KLH conjugated synthetic peptide derived from human HMW Kininogen-1 light chain:551-644/644
Format：
Liquid
Storage instructions：
Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.
Concentration：
1mg/ml
Clonality：
Polyclonal
Isotype：
IgG
Applications：
WB=1:500-2000ELISA=1:5000-10000IHC-P=1:100-500IHC-F=1:100-500IF=1:50-200（Paraffin sections need to do antigen repair）not yet tested in other applications.optimal dilutions/concentrations should be determined by the end user.
Host：
Rabbit
Product Overview：
Sample:liver(mouse) Lysate at 40 ugPrimary: Anti-Kininogen-1 light chain (SL9504R) at 1/300 dilutionSecondary: IRDye800CW Goat Anti-Rabbit IgG at 1/20000 dilutionPredicted band size: 28/70kDObserved band size: 28 kDSample:Placenta (Mouse) Lysate at 40 ugPrimary: Anti- Kininogen-1 light chain (SL9504R)at 1/300 dilutionSecondary: IRDye800CW Goat Anti-Rabbit IgG at 1/20000 dilutionPredicted band size: 28 kDObserved band size: 28 kD
This gene uses alternative splicing to generate two different proteins- high molecular weight kininogen (HMWK) and low molecular weight kininogen (LMWK). HMWK is essential for blood coagulation and assembly of the kallikrein-kinin system. Also, bradykinin, a peptide causing numerous physiological effects, is released from HMWK. In contrast to HMWK, LMWK is not involved in blood coagulation. Three transcript variants encoding different isoforms have been found for this gene.[provided by RefSeq, Oct 2009].
Function: 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 Specificity: Secreted in plasma. T-kinin is detected in malignant ovarian, colon and breast carcinomas, but not in benign tumors.
Post-translational modifications: 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 extracellular medium. N- and O-glycosylated. O-glycosylated with core 1 or possibly core 8 glycans.
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.
