KLK_7 _ Kallikrein_7 _ PRSS6 Antibody
- Known as:
- KLK_7 _ Kallikrein_7 _ PRSS6 Antibody
- Catalog number:
- 10416-RP01
- Product Quantity:
- 200
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- KLK_7 _ Kallikrein_7 PRSS6 Antibody
Related genes to: KLK_7 _ Kallikrein_7 _ PRSS6 Antibody
- Gene:
- KLK7 NIH gene
- Name:
- kallikrein related peptidase 7
- Previous symbol:
- PRSS6
- Synonyms:
- SCCE
- Chromosome:
- 19q13.33
- Locus Type:
- gene with protein product
- Date approved:
- 1995-06-14
- Date modifiied:
- 2015-11-13
Related products to: KLK_7 _ Kallikrein_7 _ PRSS6 Antibody
Related articles to: KLK_7 _ Kallikrein_7 _ PRSS6 Antibody
- Mounting evidence suggests that the kallikrein-related peptidase family is dysregulated in thyroid cancer. However, previous analyses of kallikrein-related peptidase 7 (KLK7) expression patterns have yielded inconsistent results. In this study, KLK7 expression was examined in different histological types of thyroid cancer using immunohistochemistry. We found no detectable KLK7 immunoreactivity in the follicular epithelium of normal thyroid tissue or follicular adenomas. Weak KLK7 expression was observed in papillary (mean H-score 47) and follicular carcinomas (mean H-score 29), with moderate expression in anaplastic cancers (mean H-score 88; P for trend < 0.001). Membranous and cytoplasmic staining was validated using two independent antibodies and small interfering RNA (siRNA) knockdown controls. These observations were consistent with our bioinformatics analysis, which demonstrated that KLK7 was upregulated in less differentiated thyroid cancer and inversely correlated with thyroid differentiation scores. Knockdown of KLK7 expression through transfection with siRNA significantly impaired the viability, clonogenicity, and migratory abilities of thyroid cancer cells. This was accompanied by upregulation of E-cadherin and integrin-β1, along with elevated levels of the KLK7 substrates midkine and tenascin-C. Taken together, our results indicate that KLK7 is overexpressed in thyroid cancer and is linked to disease progression and dedifferentiation, partly by disrupting cell adhesion networks. KLK7 may therefore serve as a biomarker for aggressive thyroid cancer and a potential therapeutic target. - Source: PubMed
Publication date: 2026/04/22
Chi Shun-YuKuo Chi-YuHuang Shih-YuanCheng Shih-Ping - Differential expression of Kallikreins (KLKs) was described for established metastatic pancreatic ductal adenocarcinoma (PDAC), but their potential as markers for early detection is not known. We have performed comprehensive in silico and in situ analyses of KLK expression in PDAC at different stages of tumor development. We found that upregulation of KLK7 and KLK10 RNA and protein occurs early in tumor development and marks carcinoma in-situ lesions (stage 0, PanIN3) and early-stage (stage 1) PDAC, while non-cancerous low grade lesions stain negative for these proteases. Moreover, both KLKs are co-expressed with desmoglein-3 (DSG3) in PDAC cell lines as well as PDAC samples from treatment naïve patients. DSG3 serves as a substrate for both KLK7 and KLK10 resulting in a 30 kDa extracellular fragment. Overall, our data suggest that analyses for expression of KLK7 and KLK10 as well as their substrates could have potential as diagnostic biomarkers to distinguish non-cancerous low-grade lesions from earliest cancerous lesions in the pancreas. - Source: PubMed
Publication date: 2026/04/13
Eisenhauer JillianArgo RyanMartinez Alicia K FlemingMaldosevic EmirBastea Ligia IWehrkamp Cody JDöppler Heike REdenfield Brandy HLewis Jason TWallace Michael BStorz Peter - The serine protease KLK7 contributes to several skin disorders and tumorigenesis, making it an attractive drug target. Owing to structural similarities in the S1 binding pocket between human KLK7 and certain trypsin-like serine proteases harboring an Ala at position 190, compounds containing a chlorine-substituted benzylamide as P1 group were screened for KLK7 inhibition. Further optimization yielded the substrate analog inhibitor Bzls-d-hTyr-Pro-2-aminomethyl-5-chloro-benzylamide ( value 29.3 nM), which, however, had insufficient selectivity against the tested clotting proteases. Guided by a published KLK7 crystal structure, a second, more selective non-peptide inhibitor series was synthesized. The best derivatives ( values <100 nM) contain a chlorine-substituted aromatic P1 group and additionally address the non-prime region of KLK7. Murine Klk7 is poorly inhibited by these compounds; however, mutating threonine 190 in the S1 pocket to alanine restored the inhibitory potency. The new inhibitors effectively block KLK7-mediated functions, including chemokine cleavage and moesin gene upregulation, without cytotoxicity towards murine ovarian cancer cells. Moreover, tumors derived from ovarian cancer cells overexpressing either wild-type or mutated Klk7 reduced overall survival in mice compared to vector control cells. Together, these findings establish a robust inhibitor-enzyme system to evaluate human KLK7 inhibitors in a preclinical mouse model. - Source: PubMed
