Collagen, Type VIII, alpha 1 (COL8A1) ELISA Kits

Mouse (Murine) Collagen, Type VIII, alpha 1 (COL8A1) Interaktionspartner

1. Lack of collagen VIII reduces myofibroblast differentiation and fibrosis and promotes early mortality and left ventricle dilatation in response to pressure overload in mice.

2. Type VIII collagen signals via beta1 integrin and RhoA to regulate MMP-2 expression and smooth muscle cell migration.

3. Type VIII collagen mediates vessel wall remodeling after arterial injury and fibrous cap formation in atherosclerosis.

4. in contrast to diabetic wild-type mice EMT-like changes were attenuated in diabetic Col8alpha1/alpha2-KO mice, indicating that collagen VIII may be 1 of the major inducers of epithelial-to-mesenchymal transition-like changes in kidneys of diabetic wild-type mice

5. Type VIII collagen significantly modulates the effect of TGF-beta1 on mesangial cells and may therefore play a role in the pathogenesis of diabetic nephropathy.

6. Crystal structure of mouse alpha1(VIII)(3) NC1 domain trimer at 1.9 A resolution. Surface of collagen VIII NC1 trimer has three strips of partially exposed aromatic residues, likely involved in supramolecular assemblies.

7. These data indicate that type VIII collagen plays an important role in glial scar formation during the repair process by astrocytes.

8. Smooth muscle cells can modify the matrix microenvironment by producing type VIII collagen, using it to overlay type I collagen, and generating a substrate favorable for migration

9. Downregulation of COL8A1 expression sensitized hepatocarcinoma cells to the action of D-limonene, impeded cell proliferation, and led to decreased invasiveness, indicating that COL8A1 might serve as a target for gene therapy in hepatocarcinoma.

10. Oxidized phospholipids induce type VIII collagen expression and vascular smooth muscle cell migration.

11. Lack of type VIII collagen confers renoprotection in diabetic nephropathy in a knockout mouse model.

Human Collagen, Type VIII, alpha 1 (COL8A1) Interaktionspartner

1. We demonstrated the presence of Col8a1 in Bruch's membrane, further supporting the role of COL8A1 variants in AMD pathogenesis. Protein-altering variants in COL8A1 may alter the integrity of Bruch's membrane, contributing to the accumulation of drusen and the development of AMD.

2. Polymorphisms in COL8A1 is associated with Polycystic ovary syndrome and type-2 diabetes.

3. COL8A1 was identified and proved to be correlated with the progression and prognosis of human colon adenocarcinoma, probably through regulating focal adhesion-related pathways.

4. High COL8A1 level is associated with chronic obstructive pulmonary disease and cancer.

5. The COL8A1 rs13095226 polymorphism is not associated with nAMD or PCV, which suggesting this gene maybe not a susceptibility gene locus for neovascular age-related macular degeneration (nAMD) or polypoidal choroidal vasculopathy (PCV) in Chinese subjects.

6. High COL8A1 expression is associated with early loss of kidney function.

7. Data indicate that complement factor H (CFH) R1210C and common variants in COL8A1 and RAD51B plus six genes contribute predictive information for advanced macular degeneration (AMD) beyond macular and behavioral phenotypes.

8. The results are consistent with the proposal that rare CNVs play a role in TS aetiology and suggest a possible role for rearrangements in the COL8A1 and NRXN1 gene regions.

9. In addition, eight genes classified as 'second tier' hits in the original study (PAX7, THADA, COL8A1/FILIP1L, DCAF4L2, GADD45G, NTN1, RBFOX3 and FOXE1) showed evidence of linkage and association in this replication sample.

10. The purpose of this study is to evaluate COL8A1 and COL8A2 as candidate genes for thin central corneal thickness in human primary open angle glaucoma patients.

11. The absence of pathogenic mutations identified in the COL8A1 or COL8A2 genes in affected members of 15 pedigrees with familial FECD (Fuchs endothelial corneal dystrophy) indicates that other genetic factors are involved.

12. The absence of pathogenic mutations in COL8A1 and COL8A2 in patients with keratoconus indicates that other genetic factors are involved in the pathogenesis of this corneal ectatic disorder.