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Transcobalamin I (TC-1), also known as haptocorrin (HC), R-factor, and R-protein is encoded in the human by the TCN1 gene. TC-1 is a glycoprotein produced by the salivary glands of the mouth. It primarily serves to protect cobalamin (Vitamin B12) from acid degradation in the stomach by producing a HC-Vitamin B 12 complex.
The same cells in the stomach that produce gastric hydrochloric acid, the parietal cells, also produce a molecule called the intrinsic factor (IF), which binds the B 12 after its release from haptocorrin by digestion, and without which only 1% of vitamin B 12 is absorbed. Intrinsic factor (IF) is a glycoprotein, with a molecular weight of 45 kDa.
Christmas factor: 4 × 10 −6: Stuart factor: 5 × 10 −6: Plasma thrmb. anteced. 4 × 10 −6: Hageman factor: 2.9 × 10 −5: Fibrin-stabilizing factor: 1 × 10 −5: Fibrin split products <1 × 10 −5: Fletcher factor: 5 × 10 −5: Fitzgerald factor: 7 × 10 −5: von Willebrand factor: 7 × 10 −6: Cobalamin (Vitamin B 12) Needed for ...
The factor VIII protein has a half-life of 12 hours in the blood stream when stabilized by the von Willebrand factor. [ 20 ] No longer protected by vWF, activated FVIII is proteolytically inactivated in the process (most prominently by activated protein C and factor IXa ) and quickly cleared from the blood stream.
Contrary to popular belief, haemoglobin is not a blood protein, as it is carried within red blood cells, rather than in the blood serum. Serum albumin accounts for 55% of blood proteins, [1] is a major contributor to maintaining the oncotic pressure of plasma and assists, as a carrier, in the transport of lipids and steroid hormones.
Acid–base and blood gases are among the few blood constituents that exhibit substantial difference between arterial and venous values. [6] Still, pH, bicarbonate and base excess show a high level of inter-method reliability between arterial and venous tests, so arterial and venous values are roughly equivalent for these. [44]
The affinity of this protein for factor Xa is increased 1000-fold by the presence of protein Z, while it does not require protein Z for inactivation of factor XI. Defects in protein Z lead to increased factor Xa activity and a propensity for thrombosis. The half life of factor X is 40–45 hours.
The blood coagulation and Protein C pathway.. Factor IX is produced as a zymogen, an inactive precursor.It is processed to remove the signal peptide, glycosylated and then cleaved by factor XIa (of the contact pathway) or factor VIIa (of the tissue factor pathway) to produce a two-chain form, where the chains are linked by a disulfide bridge.