Disease relevance of Cd2ap

• The severity of kidney disease in Cd2ap mutant mice may have eclipsed manifestation of defects in other tissues [1].
• Congenital nephrotic syndrome in mice lacking CD2-associated protein [2].
• Mice born without CD2-associated protein (CD2AP) develop renal failure and nephrotic syndrome about 4 weeks after birth and die around 6 weeks of age [3].
• CD2-associated protein (CD2AP) is an adapter protein associating with several membrane proteins, including nephrin, mutated in congenital nephrotic syndrome of the Finnish type, and polycystin-2, mutated in type 2 autosomal dominant polycystic kidney disease [4].
• Mice lacking CD2-associated protein (CD2AP-/-) develop glomerular lesions resembling human focal segmental glomerulosclerosis (FSGS) between 3-4 weeks of age and die approximately 2 weeks later from massive proteinuria and renal failure [5].

High impact information on Cd2ap

• CD2-associated protein (CD2AP) is an 80-kilodalton protein that is critical for stabilizing contacts between T cells and antigen-presenting cells [2].
• Increased ferritin permeability was not observed in nephrotic CD2-associated protein-null (Cd2ap-/-) mice, which have a primary podocyte defect [6].
• A novel role for the adaptor molecule CD2-associated protein in transforming growth factor-beta-induced apoptosis [7].
• CD2-associated protein (CD2AP) is an adaptor molecule involved in T cell receptor signaling and podocyte homeostasis [7].
• We have found that METS-1/CD2AP (hereafter referred to as CD2AP) is expressed at lower levels in renal tubular epithelial cells in the adult kidney, particularly in distal nephron segments [8].

Anatomical context of Cd2ap

• CD2-associated protein (CD2AP) expression in podocytes rescues lethality of CD2AP deficiency [3].
• CD2-associated protein directly interacts with the actin cytoskeleton [4].

Associations of Cd2ap with chemical compounds

• Kidneys from Cd2ap -/- mice initially exhibited normal nephrin localization, but as the mice aged and foot processes became effaced, nephrin disappeared [1].

References