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Mouse Anti-Kng1 Recombinant Antibody (CBYJT-1412) (CBMAB-T0435-YJ)

Provided herein is a Mouse monoclonal antibody, which binds to Kng1 (Kininogen 1). The antibody can be used for immunoassay techniques, such as WB, ICC, IHC-P, ELISA.
See all Kng1 antibodies

Summary

Host Animal
Mouse
Specificity
Rat
Clone
CBYJT-1412
Antibody Isotype
IgG
Application
WB, ICC, IHC-P, ELISA

Basic Information

Immunogen
The antibody is a mouse monoclonal antibody raised against KNT1. It has beenselected for its ability to recognize KNT1 in immunohistochemical staining andwestern blotting
Specificity
Rat
Antibody Isotype
IgG
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Buffer
PBS, pH 7.4
Storage
Store at 4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
Kininogen 1
Introduction
Kininogens are plasma glycoproteins with a number of functions: As precursor of the active peptide bradykinin they effect smooth muscle contraction, induction of hypotension and increase of vascular permeability; They function in blood coagulation by helping to position optimally prekallikrein and factor XI next to factor XII; They are inhibitor of thiol proteases.
Entrez Gene ID
288001
UniProt ID
P08932
Alternative Names
Kng1l1; kininogen
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.
Biological Process
Antimicrobial humoral immune response mediated by antimicrobial peptideIDA:UniProtKB
Blood coagulationIEA:UniProtKB-KW
Inflammatory responseIEA:UniProtKB-KW
Killing of cells of other organismIDA:UniProtKB
Negative regulation of blood coagulationManual Assertion Based On ExperimentIDA:UniProtKB
Negative regulation of cell adhesionManual Assertion Based On ExperimentIDA:UniProtKB
Negative regulation of endopeptidase activityManual Assertion Based On ExperimentIBA:GO_Central
Negative regulation of proteolysisManual Assertion Based On ExperimentIDA:UniProtKB
Positive regulation of apoptotic process1 PublicationNAS:UniProtKB
Positive regulation of cytosolic calcium ion concentrationManual Assertion Based On ExperimentIDA:UniProtKB
VasodilationIEA:UniProtKB-KW
Cellular Location
Secreted, extracellular space
Involvement in disease
High molecular weight kininogen deficiency (HMWK deficiency):
Autosomal recessive coagulation defect. Patients with HWMK deficiency do not have a hemorrhagic tendency, but they exhibit abnormal surface-mediated activation of fibrinolysis.
PTM
Bradykinin is released from kininogen by plasma kallikrein.
Hydroxylation of Pro-383 oCcurs prior to the release of bradykinin.
Phosphorylated by FAM20C in the extracellular medium.
N- and O-glycosylated. O-glycosylated with core 1 or possibly core 8 glycans.

Adenaeuer, A., Barco, S., Trinchero, A., Krutmann, S., Nazir, H. F., Ambaglio, C., ... & Rossmann, H. (2023). Severe high-molecular-weight kininogen deficiency: clinical characteristics, deficiency–causing KNG1 variants, and estimated prevalence. Journal of thrombosis and haemostasis, 21(2), 237-254.

Cheng, X., Liu, D., Song, H., Tian, X., Yan, C., & Han, Y. (2021). Overexpression of Kininogen-1 aggravates oxidative stress and mitochondrial dysfunction in DOX-induced cardiotoxicity. Biochemical and biophysical research communications, 550, 142-150.

Vijay, A., Kassab, M. B., Shim, Y. J., Swaidani, S., Mauskapf, A., McCrae, K. R., & Jaffer, F. A. (2021). Protective Effects of Kininogen-1 Gene Deficiency in Mouse Models of Venous Thrombosis. Blood, 138, 289.

Adenaeuer, A., Barco, S., Trinchero, A., Nazir, H., Krutmann, S., Ambaglio, C., ... & Lämmle, B. (2021). Severe High Molecular Weight Kininogen (HK) Deficiency: Clinical Characteristics, Deficiency-Causing KNG1 Variants in Reported and New Cases, and Estimated Prevalence. Blood, 138(Supplement 1), 3200-3200.

Jeong, D., Goo, J. Y., Kim, H. K., Chong, S. Y., & Kang, M. S. (2020). The first korean case of high-molecular-weight kininogen deficiency, with a novel variant, c. 488delG, in the KNG1 gene. Annals of laboratory medicine, 40(3), 264.

Wang, W., Wang, S., & Zhang, M. (2020). Evaluation of kininogen 1, osteopontin and α‑1‑antitrypsin in plasma, bronchoalveolar lavage fluid and urine for lung squamous cell carcinoma diagnosis. Oncology letters, 19(4), 2785-2792.

Yu, J., Huang, Y., Lin, C., Li, X., Fang, X., Zhong, C., ... & Zheng, S. (2018). Identification of kininogen 1 as a serum protein marker of colorectal adenoma in patients with a family history of colorectal cancer. Journal of Cancer, 9(3), 540.

Xu, J., Fang, J., Cheng, Z., Fan, L., Hu, W., Zhou, F., & Shen, H. (2018). Overexpression of the Kininogen-1 inhibits proliferation and induces apoptosis of glioma cells. Journal of Experimental & Clinical Cancer Research, 37, 1-15.

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For research use only. Not intended for any clinical use.

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