mouse anti collagen type vi alpha 1 chain col6a1 (Proteintech)
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Proteintech
mouse anti collagen type vi alpha 1 chain col6a1
Mouse Anti Collagen Type Vi Alpha 1 Chain Col6a1, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 62 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mouse+anti+collagen+type+vi+alpha+1+chain+col6a1/Collagen+Type+VI+Antibody/pm41435451-95-44-52
Average 94 stars, based on 62 article reviews
Mouse Anti Collagen Type Vi Alpha 1 Chain Col6a1, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 62 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mouse+anti+collagen+type+vi+alpha+1+chain+col6a1/Collagen+Type+VI+Antibody/pm41435451-95-44-52
Average 94 stars, based on 62 article reviews
mouse anti collagen type vi alpha 1 chain col6a1 - by Bioz Stars,
2026-09
94/100 stars
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Incubation:Article Title: Decoding vascular aging: Substrate stiffness and shear stress orchestrate endothelial inflammation and remodelling via mechanosensitive pathways. Article Snippet: Vascular ageing is a major contributor to cardiovascular disease and is closely linked to vascular stiffness.. Stiffening of the vascular wall disrupts endothelial homeostasis and promotes chronic inflammation, yet the underlying mechanisms remain poorly understood due to technological limitations.. Here, we used a previously developed in vitro microfluidic model to investigate how biomechanical forces, specifically substrate stiffness and shear stress, interact to regulate endothelial cell behaviour. Binding Assay:Article Title: Decoding vascular aging: Substrate stiffness and shear stress orchestrate endothelial inflammation and remodelling via mechanosensitive pathways. Article Snippet: Vascular ageing is a major contributor to cardiovascular disease and is closely linked to vascular stiffness.. Stiffening of the vascular wall disrupts endothelial homeostasis and promotes chronic inflammation, yet the underlying mechanisms remain poorly understood due to technological limitations.. Here, we used a previously developed in vitro microfluidic model to investigate how biomechanical forces, specifically substrate stiffness and shear stress, interact to regulate endothelial cell behaviour. |