1996
DOI: 10.1074/jbc.271.35.20973
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Ubiquitination of Protein Kinase C-α and Degradation by the Proteasome

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Cited by 146 publications
(96 citation statements)
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References 29 publications
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“…The end result may be a transient down-regulation of the PKC. The existence of a proteasome complex, as shown in recent in vitro studies to enhance degradation of PKC (Lee et al, 1996), may well be involved. One general comment regarding the neurotoxic action of TeTx: to date, neither transglutaminase stimulation nor PKC translocation has been reported for most clostridial neurotoxins.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…The end result may be a transient down-regulation of the PKC. The existence of a proteasome complex, as shown in recent in vitro studies to enhance degradation of PKC (Lee et al, 1996), may well be involved. One general comment regarding the neurotoxic action of TeTx: to date, neither transglutaminase stimulation nor PKC translocation has been reported for most clostridial neurotoxins.…”
Section: Discussionmentioning
confidence: 99%
“…In the case of TeTx, no evidence exists for a cotranslocation of calpain; although from the present data, partial down-regulation is noteworthy. The proteasome complex has also been described as responsible for PKC degradation (Lee et al, 1996).…”
Section: Discussionmentioning
confidence: 99%
“…PKCs via the ubiquitin/proteasome system [76,77] and studies have shown that dephosphorylation of PKCs at the A-loop, TM and HM sites occurs prior to downregulation [78]. Dephosphorylation of PKCs in cells was initially shown to be sensitive to okadaic acid, which implicated the PP2a-like phosphatases in this process [79,80,75].…”
Section: Dephosphorylation Of Pkcmentioning
confidence: 99%
“…Previous studies and our own studies ( Figure 1) indicated that HC11 cells express at least four isoforms of PKC, a, d, e, and z, amongst which PKCz is the only one that is not responsive to activation by TPA. It is known that the treatment of cells with TPA initially leads to activation and translocation of responsive PKC isoforms, and that this is often followed by subsequent proteolytic downregulation of these proteins due to ubiquitin-mediated degradation and to the sensitivity of the conformation of activated PKCs to cellular proteases (Kishimoto et al, 1989;Lu et al, 1998;Lee et al, 1996;Savart et al, 1992). After treating HC11 cells with 100 ng/ml TPA, Western blot analysis of solubilized total cell lysates showed no alterations in the protein levels of PKCz, but there was a marked loss of PKCd and PKCe within 1 h after the addition of TPA (Figure 1).…”
Section: E Ects Of Tpa On Growth and Expression Of Endogenous Isoformmentioning
confidence: 99%