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These data identify a key mechanistic link between transient PKC activation and long-term Ca(2+) handling defects through PKC-induced actin cytoskeletal rearrangement and resultant T-tubule damage.
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PKCalpha combines a measure of recent, nearby synaptic plasticity with local synaptic input, enabling complex cellular computations such as heterosynaptic facilitation of plasticity necessary for efficient hippocampus-dependent learning
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Together, these data suggest that global deletion of PKCa results in reduced MAP due to decreased vascular contractility.
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High Prkca expression is associated with kidney fibrosis.
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Prkca-mediated phosphorylation of LSD1 is required for presynaptic plasticity and hippocampal learning and memory.
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Deleting the Prkca gene, which encodes PKCalpha, reverses diabetes-induced autophagy impairment, cellular organelle stress and apoptosis, leading to an NTD reduction. PKCalpha increases the expression of miR-129-2, which is a negative regulator of autophagy. miR-129-2 represses autophagy by directly targeting PGC-1alpha, a positive regulator for mitochondrial function, which is disturbed by maternal diabetes.
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Its pathway may promote reactive oxygen species generation in the early state Alzheimer's disease and eventually contribute to the exacerbation of pathological phenotype
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This indicates a role for PKC in dynamically controlling the trafficking of SNAT3 transporters in astrocytes in situ.
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Results show that de novo polarisation of the embryo at the 8-cell stage is directed by phospholipase C (PLC) and protein kinase C (PKC).
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LAV-BPIFB4 isoform modulates eNOS signalling through Ca2+/PKC-alpha-dependent mechanism.
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However, the mechanism that induces release of IL-6 from skeletal muscle cells remains unknown. Here we show that heat increases IL-6 in skeletal muscle cells through the transient receptor potential vannilloid 1, PKC, and cAMP response element-binding protein signal transduction pathway.
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protein kinase Calpha (PKCalpha) gain of function mutations may promote synaptic defects in Alzheimer's disease
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Erk5 MAP kinase is activated in response to PDGF-BB in the smooth muscle cell line MOVAS in a manner dependent on Mekk2, Mek1/2, Mek5, PI3-kinase and protein kinase C (PKC).
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PKC-alpha plays a crucial role in the pathophysiology of peritoneal membrane dysfunction induced by peritoneal dialysis fluids, and its therapeutic inhibition might be a valuable treatment option for peritoneal dialysis patients.
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these results identify PKCalpha and HMGB1 as important co-regulators involved in hydrogen peroxide-induced poly-ADP-ribose formation.
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the present study demonstrates that nNOS-derived NO signaling modulated by spinal Sig-1R activation increases Nox2 activity and concomitant ROS production, which leads to a ROS-induced increase in PKC-dependent pGluN1 expression in the spinal cord dorsal horn and the development of pain hypersensitivity
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We conclude that synaptotagmin-1 phosphorylation is an essential step in PKC-dependent potentiation of synaptic transmission, acting downstream of the two other essential DAG/PKC substrates, Munc13-1 and Munc18-1.
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These data indicate that LPA increases CCN2 expression through the activation of PKC and PKA. Thus, the regulatory functions of the PKC and PKA pathways are implicated in the LPA-induced increase in CCN2 expression
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Kinocilium is essential for proper localization of Lgn, as well as Gai and aPKC, suggesting that cilium function plays a role in positioning of apical proteins critical for hearing.
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Social defeat-driven PKA activation in the basolateral amygdala is actually a compensatory rather than pathogenic response in the homeostasis.