3.4.21.B10: neurosin
This is an abbreviated version!
For detailed information about neurosin, go to the full flat file.
Word Map on EC 3.4.21.B10
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3.4.21.B10
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kallikreins
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trypsin-like
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medicine
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klk8
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par1
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diagnostics
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immunofluorometric
- 3.4.21.B10
- kallikreins
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trypsin-like
- medicine
- klk8
- par1
- diagnostics
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immunofluorometric
Reaction
proteolytic cleavage of polypeptides =
Synonyms
GK, hK6, KAL-B, kallikrein 6, kallikrein-6, kallikrein-related peptidase, kallikrein-related peptidase 6, KLK6, KRP/hK6, myelencephalonspecific protease, neurosin, protease M, S01.236, serine protease 18, serine protease 9, SP59, tissue kallikrein 6, zyme
ECTree
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General Information
General Information on EC 3.4.21.B10 - neurosin
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evolution
the enzyme is a member of the human kallikrein gene family of secreted serine proteases
malfunction
metabolism
physiological function
additional information
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ERK1/2 signaling in cerebellar granule neurons and in the NSC34 spinal cord motoneuron cell line is reduced by lipopeptide inhibitors of PAR1 or PAR2, and PAR1 genetic deletion, which reduces the neurotoxic effects of the enzyme
malfunction
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KLK6 knockout mice have thinner epidermis and decreased keratinocyte proliferation. The keratinocytes in wild type and KLK6 knockout epidermis are equally sensitive to acute anti-proliferative effect of fluocinolone acetonide. The development of proliferative resistance during chronic treatment is reduced in knockout epidermis
malfunction
KLK6-deficient primary cortical neurons have increased ability for alpha-synuclein fibril uptake
malfunction
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ERK1/2 signaling in cerebellar granule neurons and in the NSC34 spinal cord motoneuron cell line is reduced by lipopeptide inhibitors of PAR1 or PAR2, and PAR1 genetic deletion, which reduces the neurotoxic effects of the enzyme
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kallikrein 6 and thrombin are important regulators of neural pathophysiology and neurotoxic
metabolism
KLK6 can be a major player in the turnover of alpha-synuclein species
metabolism
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mechanism of epidermal regeneration after glucocorticoid-induced atrophy via KLK6 activation
metabolism
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kallikrein 6 and thrombin are important regulators of neural pathophysiology and neurotoxic
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KLK6 is an epigenetically regulated tumor suppressor in human breast cancer. KLK6 re-expression in nonexpressing MDA-MB-231 breast tumor cells results in significant down-regulation of vimentin which represents an established marker of epithelial transition to mesenchymal transition of tumor cells and in concomitant upregulation of calreticulin and epithelial markers cytokeratin 8 and 19. Stable expression of KLK6 reduces proliferation rates, motility, and anchorage-independent growth of MDA-MB-231 cells
physiological function
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KLK6 promotes lymphocyte survival by a mechanism that depends in part on activation of protease-activated receptor 1. Recombinant KLK6 significantly reduces cell death under resting conditions and in response to camptothecin, dexamethasone, staurosporine and Fas-ligand. Immune cell survival promoting effects of KLK6 include both T and B lymphocytes and involve up regulation of the pro-survival protein B-cell lymphoma-extra large and inhibition of the pro-apoptotic protein Bcl-2-interacting mediator of cell death
physiological function
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KLK6 promotes lymphocyte survival by a mechanism that depends in part on activation of protease-activated receptor 1. Recombinant KLK6 significantly reduces cell death under resting conditions and in response to camptothecin, dexamethasone, staurosporine and Fas-ligand. Immune cell survival promoting effects of KLK6 include both T and B lymphocytes and involve up regulation of the pro-survival protein B-cell lymphoma-extra large and inhibition of the pro-apoptotic protein Bcl-2-interacting mediator of cell death
physiological function
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recombinant Klk6 protein significantly induces melanoma cell migration and invasion accompanied by an accelerated intracellular Ca2+ flux. KLK6-induced intracellular Ca2+ flux and tumor cell invasion critically depends on the protease-activated receptor 1
physiological function
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involvement of Klk6 in chronic progressive demyelinating disease, regulatory activities for kallikrein 6 in the development and progression of central nervous system inflammation and demyelination, overview
physiological function
