Synthetic peptide within Human Kininogen 1 aa 600-700. The exact sequence is proprietary.
Human plasma, platelet and ovarian cancer lysates; Human kidney tissue, Human ovarian adenocarcinoma tissue.
Mouse, Rat: We have preliminary internal testing data to indicate this antibody may not react with these species. Please contact us for more information.
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMab® patents
We are constantly working hard to ensure we provide our customers with best in class antibodies. As a result of this work we are pleased to now offer this antibody in purified format. We are in the process of updating our datasheets. The purified format is designated 'PUR' on our product labels. If you have any questions regarding this update, please contact our Scientific Support team.
This product is a recombinant rabbit monoclonal antibody.
Shipped at 4°C. Store at -20°C. Stable for 12 months at -20°C.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
1/10000 - 1/50000. Detects a band of approximately 45, 56, 120 kDa (predicted molecular weight: 48, 72 kDa).
1/10 - 1/100.
1/100 - 1/250. Perform heat mediated antigen retrieval before commencing with IHC staining protocol.
Heat up to 98 degrees C, below boiling, and then let cool for 10-20 min
(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.
Secreted in plasma. T-kinin is detected in malignant ovarian, colon and breast carcinomas, but not in benign tumors.
Involvement in disease
Defects 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.
Contains 3 cystatin domains.
Bradykinin 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.
Yu J et al. Identification of Kininogen 1 as a Serum Protein Marker of Colorectal Adenoma in Patients with a Family History of Colorectal Cancer. J Cancer9:540-547 (2018).
Read more (PubMed: 29535795) »
Schrödter S et al. Identification of the dopamine transporter SLC6A3 as a biomarker for patients with renal cell carcinoma. Mol Cancer15:10 (2016).
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