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normal enamel maturation is regulated by TGF-ss signaling through the expression of KLK4
The breakage of enamel near the dentino-enamel junction in Klk4-null mice is not due to a failure of odontoblasts to express Klk4, but it relates to a progressive hypomineralization of enamel with depth.
Effect of kallikrein 4 loss on enamel mineralization: comparison with mice lacking matrix metalloproteinase 20 (显示 MMP20 ELISA试剂盒).
expression of KLK4 correlates with the stage-associated changes in the digestion of enamel proteins
Mice lacking expression of the AmelX (显示 AMELX ELISA试剂盒), Enam (显示 ENAM ELISA试剂盒) and Mmp20 (显示 MMP20 ELISA试剂盒) genes have been generated.
Dipeptidyl peptidase I (显示 CTSC ELISA试剂盒) activates pro-KLK4 to cleave a fluorogenic peptide containing a KLK4 cleavage site in mice incisor enamel organs during amelogenesis. site.
Klk4 is essential for the removal of enamel proteins and the proper maturation of enamel crystals in mice
Results show that AMTN and KLK4 are not essential for biological processes outside of the dentition or during the secretory stage of amelogenesis. Both KLK4 and AMTN proved to be essential for the maturation of dental enamel, a process that requires the removal of extracellularmatrix proteins and the deposition of ions on the sides of enamel crystallites.
The KLK4 protein is localized in the cytoplasm of tumor and stroma cells.
KLK4 as a potential multifunctional regulator of prostate cancer progression.
Low KLK4 expression is associated with lupus nephritis.
KLK4 may contribute to the metastasis of OSCC through the PI3 K (显示 PIK3CA ELISA试剂盒)/AKT (显示 AKT1 ELISA试剂盒) signaling pathway
KLK4 acts as an oncogene (显示 RAB1A ELISA试剂盒) in OSCC cells, and targeting KLK4 may be a promising method for OSCC therapy.
Studied a 70-kb region surrounding KLK4 in East Asian population; found within combined unusual low levels of diversity, high frequency variants with significant levels of population differentiation.
Novel homozygous mutations in the KLK4 (c.620_621delCT, p.Ser207Trpfs*38) were identified in amelogenesis imperfecta consanguinity. Mutant KLK4 was degraded intracellularly and became inactive.
this study provides supportive evidence in favor of a prognostic value for KLK4 in OSCC and suggests that KLK4 could serve as a potential therapeutic target in patients with oral cancer.
Human ephrin-B2 (显示 EFNB2 ELISA试剂盒) is poorly cleaved by KLK4 while the homologous mouse is not.
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. In some tissues its expression is hormonally regulated. The expression pattern of a similar mouse protein in murine developing teeth supports a role for the protein in the degradation of enamel proteins. Alternate splice variants for this gene have been described, but their biological validity has not been determined.
kallikrein 4 (prostase, enamel matrix, prostate)
, protease, serine 17 (enamel matrix, prostate)
, androgen-regulated message 1
, enamel matrix serine protease 1
, enamel matrix serine proteinase 1
, kallikrein-like protein 1
, serine protease 17
, Enamel matrix serine proteinase 1