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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Kallikrein-related peptidase 5

KLK5, kallikrein 5, SCTE
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 expression is up-regulated by estrogens and progestins. The encoded protein is secreted and may be involved in desquamation in the epidermis. Alternative splicing results in multiple transcript variants encoding the same protein. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Kallikrein, KLK6, Trypsin, KLK14, SPINK5
Papers on KLK5
The serine protease inhibitor of Kazal-type 9 (SPINK9) is expressed in lichen simplex chronicus, actinic keratosis and squamous cell carcinoma.
New
Meyer-Hoffert et al., Kiel, Germany. In Arch Dermatol Res, Feb 2016
SPINK9 is a specific inhibitor of the serine protease kallikrein-related peptidase 5 (KLK5), which contributes to the desquamation process of the stratum corneum.
Skin pH Is the Master Switch of Kallikrein 5-Mediated Skin Barrier Destruction in a Murine Atopic Dermatitis Model.
New
Tanaka et al., Fuchū, Japan. In J Invest Dermatol, Jan 2016
Alkalinization of the skin of asymptomatic NC/Tnd mice housed in specific pathogen-free conditions induced kallikrein 5 and activated protease-activated receptor 2, resulting in thymic stromal lymphopoietin secretion and a cutaneous T-helper 2 allergic response.
Adaptive Evolution Favoring KLK4 Downregulation in East Asians.
New
Seixas et al., Porto, Portugal. In Mol Biol Evol, Jan 2016
encodes 15 serine proteases, including neighboring genes (KLK3, KLK2, KLK4, and KLK5) with key roles in the cascades of semen liquefaction, tooth enamel maturation, and skin desquamation.
Subantimicrobial-dose doxycycline monohydrate in dermatology.
New
Wollina, Dresden, Germany. In Wien Med Wochenschr, Dec 2015
UNASSIGNED: Subantimicrobial doxycycline is an anti-inflammatory drug that decreases cathelicidin, kallikrein 5, reactive oxygen species, nitric oxide, and matrix metalloproteinases.
Inhibitors of kallikrein-related peptidases 7 and 5 by grafting serpin reactive center loop sequences onto sunflower trypsin inhibitor-1 (SFTI-1).
New
Beck-Sickinger et al., Leipzig, Germany. In Chembiochem, Dec 2015
To develop peptidic protease inhibitors kallikrein-related peptidases 7 (KLK7) and 5 (KLK5) were chosen.
Skin pH is the Master Switch of Kallikrein 5-Mediated Skin Barrier Destruction in a Murine Atopic Dermatitis Model.
New
Tanaka et al., Fuchū, Japan. In J Invest Dermatol, Oct 2015
Alkalinization of the skin of asymptomatic NC/Tnd mice housed in specific pathogen-free (SPF) conditions induced KLK5 and activated the protease-activated receptor 2 (PAR2), resulting in thymic stromal lymphopoietin (TSLP) secretion and a cutaneous T-helper 2 allergic response.
KLK5 Inactivation Reverses Cutaneous Hallmarks of Netherton Syndrome.
New
Hovnanian et al., Paris, France. In Plos Genet, Sep 2015
Spink5⁻/⁻ mice recapitulate the NS phenotype, display enhanced epidermal Klk5 and Klk7 protease activities and die within a few hours after birth because of a severe skin barrier defect.
Human kallikrein 5 as a novel prognostic biomarker for triple-negative breast cancer: tissue expression analysis and relationship with disease course.
Tong et al., China. In Genet Mol Res, 2014
The purposes of this study were to analyze the expression and distribution of human kallikrein 5 (hK5) in triple-negative breast cancer (TNBC) tissues, to establish a standard operating procedure (SOP) for its immunohistochemical assay, and to evaluate the possibility of hK5 being a prognostic biomarker for TNBC.
The Co-Expression of Kallikrein 5 and Kallikrein 7 Associates with Poor Survival in Non-HPV Oral Squamous-Cell Carcinoma.
Koole et al., Utrecht, Netherlands. In Pathobiology, 2014
Serine protease inhibitor Kazal-type 5 (SPINK5) is the inhibitor of kallikrein 5 (KLK5) and KLK7.
