======= KNG1 =======
== Gene Information ==
* **Official Symbol**: KNG1
* **Official Name**: kininogen 1
* **Aliases and Previous Symbols**: N/A
* **Entrez ID**: [[https://www.ncbi.nlm.nih.gov/gene/?term=3827|3827]]
* **UniProt**: [[https://www.uniprot.org/uniprot/P01042|P01042]]
* **Interactions**: [[https://thebiogrid.org/search.php?search=KNG1&organism=9606|BioGRID]]
* **PubMed articles**: [[https://www.ncbi.nlm.nih.gov/pubmed/?term=gene%20KNG1|Open PubMed]]
* **OMIM**: [[https://omim.org/entry/612358|Open OMIM]]
== Function Summary ==
* **Entrez Summary**: 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. Bradykinin also functions as an antimicrobial peptide with antibacterial and antifungal activity. 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, Nov 2014].
* **UniProt Summary**: (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.
|Cystatin|
|blood coagulation, intrinsic pathway|
|blood coagulation, fibrin clot formation|
|protein activation cascade|
|vasodilation|
|cysteine-type endopeptidase inhibitor activity|
|negative regulation of blood coagulation|
|negative regulation of hemostasis|
|negative regulation of coagulation|
|positive regulation of blood vessel diameter|
|platelet alpha granule lumen|
|negative regulation of wound healing|
|regulation of blood coagulation|
|regulation of hemostasis|
|regulation of coagulation|
|negative regulation of response to wounding|
|platelet degranulation|
|regulation of wound healing|
|regulation of blood vessel diameter|
|regulation of tube diameter|
|regulation of tube size|
|blood microparticle|
|regulation of response to wounding|
|vascular process in circulatory system|
|heparin binding|
|negative regulation of endopeptidase activity|
|negative regulation of peptidase activity|
|negative regulation of cell adhesion|
|positive regulation of cytosolic calcium ion concentration|
|blood coagulation|
|coagulation|
|hemostasis|
|endoplasmic reticulum lumen|
|regulation of cytosolic calcium ion concentration|
|signaling receptor binding|
|negative regulation of proteolysis|
|post-translational protein modification|
|negative regulation of response to external stimulus|
|collagen-containing extracellular matrix|
|blood circulation|
|circulatory system process|
|regulation of endopeptidase activity|
|cellular calcium ion homeostasis|
|regulation of peptidase activity|
|calcium ion homeostasis|
|negative regulation of hydrolase activity|
|cellular divalent inorganic cation homeostasis|
|wound healing|
|divalent inorganic cation homeostasis|
|regulation of body fluid levels|
|inflammatory response|
|regulation of anatomical structure size|
|cellular metal ion homeostasis|
|response to wounding|
|metal ion homeostasis|
|cellular cation homeostasis|
|positive regulation of apoptotic process|
|cellular ion homeostasis|
|positive regulation of programmed cell death|
|regulation of cell adhesion|
|positive regulation of cell death|
|regulated exocytosis|
|cation homeostasis|
|inorganic ion homeostasis|
|regulation of proteolysis|
|cellular chemical homeostasis|
|ion homeostasis|
|negative regulation of catalytic activity|
|exocytosis|
|zinc ion binding|
|cellular homeostasis|
|secretion by cell|
|negative regulation of cellular protein metabolic process|
|export from cell|
|regulation of response to external stimulus|
|negative regulation of protein metabolic process|
|chemical homeostasis|
|secretion|
|negative regulation of molecular function|
|negative regulation of multicellular organismal process|
|regulation of hydrolase activity|
|G protein-coupled receptor signaling pathway|
|defense response|
|regulation of response to stress|
|regulation of apoptotic process|
|regulation of programmed cell death|
|extracellular space|
|negative regulation of response to stimulus|
|homeostatic process|
|regulation of cell death|
|extracellular region|
|vesicle-mediated transport|
|system process|
\\
=== CRISPR Data ===
No hits were found.
No correlation found to any other genes in chemogenomics.
Global Fraction of Cell Lines Where Essential: 0/739
^Tissue^Fraction Of Cell Lines Where Essential^
|1290807.0|0/1|
|909776.0|0/1|
|bile duct|0/28|
|blood|0/28|
|bone|0/26|
|breast|0/33|
|central nervous system|0/56|
|cervix|0/4|
|colorectal|0/17|
|esophagus|0/13|
|fibroblast|0/1|
|gastric|0/16|
|kidney|0/21|
|liver|0/20|
|lung|0/75|
|lymphocyte|0/16|
|ovary|0/26|
|pancreas|0/24|
|peripheral nervous system|0/16|
|plasma cell|0/15|
|prostate|0/1|
|skin|0/24|
|soft tissue|0/9|
|thyroid|0/2|
|upper aerodigestive|0/22|
|urinary tract|0/29|
|uterus|0/5|
== Essentiality in NALM6 ==
* **Essentiality Rank**: 14588
* **Expression level (log2 read counts)**: -1.26
{{:chemogenomics:nalm6 dist.png?nolink |}}