involvement of Klk6 in chronic progressive demyelinating disease, regulatory activities for kallikrein 6 in the development and progression of central nervous system inflammation and demyelination, overview
physiological function
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kallikrein 6 is a serine protease implicated in neurodegeneration. Kallikrein 6 elicits ERK1/2 signaling in neurons by activation of protease activated receptors PAR1 and PAR2. Recombinant Klk6 triggered ERK1/2 signaling in cerebellar granule neurons and in the NSC34 spinal cord motoneuron cell line, in a PI3K and MEK-dependent fashion. Kallikrein 6 and thrombin promote degeneration of cerebellar neurons and exacerbate glutamate neurotoxicity
physiological function
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the enzyme activates G-protein coupled protease activated receptors. The enzyme serves as a molecular trigger of selected physiological processes involved in the development of astrogliosis and causes astrocytes to transform from an epitheliod to a stellate morphology and to secrete interleukin 6. It reduces expression of glial fibrillary acidic protein. Injury-induced elevations in enzyme level contribute to the development of astrogliosis in a protease activated receptor-dependent fashion. The enzyme stellation promoting activity is dependent on activation of the thrombin receptor, PAR1, the enzyme effects are blocked by the PAR1 specific inhibitor SCH79797. The kallikrein 6-induced astrocyte stellation is mediated by protein kinase C. Kallikrein 6 activates PAR1 in neurons and PAR1 and PAR2 in astrocytes to elicit intracellular Ca2+ flux and regulation of the mitogen activated protein kinase (MAPK) signaling pathway
physiological function
The enzyme plays a crucial role in ovarian cancer. Regulation of KLK6 activity is mediated mainly through (auto-)proteolytic activation or inactivation with most effi cient inhibition is achieved by endogenous antithrombin III
physiological function
kallikrein-related peptidase 6 regulates epithelial-to-mesenchymal transition
physiological function
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the enzyme can influence astrocyte plasticity through receptor-dependent mechanisms. Recombinant Klk6 evokes increases in intracellular Ca2+ in primary astrocyte monolayer cultures through activation of proteinase activated receptor 1 (PAR1). Klk6 promotes a condensation of astrocyte cortical actin leading to an elongated stellate shape and multicellular aggregation in a manner that is dependent on the presence of either PAR1 or PAR2. Klk6-evoked changes in astrocyte shape are accompanied by translocation of beta-catenin from the plasma membrane to the cytoplasm
physiological function
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kallikrein 6 is a serine protease implicated in neurodegeneration. Kallikrein 6 elicits ERK1/2 signaling in neurons by activation of protease activated receptors PAR1 and PAR2. Recombinant Klk6 triggered ERK1/2 signaling in cerebellar granule neurons and in the NSC34 spinal cord motoneuron cell line, in a PI3K and MEK-dependent fashion. Kallikrein 6 and thrombin promote degeneration of cerebellar neurons and exacerbate glutamate neurotoxicity
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physiological function
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involvement of Klk6 in chronic progressive demyelinating disease, regulatory activities for kallikrein 6 in the development and progression of central nervous system inflammation and demyelination, overview
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Klk6 and the prototypical activator of protease activated receptor 1, PAR1, thrombin, as well as PAR1 and PAR2, are each elevated in murine experimental traumatic spinal cord injury at acute or subacute time points
additional information
significant correlation between KLK6 and KLK10 expression both at the invasive front and within the main tumor, indicating a collaborative effect
additional information
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significant correlation between KLK6 and KLK10 expression both at the invasive front and within the main tumor, indicating a collaborative effect
additional information
brain-targeted neurosin accumulates throughout the CNS in neurons, astrocytes and microglia, and results in reduced accumulation of alpha-synuclein in oligodendrocytes and astrocytes with possible clearance via microglia. It also ameliorates myelin degeneration, neuropathology and behavioral deficits. The modified, brain-targeted neurosin may warrant further investigation as potential therapy for multiple system atrophy
additional information
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brain-targeted neurosin accumulates throughout the CNS in neurons, astrocytes and microglia, and results in reduced accumulation of alpha-synuclein in oligodendrocytes and astrocytes with possible clearance via microglia. It also ameliorates myelin degeneration, neuropathology and behavioral deficits. The modified, brain-targeted neurosin may warrant further investigation as potential therapy for multiple system atrophy
additional information
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Klk6 and the prototypical activator of protease activated receptor 1, PAR1, thrombin, as well as PAR1 and PAR2, are each elevated in murine experimental traumatic spinal cord injury at acute or subacute time points
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