Browse our anti-Kallikrein 6 (KLK6) Antibodies

Human Kallikrein 6 (KLK6) interaction partners

1. High KLK6 expression is associated with metastasis of colon cancer.

2. Results showed a significant downregulation of KLK6 mRNA expression in breast cancer (BC) tissue sections compared to the non-cancerous component. The expression of KLK6 is positively associated with tumor grade and is overexpressed in aggressive phenotypes such as TNBC.

3. KLK6-PAR2 expression is down-regulated and PAR1 is up-regulated when DeltaNp63beta expression is decreased, leading to EMT with enhancing migration and invasion through ERK signal reduction at the invasive front

4. KLK6 may be the key protease involved in the proteolytic modification of PFK-M.

5. Our data demonstrate for the first time increased levels of KLK6 in mucosal melanomas of the head and neck

6. Induction of autophagic processes through KLK6 expression may increase acquisition of resistance of gastric cancer cells to auranofin-induced autophagy.

7. Our data provide experimental evidence that KLK6 controls metastasis formation in colon cancer via specific downstream network of miRNA-mRNA effectors.

8. Data show that kallikrein 6 (KLK6) expression is induced in mouse and human skin during chronic glucocorticoid treatment.

9. FST and KLK6 may have significance in breast cancer detection

10. KLK6 overexpression and likely its proteolytic activity is associated with alterations in downstream miRNAs and their targets, and these differ with the molecular subtypes of breast cancer.

11. Molecular models of peptides were built into the KLK6 structure and the marked preference of the cut between the two R of the examined peptides was related to the extended conformation of the substrates

12. Our fine-mapping study has identified novel loci in the KLK6 region strongly associated with aggressive PCa.

13. mRNA expression levels of KLK6 and KLK8 in advanced serous ovarian cancer

14. Data demonstrate that elevated levels of KLK6, KLK7 and KLK9 proteins are associated with poor glioblastoma patients survival.

15. Data indicate that elevated expression of microRNA-375 in head and neck squamous cell carcinoma (HNSCC) cells significantly reduces kallikrein 6 (KLK6), kallikrein 10 (KLK10), and matrix metalloproteinase 9 (MMP9) messenger RNA expression.

16. KLK6 expression was detected in head and neck tumor cell lines (FaDu, Cal27 and SCC25), but not in HeLa cervix carcinoma cells.

17. KLK6 and KLK7 mRNA and protein overexpression is directly associated with early-stage ovarian tumors.

18. The results of this study indicated that reductions in kallikrein-6 and calpain-1 may contribute to the accumulation of alpha-synuclein in DLB.

19. KLK6 and KLK10 may be useful markers and potential therapeutic targets in gastroesophageal junction tumors

20. This study assessed the prognostic utility of human tissue kallikrein-like peptidases 6 and 10 (KLK6 and KLK10) and correlated their expression with histopathological and clinical parameters in gastric cancer.

Mouse (Murine) Kallikrein 6 (KLK6) interaction partners

1. The data are exciting because they demonstrate that Klk6 can influence astrocyte plasticity through receptor-dependent mechanisms.

2. expression strongly induced in psoriasiform epidermis; crucial for development of imiquimod-induced psoriasiform dermatitis

3. Kallikrein 6 secreted by oligodendrocytes plays a critical role in the pathogenesis of experimental autoimmune encephalomyelitis.

4. Data show that kallikrein 6 (KLK6) expression is induced in mouse and human skin during chronic glucocorticoid treatment.

5. Klk6 represents an important target for conditions in which pro-inflammatory responses play a critical role in disease development, including MS

6. KLK6 protein from 129 mice showed reduced SDS-PAGE mobility compared with that from C57BL/6 mice; recombinant KLK6 protein from 129 mice had a higher optimum pH and >15 times higher hydrolytic enzymatic activity for several substrates than that from C57BL/6 mice. These results suggest that KLKs may contribute to the genetic basis of the differences between mouse strains.

7. these data point to a novel kallikrein 6 -signaling axis in neurons that is mediated by PAR1 and PAR2 and is positioned to contribute to neurodegeneration

8. These results indicate that KLK6 plays a functional role in oligodendrocyte development and the expression of myelin proteins.

9. Neuropathological analysis following delivery of LV-Neurosin to alpha-syn tg mice resulted in reduced accumulation of alpha-syn and reversal of neurodegenerative alterations in wild type but not A53T alpha-syn tg mice

10. We have found an increase in the level of neurosin, a key negative regulator of SNCA in the Ts65Dn mouse model for Down syndrome

11. KLK6 is positioned to serve as a molecular trigger of select physiological processes involved in the development of astrogliosis

12. Klk8 is involved in the proliferation and migration of keratinocytes through Klk6 in the early stages of wound healing, and possibly in keratinocyte differentiation associated with the upregulation of PAR2 in the late stages of wound healing.

13. neurosin plays a significant role in physiological alpha-synuclein degradation and also in the pathogenesis of synucleinopathies

14. study demonstrates changes in the expression of neuropsin and protease M/neurosin in oligodendrocytes following hemisection of the spinal cord