Publication date: 2026/03/19
Steinmetzer TorstenMesa-Rangel Laury SJanghorban SadafSabzi SajadBoller CharlotteMaiwald AlexanderLang-Henkel HeikeBielesch SophiaMilisterfer JuliaMagno GiuliaBronger HolgerDarmoul DalilaMagdolen ViktorDreyer Tobias F - To elucidate the mechanism of Schizonepeta tenuifolia-Diosmetin in acne treatment using an integrated approach combining network pharmacology, molecular dynamics simulation, and experimental validation. Acne-related expression datasets were acquired from GEO, with differentially expressed genes (DEGs) identified using R. Regulatory patterns were visualized via volcano plots and heatmaps. Enrichment analyses (GO and KEGG) revealed significant biological processes and pathways. Candidate targets were screened using LASSO regression and PPI network analysis, followed by drug discovery via the Coremine Medical database. Molecular docking and dynamics simulations assessed compound-target binding stability. To evaluate the in vitro effects of diosmetin, this study employed the HaCaT keratinocyte model. Cell viability and inflammatory cytokine expression levels following drug treatment were assessed using the CCK-8 assay and ELISA, respectively. Western blot analysis was used to investigate the effects of diosmetin proteins such as NF-κB, Nrf2, and KLK7. Immunofluorescence was used to detect ROS levels and mitochondrial morphological changes. GO and KEGG enrichment analyses revealed that DEGs were significantly enriched in pathways related to mitochondrial function and ROS. PPI network analysis further identified potential hub genes. Molecular docking and dynamics simulations suggested that diosmetin, an active component of S. tenuifolia, binds strongly to KLK7. Diosmetin (Dios) restored KLK7 levels, reduced ROS accumulation, and improved mitochondrial dysfunction induced by acne. Furthermore, the study found that diosmetin significantly reduced ear swelling and alleviated inflammation, providing preliminary preclinical evidence for its treatment of acne. The pathogenesis of acne is related to inflammation and oxidative stress. The anti-acne effect of S. tenuifolia is mainly mediated by diosmetin, which can alleviate oxidative stress and reduce inflammatory responses. This study provides supportive evidence for the potential application of diosmetin in acne treatment. - Source: PubMed
Publication date: 2026/02/18
Pan YuSun RuiThomas Elizabeth RosalindPan ShiYang LinliWang WenjunChen LinLi Xiang - Netherton syndrome (NS) is a rare, severe, and often life-threatening disease for which current therapeutic approaches are limited and show variable effectiveness. NS is characterized by excessive epidermal desquamation that results in a highly defective epidermal barrier, constitutive skin inflammation, allergies, and hair abnormalities. NS develops due to loss-of-function mutations in the SPINK5 gene, which encodes the LEKTI inhibitor that regulates KLK proteases (KLK5, KLK6, KLK7, KLK13, and KLK14). These findings indicate that dysregulation of proteolytic networks underlies the extensive skin shedding and inflammation characteristic of NS. Spink5 mice recapitulate the major features of the human disease but exhibit neonatal lethality. Several double- and triple-knockout models have been generated to rescue the lethal NS phenotype, and have proved instrumental in studies aiming to elucidate the biological pathways involved in NS, and to identify and validate potential targets for drug development. These studies have established that inhibition of excessive KLK protease activity in LEKTI-deficient epidermis can reverse the cutaneous manifestations of NS. In particular, ablation of KLK5 results in a marked therapeutic response, although KLK7 or TNFα must also be inhibited to rescue the most severe (lethal) form of NS. Murine models have also been essential in proving or disproving putative pathways and/or therapeutic targets proposed from in vitro studies or patient case studies. Collectively, these models have provided a deeper understanding of the epidermal proteolytic cascades involved in NS pathology and in normal skin renewal. Moreover, these models offer a platform in which disease-specific candidate therapeutics can be tested and preclinically validated. © 2026 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland. - Source: PubMed
Publication date: 2026/01/09
Zingkou EleniBisyris EvangelosPampalakis GeorgiosSotiropoulou Georgia