Disease relevance of Ggcx

• Enhanced renal vitamin-K-dependent gamma-glutamyl carboxylase activity in experimental rat urolithiasis [1].
• Gamma-glutamyl-carboxylase activity was increased by vitamin K-deficiency but not inhibited by testosterone or NMTT [2].

High impact information on Ggcx

• Molecular cloning of matrix Gla protein: implications for substrate recognition by the vitamin K-dependent gamma-carboxylase [3].
• The renal vitamin K-dependent gamma-glutamyl carboxylase was present in microsomes prepared from the renal cortex as well as the inner and outer medulla of several species [4].
• Cloning of rat vitamin K-dependent gamma-glutamyl carboxylase and developmentally regulated gene expression in postimplantation embryos [5].
• Gla-containing proteins have glutamic acid residues that must by gamma-carboxylated by vitamin-K-dependent gamma-carboxylase to enable them to bind calcium and function normally [6].
• The relative utilization of phylloquinone and menaquinone-9 (MK-9) as substrates for the microsomal vitamin K-dependent gamma-glutamyl carboxylase was determined in a rat model [7].

Biological context of Ggcx

• The vitamin K-dependent gamma-glutamyl carboxylase gene was cloned from a rat liver genomic DNA library and the structural organization of this gene was determined [8].
• A positive correlation was observed between lipid peroxidation and the renal gamma-glutamyl carboxylase activity [1].

Anatomical context of Ggcx

• Both K1 and MK-4 are cofactors for the endoplasmic reticulum enzyme gamma-glutamyl carboxylase but have a structurally different aliphatic side chain [9].
• An acetone powder, prepared from the liver microsomes of vitamin K-deficient rats, retains an active vitamin K-dependent gamma-glutamyl carboxylase [10].

Associations of Ggcx with chemical compounds

• We have shown previously that the in vitro activity of the renal vitamin K-dependent gamma-glutamyl carboxylase toward synthetic oligopeptide substrates is stimulated by administration of either parathyroid hormone (PTH) or 1,25-dihydroxycholecalciferol [1,25(OH)2D3] to rats [(1983) J. Biol. Chem. 258, 12783-12786] [11].
• Responses of renal and hepatic vitamin K dependent gamma-glutamyl carboxylase substrates to warfarin and vitamin K treatments [12].

References