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anti-Human Kallikrein 6 Antibodies:
anti-Rat (Rattus) Kallikrein 6 Antibodies:
anti-Mouse (Murine) Kallikrein 6 Antibodies:
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Human Polyclonal Kallikrein 6 Primary Antibody for ELISA - ABIN545336
Pampalakis, Kurlender, Diamandis, Sotiropoulou: Cloning and characterization of novel isoforms of the human kallikrein 6 gene. in Biochemical and biophysical research communications 2004
Show all 3 Pubmed References
Human Polyclonal Kallikrein 6 Primary Antibody for ELISA - ABIN545337
Bayés, Tsetsenis, Ventura, Vendrell, Aviles, Sotiropoulou: Human kallikrein 6 activity is regulated via an autoproteolytic mechanism of activation/inactivation. in Biological chemistry 2004
Show all 3 Pubmed References
Human Monoclonal Kallikrein 6 Primary Antibody for ELISA, WB - ABIN519338
Lou, Si, Chen, Sun, Zhang, Niu, Hu: Correlation between KLK6 expression and the clinicopathological features of glioma. in Contemporary oncology (Pozna?, Poland) 2014
Mouse (Murine) Polyclonal Kallikrein 6 Primary Antibody for ELISA, WB - ABIN4328114
Iwata, Maruyama, Akagi, Hashikawa, Kanazawa, Tsuji, Nukina: Alpha-synuclein degradation by serine protease neurosin: implication for pathogenesis of synucleinopathies. in Human molecular genetics 2003
KLK6 expression is significantly downregulated in healthy palatal mucosa of smokers
KLK6 is an important molecular link in the development of skin inflammation.
High KLK6 expression is associated with metastasis of colon cancer.
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.
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
KLK6 may be the key protease involved in the proteolytic modification of PFK-M.
Our data demonstrate for the first time increased levels of KLK6 in mucosal melanomas of the head and neck
Induction of autophagic processes through KLK6 expression may increase acquisition of resistance of gastric cancer cells to auranofin-induced autophagy.
Our data provide experimental evidence that KLK6 controls metastasis formation in colon cancer via specific downstream network of miRNA-mRNA effectors.
Data show that kallikrein 6 (KLK6) expression is induced in mouse and human skin during chronic glucocorticoid treatment.
FST and KLK6 may have significance in breast cancer detection
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.
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
Our fine-mapping study has identified novel loci in the KLK6 region strongly associated with aggressive PCa.
mRNA expression levels of KLK6 and KLK8 in advanced serous ovarian cancer
Data demonstrate that elevated levels of KLK6, KLK7 and KLK9 proteins are associated with poor glioblastoma patients survival.
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.
KLK6 expression was detected in head and neck tumor cell lines (FaDu, Cal27 and SCC25), but not in HeLa cervix carcinoma cells.
KLK6 and KLK7 mRNA and protein overexpression is directly associated with early-stage ovarian tumors.
The results of this study indicated that reductions in kallikrein-6 and calpain-1 may contribute to the accumulation of alpha-synuclein in DLB.
The data are exciting because they demonstrate that Klk6 can influence astrocyte plasticity through receptor-dependent mechanisms.
expression strongly induced in psoriasiform epidermis; crucial for development of imiquimod-induced psoriasiform dermatitis
Kallikrein 6 secreted by oligodendrocytes plays a critical role in the pathogenesis of experimental autoimmune encephalomyelitis.
Klk6 represents an important target for conditions in which pro-inflammatory responses play a critical role in disease development, including MS
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.
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
These results indicate that KLK6 plays a functional role in oligodendrocyte development and the expression of myelin proteins.
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
We have found an increase in the level of neurosin, a key negative regulator of SNCA in the Ts65Dn mouse model for Down syndrome
KLK6 is positioned to serve as a molecular trigger of select physiological processes involved in the development of astrogliosis
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.
neurosin plays a significant role in physiological alpha-synuclein degradation and also in the pathogenesis of synucleinopathies
study demonstrates changes in the expression of neuropsin and protease M/neurosin in oligodendrocytes following hemisection of the spinal cord
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. The encoded enzyme is regulated by steroid hormones. In tissue culture, the enzyme has been found to generate amyloidogenic fragments from the amyloid precursor protein, suggesting a potential for involvement in Alzheimer's disease. Multiple alternatively spliced transcript variants that encode different isoforms have been identified for this gene.
, protease M
, serine protease 18
, serine protease 9
, kallikrein 6 (neurosin)
, kallikrein 6 (neurosin, zyme)
, protease serine 9 (neurosin)
, protease, serine, 9
, brain serine protease
, kallikrein 29
, kallikrein 6
, myelencephalon-specific protease
, myofibril-bound protease
, protease, serine, 18