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Structures of BbKI complexed with the catalytic domain of human plasma kallikrein were modeled, as well as those with KLK4 and KLK7, and the structures were analyzed in order to identify the interactions that are responsible for inhibitory potency.
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The functional role of glycosylation in prostate-specific KLK4 could pave the way to a deeper understanding of their biology and to medical applications.
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In pregnant women with KLK-4 gene polymorphisms A/A and G/A genotypes the rate of tooth decay growth increases in spite of applying the ternary calcium-phosphate-fluoride-containing gel.
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Authors demonstrated that KLF4 was induced by ER stress in melanoma cells, and increased KLF4 inhibited cell apoptosis and promoted cell metastasis. Further mechanistic studies revealed that KLF4 directly bound to the promoter of NUCB2, facilitating its transcription.
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During the descriptive analysis, the variables ethnicity, biofilm, and gingivitis and the markers rs2242670 and rs2978642 were statistically significant. In the multivariate analysis, the marker rs2242670 and the variable biofilm maintained statistical significance. Genetic variations in the KLK4 gene may contribute to dental decay.
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Epithelial-derived KLK4 promotes tumour progression by actively promoting cancer-associated fibroblasts differentiation in the prostate stromal microenvironment.
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structural analysis of mechanism of KLK4 inhibition
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These findings prompt a new mechanistic model and line of enquiry into the role of KLK4 in enamel hardening and malformation.
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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.
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The KLK4 protein is localized in the cytoplasm of tumor and stroma cells.
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KLK4 as a potential multifunctional regulator of prostate cancer progression.
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Low KLK4 expression is associated with lupus nephritis.
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KLK4 may contribute to the metastasis of OSCC through the PI3 K/AKT signaling pathway
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KLK4 acts as an oncogene in OSCC cells, and targeting KLK4 may be a promising method for OSCC therapy.
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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.
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secreted into the extracellular microenvironment by neutrophils stimulated with bioactive mediators
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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.
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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.
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Human ephrin-B2 is poorly cleaved by KLK4 while the homologous mouse is not.
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miR-378 was predicted to target both KLK2 and KLK4 and downregulated levels detected in prostate cancer patients.
