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Bradykinin is expressed in endometriotic lesions.
Kininogen binds to the cell surface-exposed proteins of Candida parapsilosis.
Three loci showed robust, replicating association with circulating FXI levels: KNG1 (rs710446, P-value = 2.07 x 10-302), F11 (rs4253417, P-value = 2.86 x 10-193), and a novel association in GCKR (rs780094, P-value = 3.56 x10-09), here for the first time implicated in FXI regulation. The two first SNPs (rs710446 and rs4253417) also associated with partial thromboplastin time
findings show that the KNG1 locus plays a central role as a genetic determinant of the entire coagulation pathway and thrombus/clot formation
Urinary KNG1 and RBP4 clearly respond to AKI. Additionally, RBP4 could predict recovery by monitoring this protein levels over time after AKI, as RBP4 reflects patient's normalization earlier than sCr values do.
KNG1 rs710446/ rs2304456 SNPs are not related to the incidence of Alzheimer's disease in a Hunan Han Chinese population.
Low urine KNG1 expression is associated with clear cell renal cell carcinoma.
The results of this study supported the association of the epistatic interactions of ALOX5AP, THBD, and KNG1 and present novel evidence for the main effect of KNG1 gene on IS susceptibility.
Bradykinin stimulates pro-contractile signalling mechanisms in human myometrial cells and arrestin proteins play key roles in their regulation.
2 genetic loci (kininogen 1 and kallikrein B) influencing key components of the RAAS, consistent with the close interrelation between the kallikrein-kinin system and the RAAS.
Measuring plasma levels of cleaved HK may be a sensitive mean of assessing disease severity in HAE-C1-INH patients.
The antimicrobial protein kininogen evolved adaptively in mammals and human populations.
results demonstrate that HKa accelerates the onset of EPC senescence by stimulating JNK/FOXO4/MnSOD pathway, its effect is mediated by the HC
When the concentrations of IGFBP-6 or KNG1 were greater than 98.5 pg/ml or 88.5 ng/ml, respectively, they predicted the proliferative vitreoretinopathy prognosis.
uPAR mediates efferocytosis through high molecular weight kininogen interaction with phosphatidylserine on apoptotic cells
Data suggest factor XII binding/autoactivation are increased on surface of hantavirus-infected vascular endothelium; thus, activation of kallikrein-kinin system during hantavirus infection could have profound implications on capillary permeability.
The acquisition of an active site in prekallikrein as a result of binding to high-molecular-weight kininogen (HK) is a new concept for bradykinin formation and might be relevant in the pathogenesis of hereditary angiodema types I and II.
these results suggest that D5(H) of high molecular weight kininogen may modulate cell adhesion and invasion together with actinin-4.
KNG1 and F11 are the main genetic regulators of plasma FXI level.
The results showed that bradykinin stimulates Toll-like receptor 2 transcription and translation by activation of protein kinase C as well as proto-oncogene protein AKT.
Schistosome tegument contains two cysteine proteases belonging to the calpain family (SmCalp1 and SmCalp2) and these are likely responsible for the high molecular weight kininogen (HK) cleavage reported here. Schistosome cleavage of HK should help impede blood clotting and inflammation around the worms in vivo and so promote their ease of movement within the vasculature of their hosts.
mice deficient in KNG showed less severe blood-brain barrier damage and edema formation, and the local inflammatory response was reduced compared with controls.
Domain 5 of kininogen was identified as an anti-adhesive component with a potent anti-inflammatory action in a peritonitis mouse model.
His-Gly-Lys motif and lysine residue (Lys487) play essential roles in inhibition of cell adhesion and invasion in vitro and in prevention of metastasis of cancer cells in vivo
Two genes, kininogen-I and kininogen-II, are located in close proximity on chromosome 16 in a head-to-head arrangement. In liver and kidney, both genes are expressed and for each gene three alternative splice variants are synthesized.
in the kidney K2 is strongly expressed as both HMWK and LMWK, whereas K1 is not expressed as HMWK and expressed only very weakly as LMWK
mKng1 is responsible for production of plasma kininogen
The vascular compartment is the main site of AngI and bradykinin-(1-9) formation and metabolism.
Bradykinin, together with its precursor and tissue kallikrein, is continuously released into the vasculature of the isolated, perfused, lactating bovine udder.
Bradykini stimulates endothelial cell fatty acid oxidation by calmodulin-dependent kinase kinase -dependent activation of AMP-activated protein kinase (AMPK)
Promoter of ITIH4 major acute phase protein has been isolated, cloned, and proven functional by response to an inflammatory stimulus (interleukin-6) in human Hep3B cells. (inter-alpha-trypsin heavy chain 4; ITIH4)
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.
, alpha-2-thiol proteinase inhibitor
, fitzgerald factor
, high molecular weight kininogen
, williams-Fitzgerald-Flaujeac factor
, kininogen I
, kininogen II
, thiol proteinase inhibitor
, low molecular weight kininogen
, kininogen 1
, T-kininogen 2
, T-kininogen II
, low molecular weight (LMW) T-kininogen II
, major acute phase protein (alpha-1-MAP)
, ITI heavy chain H4
, inter-alpha (globulin) inhibitor H4 (plasma Kallikrein-sensitive glycoprotein)
, inter-alpha-inhibitor heavy chain 4
, inter-alpha-trypsin inhibitor family heavy chain-related protein
, inter-alpha-trypsin inhibitor heavy chain H4
, major acute phase protein