3.4.21.B43: kallikrein 12
This is an abbreviated version!
For detailed information about kallikrein 12, go to the full flat file.
Word Map on EC 3.4.21.B43
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3.4.21.B43
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kallikreins
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klk8
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atopic
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dermatitis
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kazal-type
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diagnostics
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kallikrein-like
- 3.4.21.B43
- kallikreins
- klk8
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atopic
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dermatitis
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kazal-type
- diagnostics
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kallikrein-like
Reaction
proteolytic cleavage of polypeptides =
Synonyms
hK12, K12, kallikrein 12, kallikrein-related peptidase 12, KLK12, S01.020
ECTree
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General Information
General Information on EC 3.4.21.B43 - kallikrein 12
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malfunction
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knockdown of KLK12 results in a significant downregulation of autophagy and apoptosis in Mycobacterium bovis infected bone marrow derived macrophages
metabolism
PDGF-B is probably one of the molecules linking the interaction between enzyme-induced endothelial cells and fibroblasts. Expression of both KLK12 and PDGFB genes is regulated by hypoxia in the lung tumor microenvironment
physiological function
additional information
fragmentation of CCN1 or CCN5 by KLK12 prevents vascular endothelial growth factor165 binding, whereas it also triggers the release of intact vascular endothelial growth factor and bone morphogenetic protein 2 from the CCN protein complexes. The KLK12-mediated release of transforming growth factor-beta1 and fibroblast growth factor-2 is concentration-dependent. KLK12 may indirectly regulate the bioavailability and activity of several growth factors through processing of their CCN binding partners
physiological function
cleavage of the influenza hemagglutinin precursor by host proteases, e.g. kallikrein-related peptidase 12, is a critical step in the virus life cycle. Cleavage activation of influenza hemagglutinin enables fusion with the host endosome, allowing for release of the viral genome into the host cel
physiological function
expression profile of the splice variants KLK12sv3 and KLK12sv1/KLK12sv2 of kallikrein-related peptidase 12 in breast cancer patients and their clinical significance, overview. Positive KLK12sv3 expression is associated with longer patient disease-free survival and higher progesterone receptor concentration. KLK12sv1/KLK12sv2 expression is statistically associated with KLK12sv3 expression
physiological function
proangiogenic activity of the enzyme in lung endothelial cells. The enzyme may interfere with kininostatin-related antiangiogenic activity by cleaving the D5 domain
physiological function
the enzyme induces the formation of pulmonary endothelial cell tubule-like structures. The enzyme converts the extracellular matrix- or membrane-bound precursor of platelet-derived growth factor B (PDGF-B) into a soluble active form. Both PDGF-B and vascular endothelial growth factor A (VEGF-A) take part in the induction of angiogenesis by enzyme KLK12 in a coculture model of angiogenesis that mimics endothelial tubule formation. Release of mature PDGF-B by enzyme KLK12 leads to the fibroblast-mediated secretion of VEGF-A, which stimulates endothelial cell differentiation and the formation of capillary tube-like structures. PDGF-B signaling ultimately results in cell growth, migration, and protection against apoptosis, overview
physiological function
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the enzyme regulates innate resistance of murine macrophages against Mycobacterium bovis infection by modulating autophagy and apoptosis
physiological function
the enzyme stimulates endothelial cell migration by remodeling the fibronectin matrix
KLK12 is a trypsin-like kallikrein-related peptidase that is abundant in a variety of human tissues
additional information
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KLK12 is a trypsin-like kallikrein-related peptidase that is abundant in a variety of human tissues