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Printable Handouts
Navigable Slide Index
- Introduction
- MAPK/SAPK cascades in mammalian cells
- Duration, strength of p-ERK determine cell fate
- The activation and inactivation of MAP kinases
- MKPs share basic structural features
- The MAP-kinase phosphatases families
- DUSP6/MKP-3: key properties
- MKP-3 catalytic activation on binding to ERK2
- MKP catalytic activity requires a general acid
- Acid loop displaced in the absence of substrate
- MKP-3 is expressed in FGF sites
- Removal of AER abrogates MKP-3 expression
- Inhibition of FGF or MEK1/2 abolishes MKP-3
- How do FGF induce DUSP6/MKP-3 expression?
- Inhibition of MAPK suppresses MKP-3 by FGFs
- Deletion analysis of the MKP-3 gene promoter
- In silico analysis of the DUSP6/MKP-3 promoter
- Mutated Ets abolishes the FGF response
- Ets1 and Ets2 bind to MKP-3 gene promoter
- Murine MKP-3 promoter directs expression of GFP
- DUSP6/MKP-3 summary
- The dual-specificity MAPK phosphatase family
- MKP-1 inactivates ERK, p38-alpha and JNK
- DUSP1/MKP-1 are inducible by UV-radiation
- MKP-1 is abolished in p38-alpha knockout mice
- MKP-1 unaffected by loss of p38-alpha or JNK
- UV induction of MKP-1 is rescued by p38-alpha
- p38-alpha is essential for induction of MKP-1
- UV induction of MKP-1 mediated by MSK 1/2
- MKP-1 promoter activity, p38, MSK 1/2 and CREB
- Deletion of MKP-1 increases ERK, p38 and JNK
- Cells lacking MKP-1 are acutely sensitive to UV
- Cell death when lacking MKP-1 isn't due to p38
- MKP-1(-) cell death rescued by MKP-1 mutant
- JNK1/2(-) cells not sensitised to UV
- Cross-talk between p38-alpha and JNK pathways
- Concluding remarks
- Acknowledgements
Topics Covered
- Signal transduction
- Mechanisms of MAP kinase inactivation
- Dual-specificity MAP kinase phosphatases
- Fibroblast growth factor signalling
Talk Citation
Keyse, S.M. (2011, March 16). The regulation of MAP kinase signalling by dual-specificity protein phosphatases [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved October 6, 2024, from https://doi.org/10.69645/UDCN2238.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Steve M. Keyse has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
A selection of talks on Biochemistry
Transcript
Please wait while the transcript is being prepared...
0:00
Hi, my name's Steve Keyse,
and I'm based at the University of Dundee in Scotland;
And the subject of my talk today,
is "The Regulation of Mitogen-activated Protein Kinase Signalling
by Dual-Specificity Protein Phosphatases.
0:15
This next slide shows an overview,
the mitogen and stress-activated protein kinase signalling cascades in mammalian cells.
These highly conserve signal transduction pathways,
serve to respond to a series of environmental cues
which range from growth factors and hormones,
through to cellular stresses such as pro-inflammatory cytokines and DNA damaging agents,
and elicit a wide variety of physiological responses in cells,
which range from increases in the rate of cell growth or cell differentiation,
changes in morphology and motility,
mediation of inflammatory responses,
cell cycle arrest, and even cell death.
These pathways are divided into three major families: the so-called
classical Ras-MAP kinase pathway which is
largely responsible for the response to growth factors and hormones,
and is thought primarily to influence cell growth, differentiation and survival.
There are two so-called stress-activated MAP kinase pathways
exemplified by the c-Jun amino-terminal kinases or JNKs,
and the p38 MAP kinases,
which respond primarily to cellular stress and pro-inflammatory cytokines,
and are thought to be responsible for exit from the cell cycle,
and responses to damage such as cell death.
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