KLK8 antibody
- Known as:
- KLK8 (anti-)
- Catalog number:
- orb100297
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- KLK8 antibody
Related genes to: KLK8 antibody
- Gene:
- KLK8 NIH gene
- Name:
- kallikrein related peptidase 8
- Previous symbol:
- PRSS19
- Synonyms:
- HNP, TADG14, neuropsin, ovasin
- Chromosome:
- 19q13
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-09
- Date modifiied:
- 2015-11-13
Related products to: KLK8 antibody
Related articles to: KLK8 antibody
- Blood-based biomarkers are increasingly recognized as promising tools for the diagnosis and monitoring of neurodegenerative diseases, offering a minimally invasive alternative to cerebrospinal fluid (CSF) testing. We evaluated the analytical performance and clinical utility of the Olink Target 48 Neurodegeneration panel, a novel multiplex proteomic platform based on the proximity extension assay (PEA) technology, in a large, clinically diverse dementia cohort. - Source: PubMed
Publication date: 2026/07/11
Bentivenga Giuseppe MarioMammana AngelaBaiardi SimoneVittoriosi EricaMastrangelo AndreaRuggeri EdoardoVargiu Claudia MarinaPolischi BarbaraStanzani-Maserati MichelangeloRizzo GiovanniPantieri RobertaRaggi AlbertoCapellari SabinaParchi Piero - Surgical stress reprograms monocyte/macrophage populations, rendering patients more susceptible to infections and impairing postoperative recovery. However, the underlying mechanisms remain incompletely understood. - Source: PubMed
Publication date: 2026/07/11
Hua QingYao YutingShi XintongWu ShufeiZhu XiaoyanXu Pingbo - Neuroinflammation is a central feature of Alzheimer's disease (AD), yet the mechanisms linking inflammatory protease systems to disease pathology remain incompletely understood. The kallikrein-kinin system (KKS), a major source of bradykinin, has been associated with AD mainly at the peripheral level, but its regulation within the human brain remains largely unexplored. Here, we investigated KKS activity in human AD tissue and a transgenic mouse model, with a particular focus on serine protease kallikrein-8 (KLK8). We observed that both bradykinin and bradykinin B1 receptor levels are increased in the hippocampus of AD patients, with a pronounced upregulation in females. In the TgCRND8 mouse model of AD, hippocampal bradykinin levels were also elevated, while heterozygous KLK8 knockout ameliorated this pathological effect, supporting a functional contribution of KLK8. Analysis of kallikrein expression revealed a selective increase in KLK8 in the AD hippocampus, whereas the canonical kinin-generating proteases, tissue kallikrein (KLK1) and plasma kallikrein (KLKB1), remained unchanged. In vitro cleavage assays demonstrated that recombinant human KLK8 can process both low- and high-molecular-weight kininogens, and functional assays confirmed that KLK8 increases bradykinin levels in human hippocampal tissue and plasma, an effect that was blocked by a KLK8-neutralizing antibody. Together, these findings identify KLK8 as a previously unrecognized modulator of the KKS in the AD brain. Our data support a model in which elevated KLK8 contributes to dysregulated bradykinin production and B1R signaling, providing a mechanistic link between KLK8 activity and neuroinflammation in Alzheimer's disease. - Source: PubMed
Publication date: 2026/05/14
Raza Syed AhsanPereira de Almeida PaulaFarid IdrisMacha NicoleKnoll MichaelaRoser PatrikScherbaum NorbertHerring ArneKeyvani Kathy - Early diagnosis of dementia is critical for timely treatment and management before the disease progresses to a severe stage. In this study, we aimed to evaluate plasma kallikrein-8 (KLK8) as a potential biomarker for early diagnosis at the mild cognitive impairment (MCI) stage. - Source: PubMed
Publication date: 2026/03/10
Gupta IshitaMiura MasahiroKimura AyakaTanaka SayakaTakeda ShukoNakajima TsuneoHashimoto MamoruIwata KazuhikoSegawa TatsuyaSato ToshiyukiShiosaka Sadao - Cartilage degradation, inflammation, and pyroptosis are key drivers of Osteoarthritis (OA) pathogenesis, contributing to chondrocyte impairment. However, the therapeutic potential of KLK8, a cartilage-associated protease, remains unexplored in OA. KLK8 expression was detected in meniscal/ligamentous injury (MLI)-induced OA mouse models and human OA cartilage tissues. KLK8 expression in chondrocytes stimulated with interleukin-1β (IL-1β) was also detected and quantified. Small interfering RNA (siRNA) was used to inhibit KLK8 in IL-1β-stimulated chondrocytes and its influence on the expression of cartilage catabolic factor and inflammatory factors expression were examined. The mechanism through which KLK8 regulates NF-κB activity was investigated. Chondrocyte pyroptosis were also measured. MLI-induced OA in mice were used to investigate KLK8's in vivo therapeutic potential. KLK8 expression was significantly upregulated in articular cartilage from OA patients and mice models. IL-1β stimulation increased KLK8 levels in chondrocytes in vitro. Functional assays showed that KLK8 knockdown attenuated IL-1β-induced inflammatory responses and extracellular matrix degradation in chondrocytes. KLK8 directly interacts with IκBα to promote its cytoplasmic degradation, which leads to p65 release, nuclear translocation and extended nuclear retention, thus enhancing NF-κB activity in IL-1β-stimulated chondrocytes. Furthermore, the levels of NLRP3, ASC and cleaved Caspase-1 were decreased after IL-1β stimulation in KLK8-deficient chondrocyte, indicating a stimulatory effect on NLRP3 inflammasome activation. Flow cytometry showed reduced chondrocyte pyroptosis after KLK8 knockdown, and ELISA detected decreased TNF-α, IL-6, and IL-18 levels, indicating KLK8 regulates chondrocyte pyroptosis. In vivo, KLK8 knockdown mitigated OA progression and reduced the expression of NLRP3, MMP13, COL2A1, and IL-18 in OA mice. These findings indicate that KLK8 promotes cartilage degradation, inflammation and pyroptosis via activating the NF-κB and NLRP3 inflammasome pathways. In vivo, KLK8 inhibition significantly alleviates OA progression, highlighting KLK8 as a potential therapeutic target for OA. - Source: PubMed
Publication date: 2026/02/27
Xu LibinJiang ZeyuLi Haijun