate (TRIM13, LCK, TICAM1) immune pathways. Plasma proteomic profiling revealed that ARF4, EIF4A2, and HNRNPAB (proteins involved in fundamental cellular processes) were less abundant in resilient chickens compared to both controls and susceptible birds. Our results suggest that early modulation of these pathways is associated with resilience to HPAIV and likely reflects early viral control or reduced systemic dissemination rather than the absence of infection. - Source: PubMed
Publication date: 2026/08/06
Valdez-May María JPerlas AlbertNofrarías MiquelPina-Pedrero SoniaDabad MarcValle RosaPérez MartaMoreno-León AlejandroEsteve-Codina AnnaArgilaguet JordiBertran KateriMajó Natàlia - Ischemic stroke (IS) is a cerebrovascular disease with high mortality and disability rates, currently lacking effective therapeutic targets. The STING inhibitor SN-011 shows potential in IS treatment, but its mechanism of action remains unclear. This study aims to explore the key molecular mechanisms of SN-011 in treating IS through bioinformatics approaches. IS transcriptome datasets were analyzed to identify differentially expressed genes. Mendelian randomization using brain eQTL and IS-GWAS data identified genes with causal relationships to IS. Single-cell transcriptome, pseudo-time trajectory, intercellular communication, and transcription factor regulatory network analyzes were performed. Molecular docking and DARTS-WB assay validated SN-011 binding to transcription factors. Transcriptomic analysis identified 77 intersecting genes. Mendelian randomization revealed ADGRE5 as a protective gene for IS (OR < 1), significantly downregulated in venous endothelial cells (vECs) during disease progression. Cell communication analysis showed ADGRE5-high vECs interact with immune, glial, and stromal cells via LAMININ (Lamb2-CD44, Lamb2-Itga6+Itgb1, Lamb2-Dag1 pair) and JAM signaling pathways. Transcription factor analysis identified JUNB as a negative regulator of ADGRE5. Molecular docking (-6.8 kcal/mol) combined with an in vitro DARTS-WB assay confirmed the interaction between SN-011 and JUNB. In OGD-induced endothelial cell injury models, SN-011 suppressed JUNB expression, restored ADGRE5 expression inhibited by JUNB overexpression, reversed the downregulation of LAMB2 and CD44, and reduced the expression of the pro-inflammatory cytokines IL-6 and IL-1β. Notably, blockade of LAMB2 largely abolished these protective effects, indicating that the anti-inflammatory and endothelial-protective activities of SN-011 are mediated, at least in part, through restoration of the LAMB2-CD44 signaling axis. ADGRE5 downregulation in vECs may impair vascular repair by disrupting LAMININ-mediated intercellular communication. SN-011 may exert neuroprotective effects by targeting JUNB to upregulate ADGRE5 expression and restore the vEC-centered cellular communication network, providing a theoretical basis for SN-011 as a potential IS therapeutic. - Source: PubMed
Ou XiangLingGong ZunKe - Bone invasion is a strong indicator of a poor prognosis in head and neck squamous cell carcinoma (HNSCC), although the underlying mechanisms are still unclear. Due to the limited resolution of bulk sequencing, the specific malignant epithelial cell (EPC) subpopulation responsible for bone invasion and its regulatory network have long been unclear. We developed a comprehensive cellular atlas of EPCs in bone-invasive HNSCC using single-cell transcriptome sequencing, and we carefully examined their subpopulation heterogeneity, functional states, and transcriptional regulatory networks. The primary subpopulation found to be associated with bone invasion was the C2 ITGA6⁺ EPC. Mechanistically, these intermediate transitional cells may facilitate bone invasion via an epithelial-mesenchymal transition program controlled by TP63, with connections between the tumor microenvironment regulated by LAMININ and EPHB signaling. This discovery may help develop customized treatment options by providing a novel single-cell-resolution viewpoint on the molecular associations underlying bone-invasive HNSCC. - Source: PubMed
Publication date: 2026/08/03
Guo BingSun LinChen JiananWen XutaoLiu ZhonglongZhang XinyuZhao ZhijieWang XiuxiaYang Jun - Prostate cancer (PC) is the second most common solid cancer affecting men. LncRNA PCAT19 has a carcinogenic role in multiple solid and hematological cancers. Additionally, miR-195 was significantly downregulated in multiple malignancies. Moreover, ITGA6 promotes pathways that control carcinogenesis. E-cadherin is a glycoprotein involved in epithelial cell adhesion and maintaining tissue integrity. E-cadherin loss is related to epithelial-mesenchymal transition (EMT) and cancer metastasis. This preliminary study investigated the expression of PCAT19, miR-195, ITGA6, and E-cadherin in PC tissues. - Source: PubMed
Publication date: 2026/07/29
Hussein SamiaZahra MansourShalaby Amr ASalama Mariam F ASameh RehamWaley Ahmad BarakatShawky Salma AAboafya Zahraa IMatar IhabAmgd MoamenAlgazeery Ahmed - Head and neck squamous cell carcinoma (HNSCC) exhibits marked molecular heterogeneity and diverse clinical outcomes, partly influenced by HPV status and the tumor immune microenvironment. Although tumor doubling time (TDT) reflects tumor growth kinetics and has prognostic relevance, its molecular basis in HNSCC remains unclear. - Source: PubMed
Publication date: 2026/07/23
Zhang MingchuZhao ZiwenZhu QingwenLiang ShihanSun LiminWei HualiLiu ShiweiZhao MengweiLi LifengWang Liang