KLK3(Kallikrein 3), also known as Prostate Specific Antigen (PSA), kallikrein-related peptidase 3, Gamma-seminoprotein, is a secreted protein of the glandular kallikrein subfamily of serine proteases.KLK3 contains one peptidase S1 domain.KLK3 is a glycoprotein produced almost exclusively by the prostate gland. Growing evidence suggests that many kallikreins are implicated in carcinogenesis and some have potential as novel cancer and other disease biomarkers.
Human Kallikrein 7 is a member of the tissue kallikrein family of extracellular serine proteases that is made up of 15 members. It is predominantly expressed in the skin. A major physiological function of Kallikrein 7 is to regulate the desquamation process (the shedding of corneocytes from the outer layer of the epidermis) through proteolysis of the intercellular adhesive structures between corneocytes. Dysregulation of Kallikrein 7 has been linked to several inflammatory skin diseases including atopic dermatitis, psoriasis, and Netherton syndrome. Studies have shown that Kallikrein 5 is a potential physiological activator for Kallikrein 7. The proform of Kallikrein 7 can be activated by thermolysin.
Kallikreins are a subgroup of serine proteases having diverse physiological functions. Growing evidence suggests that many Kallikreins are implicated in carcinogenesis and some have potential as novel cancer and other disease biomarkers. This gene is one of the fifteen Kallikrein subfamily members located in a cluster on chromosome 19. Its encoded protein is secreted and may play a role in suppression of tumorigenesis in breast and prostate cancers. Alternate splicing of this gene results in multiple transcript variants encoding the same protein.
Kallikrein-8, also known as Neuropsin, Serine protease 19, Serine protease TADG-14, Tumor-associated differentially expressed gene 14 protein and KLK8, is a secreted protein which belongs to thepeptidase S1 family and Kallikrein subfamily. It is a serine protease which is capable of degrading a number of proteins such as casein, fibrinogen, kininogen, fibronectin and collagen type IV. Kallikrein-8 / KLK8 plays a role in the formation and maturation of orphan and small synaptic boutons in the Schaffer-collateral pathway. It regulates Schaffer-collateral long-term potentiation in the hippocampus and is required for memory acquisition and synaptic plasticity. It is involved in skin desquamation and keratinocyte proliferation and plays a role in the secondary phase of pathogenesis following spinal cord injury. It also cleaves L1CAM in response to increased neural activity. It induces neurite outgrowth and fasciculation of cultured hippocampal neurons. Kallikrein-8 / KLK8 is expressed at high levels in serum, ascites fluid and tumor cytosol of advanced stage ovarian cancer patients and may serve as a marker of ovarian cancer. Kallikrein-8 / KLK8 may have potential clinical value for disease diagnosis or prognosis and it may also be a useful therapeutic target.
Klotho, also called Klotho-alpha, is the founding member of the Klotho family within the glycosidase-1 superfamily . Klotho is expressed in areas concerned with calcium regulation, predominantly in the kidney distal convoluted tubules, but also in the brain choroid plexus (which produces cerebrospinal fluid) and the parathyroid. A 130 kDa form found in plasma and cerebrospinal fluid is produced by proteolytic cleavage of the glycosylated 135 kDa full-length Klotho . A truncated 549 aa isoform predicted by alternative mRNA splicing has been detected in human and mice. A prominent intracellular 120 kDa form of Klotho is localized to endoplasmic reticulum and Golgi membranes. The phenotype of Klotho-deficient mice resembles premature aging, including arteriosclerosis, osteoporosis, skin atrophy, infertility, emphysema and premature death. Conversely, excess Klotho extends lifespan. Klotho acts as a cofactor for interaction of FGF-23 with FGF R1. This interaction negatively regulates 1 alpha-hydroxylase, the rate-limiting enzyme in the synthesis of 1,25(OH)2D3 (vitamin D). Klotho deficient mice show severe hyperphosphatemia and ectopic calcification of soft tissues due to excess vitamin D. Both Klotho and Klotho beta are cofactors for FGF19 binding. Klotho also shows glucuronidase activity which activates the renal ion channel TRPV5 to reabsorb urinary calcium. Klotho has been reported to downregulate insulin or IGF-1 signaling in adipocytes, to bind and antagonize Wnt molecules, and to facilitate release of parathyroid hormone.
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