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Human Caspase 6 Protein expressed in Escherichia coli (E. coli) - ABIN2487275
Basu, Lu, Sun, Moor, Akkaraju, Huang: Proteolytic activation of protein kinase C-epsilon by caspase-mediated processing and transduction of antiapoptotic signals. in The Journal of biological chemistry 2002
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Intact motor axons of Casp6 null mice had normal electrophysiological properties but, as tested serially during axonal degeneration (AxD), there was attenuated loss of excitability. Following transection, morphological features of AxD were evident in both wild type and Casp6-/- mice but the latter had evidence of slowed progression.
Caspase-6 is posttranslationally palmitoylated by the palmitoyl acyltransferase HIP14 and that the palmitoylation of Caspase-6 inhibits its activation.
Caspases and their substrates are key mediators of apoptosis.
The bactericidal activity of caspase-6-/- macrophages was impaired compared to wild type cells. Caspase-6-/- mice showed higher expression of the IL-1b gene, known to be detrimental in murine melioidosis. Expression of the IL-10 gene was also increased in caspase-6-/- mice as early as 6 hours after infection. Treatment with exogenous IL-10 rendered mice more susceptible against B. pseudomallei challenge
caspase-6 could regulate breast cancer cell invasion by modulating MMP-2 and MMP-9 expression in 4T1 tumor-associated macrophages
Casp6 is unlikely to be involved in colitis-associated tumors.
p53 activity is an important upstream regulator of caspase-6 activity in muscle tissue.
TNFalpha-induced RIP1-independent caspase-6 activation was involved in regulating the relationship between autophagy and necroptosis.
CASP6 released from axonal terminals regulates microglial TNF-alpha secretion, synaptic plasticity, and inflammatory pain.
both Caspase-3 and Caspase-6 are implicated in axon degeneration that occurs as a part of normal development.
Casp6-/- neurons are protected against excitotoxicity, nerve growth factor deprivation and myelin-induced axonal degeneration. Furthermore, Casp6-deficient mice show an age-dependent increase in cortical and striatal volume.
This study demonistrated that elimination of caspase-6 protein and activity in the BACHD mouse model does not prevent the production of a 586 aa Htt proteolytic fragment in the brain.
Neutrophil/macrophage contact activates CASP-6, producing interleukin-1 receptor-associated kinase-M (IRAK-M) cleavage and de-repression of alveolar macrophages; CASP-6 deletion protects mice from death caused by bacterial peritonitis.
Lamin A/C and caspase-6 could be valuable tools in the knowledge of oocyte in vitro destiny
p53 activation enhances XIAP inhibition-induced cell death by promoting mitochondrial release of second mitochondria-derived activator of caspases (SMAC) and by inducing the expression of caspase-6.
CREB-binding proteins are specifically targeted by caspases and calpains at the onset of neuronal apoptosis
caspase-6 and caspase-7 are activated by teratogens in early postimplantation mouse embryos
analysis of the roles of caspase-3, -6, and -7 during lens development
Mild oxidative stress represses NHE1 promoter activity and expression via an early oxidation phase blocked by reducing agents, and a late phase requiring an iron-dependent increase in caspases 3 and 6 activities.
Taken together, these results suggest that activation of caspases (6 and 7) and the subsequent cleavage of lamin A/C and PARP are involved in the morphological changes of apoptotic macrophages infected with Actinobacillus actinomycetemcomitans.
The prodomain region was found to be intrinsically disordered independent of the activation state of caspase-6; however, its complete removal resulted in the protection of the adjacent 26-32 region, suggesting that this region may play a regulatory role. The molecular details of caspase-6 dynamics in solution provide a comprehensive scaffold for strategic design of therapeutic approaches for neurodegenerative disorders.
SMSr is a novel and specific substrate of caspase-6, a non-conventional effector caspase implicated in Huntington's and Alzheimer's diseases.
Results support the possibility that the Casp6 activity in the anterior olfactory nucleus of the olfactory bulb reflects degeneration in the entorhinal cortex and suggest that Casp6 activity in the olfactory bulb could represent degeneration associated with cognitive decline and early Alzheimer disease.
These data suggest that caspase-6 deactivating mutations may contribute to multifactorial carcinogenic transformations.
Caspase-6 undergoes helix-strand transition upon substrate binding. Caspase-6 shows distinctive conformational dynamics in its 130's region Local pKa Values of Key Amino Acid Residues within the 130's Region Vary between the Unliganded (Helical) and the VEID-bound (Strand) States of Caspase-6 .
Following specific binding to and internalization into HER2-overexpressing tumor cells, the e23sFv-Fdt-casp6 protein induced tumor cell apoptosis and inhibited the proliferation of HER2-overexpressing A172 and U251MG cells in vitro, but not in U87MG cells with undetectable HER2
Results identified novel members of the CASP6 interactome and demonstrate that a number of them are involved in key signaling pathways observed in neurodegenerative diseases.
The ability of sox11 to reduce effector caspase activity was also reflected in its capacity to reduce cell death following toxic insult. Interestingly, other sox proteins also had the ability to reduce caspase-6 activity but to a lesser extent than sox11
Caspase-6 plays a role in activating caspase-3 in Tau truncation.
unmodified STAT1 is cleaved at multiple sites by caspase-3 and caspase-6 in malignant undifferentiated hematopoietic cells
p53 activity is an important upstream regulator of caspase-6 activity in Huntington's disease.
In this study, the crystal structure of a full-length CASP6 zymogen mutant, proCASP6H121A, was solved.
Caspase-6 is likely important in most tissues during early development but is less involved in adult tissues
axon regeneration promoted by suppression of CASP2 and CASP6 is CNTF-dependent and mediated through the JAK/STAT signalling pathway
Significant associations have been found between CpG sites and patient sex, including DNA methylation in CASP6, a gene that may respond to estradiol treatment, and in HSD17B12, which encodes a sex steroid hormone.
Caspase 6 activity in entorhinal cortex identifies aged individuals at risk for developing Alzheimer's disease.
Results demonstrate that in the absence of caspase 6 activity, intrinsic triggers of apoptosis induce the receptor-interacting-kinase-1-dependent production of pro-inflammatory cytokines.
binding of zinc at the exosite is the primary route of inhibition, potentially locking caspase-6 into the inactive helical conformation.
peptide binds at a tetramerization interface that is uniquely present in zymogen caspase-6, rather than binding into the active site, and acts via a new allosteric mechanism that promotes caspase tetramerization
Results showed the inhibition mechanism of CASP6 phosphorylation and laid the foundation for a new strategy of rational CASP6 drug design.
This gene encodes a protein which is a member of the cysteine-aspartic acid protease (caspase) family. Sequential activation of caspases plays a central role in the execution-phase of cell apoptosis. Caspases exist as inactive proenzymes which undergo proteolytic processing at conserved aspartic residues to produce two subunits, large and small, that dimerize to form the active enzyme. This protein is processed by caspases 7, 8 and 10, and is thought to function as a downstream enzyme in the caspase activation cascade. Alternative splicing of this gene results in two transcript variants that encode different isoforms.
, caspase 6, apoptosis-related cysteine protease
, caspase 6
, apoptotic protease Mch-2
, apoptotic protease MCH-2