Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle.
Storage bufferpH: 7.3
Preservative: 0.02% Sodium azide
Constituents: 0.5% BSA, Tris buffered saline
Concentration information loading...
PurityImmunogen affinity purified
Purification notesPurified from goat serum by ammonium sulphate precipitation followed by antigen affinity chromatography using the immunizing peptide.
Our Abpromise guarantee covers the use of ab223212 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||Use a concentration of 0.03 - 0.1 µg/ml.|
Function(1) Kininogens are inhibitors of thiol proteases; (2) HMW-kininogen plays an important role in blood coagulation by helping to position optimally prekallikrein and factor XI next to factor XII; (3) HMW-kininogen inhibits the thrombin- and plasmin-induced aggregation of thrombocytes; (4) the active peptide bradykinin that is released from HMW-kininogen shows a variety of physiological effects: (4A) influence in smooth muscle contraction, (4B) induction of hypotension, (4C) natriuresis and diuresis, (4D) decrease in blood glucose level, (4E) it is a mediator of inflammation and causes (4E1) increase in vascular permeability, (4E2) stimulation of nociceptors (4E3) release of other mediators of inflammation (e.g. prostaglandins), (4F) it has a cardioprotective effect (directly via bradykinin action, indirectly via endothelium-derived relaxing factor action); (5) LMW-kininogen inhibits the aggregation of thrombocytes; (6) LMW-kininogen is in contrast to HMW-kininogen not involved in blood clotting.
Tissue specificitySecreted in plasma. T-kinin is detected in malignant ovarian, colon and breast carcinomas, but not in benign tumors.
Involvement in diseaseDefects in KNG1 are the cause of high molecular weight kininogen deficiency (HMWK deficiency) [MIM:228960]. HMWK deficiency is an autosomal recessive coagulation defect. Patients with HWMK deficiency do not have a hemorrhagic tendency, but they exhibit abnormal surface-mediated activation of fibrinolysis.
Sequence similaritiesContains 3 cystatin domains.
modificationsBradykinin is released from kininogen by plasma kallikrein.
Hydroxylation of Pro-383 occurs prior to the release of bradykinin.
Phosphorylation sites are present in the extracelllular medium.
N- and O-glycosylated. O-glycosylated with core 1 or possibly core 8 glycans.
Cellular localizationSecreted > extracellular space.
- Information by UniProt
- Alpha-2-thiol proteinase inhibitor antibody
- BDK antibody
- BK antibody
ab223212 has not yet been referenced specifically in any publications.