1/500. Perform heat mediated antigen retrieval with citrate buffer pH 6 before commencing with IHC staining protocol.
1/2000 - 1/10000.
Component of a probable SCF-like E3 ubiquitin-protein ligase complex, which mediates the ubiquitination and subsequent proteasomal degradation of target proteins. Probably plays a role in the degradation of proteins involved in endothelial proliferation and/or differentiation (By similarity). Seems not to promote polyubiquitination and proteasomal degradation of TP53. In vitro, complexes of CUL7 with either CUL9 or FBXW8 or TP53 contain E3 ubiquitin-protein ligase activity.
Highly expressed in fetal kidney and adult skeletal muscle. Also abundant in fetal brain, as well as in adult pancreas, kidney, placenta and heart. Detected in trophoblasts, lymphoblasts, osteoblasts, chondrocytes and skin fibroblasts.
Protein modification; protein ubiquitination.
Defects in CUL7 are the cause of 3M syndrome type 1 (3M1) [MIM:273750]. An autosomal recessive disorder characterized by severe pre- and postnatal growth retardation, facial dysmorphism, large head circumference, and normal intelligence and endocrine function. Skeletal changes include long slender tubular bones and tall vertebral bodies.
Belongs to the cullin family. Contains 1 DOC domain.
ab115304, at 1/500 dilution, staining Cullin 7 in formalin-fixed, paraffin-embedded Human Brain, Cortex tissue by Immunohistochemistry, using a biotinylated goat anti-rabbit IgG secondary antibody, alkaline phosphatase-streptavidin and chromogen.