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UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining

◀ Back to CASP7

CASP7 — PRKCD

Pathways - manually collected, often from reviews:

Text-mined interactions from Literome

Basu et al., Biochemistry 1999 : Rottlerin, an inhibitor of nPKCdelta , blocked caspase-3 activation and proteolytic cleavage of nPKCdelta by cDDP
Reyland et al., J Biol Chem 1999 : Here we report that apoptosis results in the caspase dependent cleavage of protein kinase C-delta (PKCdelta) to a 40-kDa fragment, the appearance of which correlates with a 9-fold increase in PKCdelta activity
Koriyama et al., Cell Signal 1999 : Proteolytic activation of protein kinase C delta and epsilon by caspase-3 in U937 cells during chemotherapeutic agent induced apoptosis
Webb et al., Apoptosis 2000 (Inflammation) : Spontaneous neutrophil apoptosis does not require Fas ligation, but is mediated by caspases 3, 8 and possibly caspase 9 and also involves activation of protein kinase C-delta
Denning et al., Cell Death Differ 2002 : The induction of apoptosis in human keratinocytes by UV radiation involves caspase mediated cleavage and activation of protein kinase C delta (PKCdelta)
Mohamed et al., Biochem J 2002 (MAP Kinase Signaling System) : Inhibition in HeLa cells of caspase function by pharmacological inhibitors or the expression of CrmA ( cytokine response modifier A ), a viral modifier protein, blocks TNF induced apoptosis or caspase dependent protein kinase Cdelta and poly ( ADP-ribose ) polymerase protein degradation
Kitazawa et al., Neuroscience 2003 (Parkinsonian Disorders) : Dieldrin induces apoptosis by promoting caspase-3 dependent proteolytic cleavage of protein kinase Cdelta in dopaminergic cells : relevance to oxidative stress and dopaminergic degeneration
Kaul et al., Eur J Neurosci 2003 (Nerve Degeneration) : In the present study, we demonstrate that caspase-3 mediated proteolytic activation of protein kinase C delta (PKC delta) is critical in MPP+ induced oxidative stress and apoptosis
Yang et al., Mol Cell Neurosci 2004 (Nerve Degeneration) : Suppression of caspase-3 dependent proteolytic activation of protein kinase C delta by small interfering RNA prevents MPP+ induced dopaminergic degeneration ... Using RNA interference ( RNAi ), we demonstrate that caspase-3 dependent proteolytic activation of protein kinase Cdelta (PKCdelta) contributes to the degenerative process in dopaminergic neurons
Kitazawa et al., Neurotoxicology 2004 : We also demonstrated that protein kinase Cdelta (PKCdelta) , a member of a novel PKC family of proteins, is proteolytically activated by caspase-3 to mediate apoptotic cell death processes
Voss et al., J Biol Chem 2005 (Inflammation) : Regulation of monocyte apoptosis by the protein kinase Cdelta dependent phosphorylation of caspase-3
Hanrott et al., Eur J Neurosci 2008 : In an in vitro cellular model, we reported that 6-hydroxydopamine ( 6-OHDA ) induces apoptotic cell death via the induction of mitochondrial dysfunction, the activation of caspase 3 and the consequent proteolytic activation of the redox-sensitive kinase, protein kinase C (PKC)delta , in PC12 cells
Kanthasamy et al., Molecular brain 2008 (Nerve Degeneration...) : Environmental neurotoxin dieldrin induces apoptosis via caspase-3 dependent proteolytic activation of protein kinase C delta (PKCdelta) : Implications for neurodegeneration in Parkinson 's disease ... Furthermore, dieldrin caused the caspase dependent proteolytic cleavage of protein kinase C delta ( PKCd ) into 41 kDa catalytic and 38 kDa regulatory subunits in N27 cells as well as in brain slices
Cunningham et al., Endocrinology 2009 : Androgens induce dopaminergic neurotoxicity via caspase-3 dependent activation of protein kinase Cdelta
Zhang et al., Toxicol Appl Pharmacol 2011 : We previously demonstrated that caspase-3 dependent proteolytic activation of protein kinase C delta ( PKCd ) plays a key role in Mn-induced apoptotic cell death in dopaminergic neurons
Arango et al., Biochem Pharmacol 2012 : Apigenin induced DNA damage was mediated by p38 and protein kinase C-delta ( PKCd ), yet was independent of reactive oxygen species or caspase activity