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FLASH GENE

Symbol

KLK12

contributors: mct - updated : 22-04-2020

HGNC name	kallikrein 12
HGNC id	6360

FLASH GENE DNA RNA EXPRESSION PROTEIN DISORDER ANIMAL & CELL MODELS

PROTEIN

PHYSICAL PROPERTIES

STRUCTURE

motifs/domains

isoforms

Precursor

secreted as an inactive pro-enzyme, which is able to autoactivate to gain enzymatic activity

HOMOLOGY

interspecies

homolog to murine neuropsin

Homologene

FAMILY

kallikrein gene family

CATEGORY

enzyme

SUBCELLULAR LOCALIZATION	extracellular
	intracellular
	intracellular,cytoplasm,cytosolic,granule

basic FUNCTION	involved in pathogenesis and/or progression of certain cancer types
	possesses trypsin-like activity, cleaving peptide bonds after both arginine and lysine
	may participate in enzymatic cascades involving other kallikreins
	may indirectly regulate the bioavailability and activity of several growth factors through processing of their CCN binding partners
	involvement of KLK12 in different homeostatic and disease pathways through modulation of growth factor availability and/or activity
	play a critical role in controlling normal angiogenesis
	KLK12-mediated proteolysis of CYR61 and WISP3 can reduce or abolish the binding of VEGFA, BMP2, and TGFB1
	KLK12-mediated hydrolysis of CCNs may be involved in the modulation of the bioavailability and/or activity of several growth factors including VEGFA, BMP2, TGFB1, and FGF2
	may play an important role in angiogenesis modulating proangiogenic factor bioavailability and activating the kinin receptor B2 pathway
	proangiogenic activity of KLK12 in lung endothelial cells was not related to a kinin release
	KLK5, KLK12 are involved in the cleavage activation of human-adapted influenza virus subtypes
	KLK12 proangiogenic effect is mediated through several molecular mechanisms
	plays likely a tumor-supporting role in Triple-negative breast cancer (TNBC)

CELLULAR PROCESS

protein, degradation

PHYSIOLOGICAL PROCESS

PATHWAY

metabolism

signaling

a component

INTERACTION

DNA

RNA

small molecule

protein	might be responsible for the shedding of CYR61 from the cell surface
	can target all six members of the CCN family at different proteolytic sites (WISP1, WISP2, WISP3, CYR61, CTGF, NOV)
	interacting with CYR61 and WISP3 (fragmentation of CYR61 and WISP3 by KLK12 on cells of the tumor microenvironment, including neoplastic and endothelial cells)
	angiogenesis is stimulated by KLK12 acting via a PDGFB-dependent paracrine pathway
	efficiently cleaved the extracellular matrix proteins fibronectin and tenascin, both of which are involved in the regulation of endothelial cell adhesion and migration

cell & other

REGULATION

induced by

steroid hormone

ASSOCIATED DISORDERS

corresponding disease(s)

Other morbid association(s)

Type Gene Modification Chromosome rearrangement Protein expression Protein Function tumoral     --low   in breast cancer tumoral     --over   in prostate cancer tumoral     --over   in Gastric cancer tissue

Susceptibility

Variant & Polymorphism

Candidate gene
Marker	may have potential use as a cancer biomarker
	KLK12 might serve as a novel diagnosis and prognosis biomarker in gastric cancer
Therapy target

ANIMAL & CELL MODELS