Ask about this productRelated genes to: KLK13 Blocking Peptide
- Gene:
- KLK13 NIH gene
- Name:
- kallikrein related peptidase 13
- Previous symbol:
- -
- Synonyms:
- KLK-L4
- Chromosome:
- 19q13.41
- Locus Type:
- gene with protein product
- Date approved:
- 2000-03-16
- Date modifiied:
- 2016-11-15
Related products to: KLK13 Blocking Peptide
Related articles to: KLK13 Blocking Peptide
- Urine offers a noninvasive and low-cost source of disease biomarkers, yet most proteomic studies have targeted single conditions. Using deep proteomic profiling and machine learning, we evaluated whether urinary protein signatures distinguish early-stage cancer, neurologic, and metabolic diseases from healthy controls. - Source: PubMed
Publication date: 2026/07/30
Budnik BogdanAmirkhani HosseinWeinberger KlausNedjat SaharnazForouzanfar Mohammad HAfshin Ashkan - Diabetic kidney disease (DKD) is a major complication of diabetes, but circulating proteins linking glycaemic stress to kidney injury remain unclear. We aimed to identify glycaemia-linked plasma proteins associated with DKD risk and assess their treatment responsiveness. - Source: PubMed
Publication date: 2026/05/19
Liu DuankeLin XinjieXie JunqingChen LiWang Ningli - Primary acquired nasolacrimal duct obstruction (PANDO) is a common cause of epiphora in adults, yet the biochemical environment within the nasolacrimal duct (NLD) remains poorly understood. This study aimed to characterize the proteomic composition of NLD lavage fluid and identify subtype-specific molecular features distinguishing membranous and mucinous obstruction. Paired tear and NLD lavage fluid (NLD-LF) samples were collected from patients undergoing dacryoendoscopic recanalization, and proteomic profiling was performed using LC-MS/MS. A total of 1345 proteins were identified in NLD-LF and 767 in tear fluid, revealing a distinct NLD-specific proteome. Although the membranous and mucinous subtypes shared broadly similar protein compositions, differentially expressed proteins highlighted divergent biochemical pathways. The membranous subtype showed enrichment of keratinization-related processes involving , , and , suggesting epithelial remodeling and cornification. In contrast, the mucinous subtype exhibited upregulation of proteins involved in lipid metabolism, carboxylic acid biosynthesis, and sulfur compound metabolism, including , , and , indicating metabolic conditions that promote mucin-lipid interactions, glycan sulfation, and redox-dependent mucin cross-linking. These findings provide new insights into the protein composition of NLD lavage fluid and suggest molecular differences between the membranous and mucinous obstruction subtypes. - Source: PubMed
Publication date: 2026/03/12
You HeejeongBang WonseokKang ByeongsooBack SeunghoonPark JunyoungJu MinjungPark Jong-MoonLew Helen - Ovarian cancer remains a formidable therapeutic challenge due to late diagnosis, high recurrence rates, and limited treatment options. Mesothelin (MSLN) is highly expressed in ovarian cancer, making it a promising target for immunotherapy. Given this target profile, the authors developed a novel T-cell receptor (TCR)-like chimeric antigen receptor (CAR) T-cell therapy targeting MSLN, designated KT127. - Source: PubMed
Shan YiyangDing BoJi FengLin HaoShi WeiweiWang EnxiuWang ChenShen Yang - 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