Endoplasmic reticulum stress: key promoter of rosacea pathogenesis.
Review
Melnik, Osnabrück, Germany. In Exp Dermatol, 2014
Recent scientific interest in the pathogenesis of rosacea focuses on abnormally high facial skin levels of cathelicidin and the trypsin-like serine protease kallikrein 5 (KLK5) that cleaves the cathelicidin precursor protein into the bioactive fragment LL-37, which exerts crucial proinflammatory, angiogenic and antimicrobial activities.
Netherton syndrome: defective kallikrein inhibition in the skin leads to skin inflammation and allergy.
Review
Hovnanian et al., In Biol Chem, 2014
Studies in mouse models and in NS patients have established that unopposed kallikrein 5 activity triggers stratum corneum detachment and activates PAR-2 signaling, leading to the autonomous production of pro-allergic and pro-inflammatory mediators.
Current drug therapies for rosacea: a chronic vascular and inflammatory skin disease.
Review
Huynh et al., Winston-Salem, United States. In J Manag Care Spec Pharm, 2014
Aberrant cathelicidin expression, elevated kallikrein 5 (KLK5) proteolytic activity, and altered toll-like receptor 2 (TLR2) expression have been reported in rosacea skin leading to the production of proinflammatory cytokines.
Kallikrein 5-mediated inflammation in rosacea: clinically relevant correlations with acute and chronic manifestations in rosacea and how individual treatments may provide therapeutic benefit.
Review
Del Rosso et al., Henderson, United States. In J Clin Aesthet Dermatol, 2014
Although the pathogenesis of rosacea is not fully understood, recent evidence in vitro as well as in vivo has supported the role of increased levels of the trypsin-like serine protease, kallikrein 5, in initiating an augmented inflammatory response in rosacea.
Netherton syndrome: skin inflammation and allergy by loss of protease inhibition.
Review
Hovnanian, Paris, France. In Cell Tissue Res, 2013
In vitro and in vivo studies in murine models and in NS patients have cast light on the pathogenesis of the disease and shown that LEKTI deficiency results in unopposed kallikrein-related peptidase 5 (KLK5) and KLK7 activities and to the overactivity of a new epidermal protease, elastase 2 (ELA2).
Characterization of SPINK9, a KLK5-specific inhibitor expressed in palmo-plantar epidermis.
GeneRIF
Brattsand et al., Umeå, Sweden. In Biol Chem, 2012
the inhibition and binding of different SPINK9 variants towards KLK5, KLK7, KLK8 and KLK14
MiR-382 targeting of kallikrein 5 contributes to renal inner medullary interstitial fibrosis.
GeneRIF
Liang et al., Milwaukee, United States. In Physiol Genomics, 2012
Data support a completely novel mechanism in which miR-382 targets kallikrein 5 and contributes to the development of renal inner medullary interstitial fibrosis.
Evaluation of kallikrein-related peptidase 5 expression and its significance for breast cancer patients: association with kallikrein-related peptidase 7 expression.
GeneRIF
Karameris et al., Athens, Greece. In Anticancer Res, 2011
Significant co-expression of KLKs 5 and 7 was observed in the same cancer samples. Increased KLK5 expression was a statistically significant independent prognostic factor for DFS and OS of patients
Circulating biomarker tissue kallikrein-related peptidase KLK5 impacts ovarian cancer patients' survival.
GeneRIF
Schmitt et al., München, Germany. In Ann Oncol, 2011
Increased serum and ascitic fluid KLK5 levels are associated with poor patient outcome, thus underlining the importance of KLK5 as a biomarker for early detection as well as for disease management in ovarian cancer.
Kallikreins 5, 6 and 10 differentially alter pathophysiology and overall survival in an ovarian cancer xenograft model.
GeneRIF
Vanderhyden et al., Ottawa, Canada. In Plos One, 2010
Loss of KLK5 is associated with ovarian cancer.
Increased serine protease activity and cathelicidin promotes skin inflammation in rosacea.
Impact
Gallo et al., San Diego, United States. In Nat Med, 2007
These cathelicidin peptides are a result of a post-translational processing abnormality associated with an increase in stratum corneum tryptic enzyme (SCTE) in the epidermis.
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