- •Protein phosphorylation as a switch in cellular functioning
- •Cyclic AMP and the amplification of signals
- •Protein kinase A
- •Protein kinase A and the regulation of transcription
- •Activation of the CREB transcription factor
- •Attenuation of the cAMP response elements by dephosphorylation
- •Protein kinase A and the activation of ERK
- •Actions of cAMP not mediated by PKA
- •Regulation of ion channels by cyclic nucleotides
- •Epac, a guanine nucleotide exchange factor directly activated by cAMP
- •Protein kinase C
- •Discovery of a phosphorylating activity independent cAMP
- •The protein kinase C family
- •Structural domains and activation of protein kinase C
- •The C1–C4 regions
- •Activation of protein kinase C
- •Multiple sources of diacylglycerol and other lipids activate protein kinase C
- •Differential localization of PKC isoforms
- •Different types of PKC-binding proteins
- •Holding back the PKC response
- •A matter of life or death: PKC signalling complexes in the evasion of the fly-swat
- •Phorbol ester and inflammation
- •References
Signal Transduction
FIG 9.14 Induction of an inflammatory response by phorbol ester; effects of PMA.
The processes indicated result in tumor, calor, rubor, and dolor, four well-recognized characteristics of the inflammatory response.
AP-1 complex.93,94 PMA also causes degranulation of neutrophils, releasing proinflammatory cytokines and matrix proteases. It also activates the respiratory burst,95 vital for first line host defence and also implicated in the tissue destruction associated with chronic inflammatory disease.
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