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Vitamin K is a family of structurally similar, fat-soluble vitamers found in foods and marketed as dietary supplements. [1] The human body requires vitamin K for post-synthesis modification of certain proteins that are required for blood coagulation ("K" from Danish koagulation, for "coagulation") or for controlling binding of calcium in bones and other tissues. [2]
VKAs diminish vitamin K levels in the body and inhibit the synthesis of vitamin K dependent clotting factors. [27] Thus, by inhibiting vitamin K, a key element by which the body produces clots, the risk of prolonged bleeding increases. [28] Traditionally, vitamin K has been used as a reversal agent for VKAs.
Gamma-glutamyl carboxylase is an enzyme that catalyzes the posttranslational modification of vitamin K-dependent proteins.Many of these vitamin K-dependent proteins are involved in coagulation so the function of the encoded enzyme is essential for hemostasis. [5]
“Vitamin K is a fat-soluble vitamin, so your body stores it in fat tissue and the liver,” Heather Viola, DO, Primary Care Physician at Mount Sinai Doctors-Ansonia, tells Fortune.
5627 19128 Ensembl ENSG00000184500 ENSMUSG00000022912 UniProt P07225 Q08761 RefSeq (mRNA) NM_000313 NM_001314077 NM_011173 RefSeq (protein) NP_000304 NP_001301006 NP_035303 Location (UCSC) Chr 3: 93.87 – 93.98 Mb Chr 16: 62.67 – 62.75 Mb PubMed search Wikidata View/Edit Human View/Edit Mouse Protein S (also known as PROS) is a vitamin K -dependent plasma glycoprotein synthesized in the ...
This intracellular sensor detects low cholesterol levels and stimulates endogenous production by the HMG-CoA reductase pathway, as well as increasing lipoprotein uptake by up-regulating the LDL-receptor. Regulation of this pathway is also achieved by controlling the rate of translation of the mRNA, degradation of reductase and phosphorylation.
Human Chr 3. In terms of the cause of protein S deficiency it can be in inherited via autosomal dominance.A mutation in the PROS1 gene triggers the condition. The cytogenetic location of the gene in question is chromosome 3, specifically 3q11.1 [6] [7] Protein S deficiency can also be acquired due to vitamin K deficiency, treatment with warfarin, liver disease, kidney disease, chemotherapy ...
The availability of reduced vitamin K is of importance for activation vitamin K 2,3-epoxide. The reduction of vitamin K epoxide is then responsible for the carboxylation of glutamic acid residues in some blood-clotting proteins, including factor VII, factor IX, and factor X. [5] [7] VKORC1 is of therapeutic interest both for its role in ...