african green monkey kidney fibroblast like cell line cos7 (ATCC)
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African Green Monkey Kidney Fibroblast Like Cell Line Cos7, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 7941 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/african+green+monkey+kidney+fibroblast+like+cos7+cell+line/COS-7/pm41708853-934-9-20
Average 99 stars, based on 7941 article reviews
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Cell Culture:Article Title: SigmaR1 is an auxiliary translocon factor with lipid-binding activity that regulates protein and lipid droplet homeostasis Article Snippet: .. Article Title: Tex2 is required for lysosomal functions at TMEM55-dependent ER membrane contact sites. Article Snippet: .. Cell culture, transfection, and RNAi The Article Title: Sec23IP recruits VPS13B/COH1 to ER exit site-Golgi interface for tubular ERGIC formation. Article Snippet: VPS13B/COH1 is the only known causative factor for Cohen syndrome, an early-onset autosomal recessive developmental disorder with intellectual inability, developmental delay, joint hypermobility, myopia, and facial dysmorphism as common features, but the molecular basis of VPS13B/COH1 in pathogenesis remains largely unclear.. Here, we identify Sec23 interacting protein (Sec23IP) at the ER exit site (ERES) as a VPS13B adaptor that recruits VPS13B to ERES–Golgi interfaces.. VPS13B interacts directly with Sec23IP via the VPS13 adaptor binding domain (VAB), and the interaction promotes the association between ERES and the Golgi. Transfection:Article Title: Tex2 is required for lysosomal functions at TMEM55-dependent ER membrane contact sites. Article Snippet: .. Cell culture, transfection, and RNAi The Article Title: Sec23IP recruits VPS13B/COH1 to ER exit site-Golgi interface for tubular ERGIC formation. Article Snippet: VPS13B/COH1 is the only known causative factor for Cohen syndrome, an early-onset autosomal recessive developmental disorder with intellectual inability, developmental delay, joint hypermobility, myopia, and facial dysmorphism as common features, but the molecular basis of VPS13B/COH1 in pathogenesis remains largely unclear.. Here, we identify Sec23 interacting protein (Sec23IP) at the ER exit site (ERES) as a VPS13B adaptor that recruits VPS13B to ERES–Golgi interfaces.. VPS13B interacts directly with Sec23IP via the VPS13 adaptor binding domain (VAB), and the interaction promotes the association between ERES and the Golgi. |
