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C. elegans SUR-6/PR...
C. elegans SUR-6/PR55 cooperates with LET-92/protein phosphatase 2A and promotes Raf activity independently of inhibitory Akt phosphorylation sites
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- Kao, Gautam (författare)
- Department of Genetics, University of Pennsylvania, Philadelphia, USA
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- Tuck, Simon (författare)
- Umeå universitet,Umeå centrum för molekylär patogenes (UCMP) (Medicinska fakulteten)
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- Baillie, David (författare)
- Department of Biological Sciences, Simon Fraser University, Canada
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- Sundaram, Meera V. (författare)
- Department of Genetics, University of Pennsylvania, Philadelphia, USA
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(creator_code:org_t)
- Cambridge : Company of Biologists Limited, 2004
- 2004
- Engelska.
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Ingår i: Development. - Cambridge : Company of Biologists Limited. - 0950-1991 .- 1477-9129. ; 131:4, s. 755-765
- Relaterad länk:
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http://www.ncbi.nlm....
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http://dev.biologist...
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https://urn.kb.se/re...
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https://doi.org/10.1...
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Abstract
Ämnesord
Stäng
- Protein phosphatase 2A (PP2A) can both positively and negatively influence the Ras/Raf/MEK/ERK signaling pathway, but its relevant substrates are largely unknown. In C. elegans, the PR55/B regulatory subunit of PP2A, which is encoded by sur-6, positively regulates Ras-mediated vulval induction and acts at a step between Ras and Raf. We show that the catalytic subunit (C) of PP2A, which is encoded by let-92, also positively regulates vulval induction. Therefore SUR-6/PR55 and LET-92/PP2A-C probably act together to dephosphorylate a Ras pathway substrate. PP2A has been proposed to activate the Raf kinase by removing inhibitory phosphates from Ser259 from Raf-1 or from equivalent Akt phosphorylation sites in other Raf family members. However, we find that mutant forms ofC. elegans LIN-45 RAF that lack these sites still require sur-6. Therefore, SUR-6 must influence Raf activity via a different mechanism. SUR-6 and KSR (kinase suppressor of Ras) function at a similar step in Raf activation but our genetic analysis suggests that KSR activity is intact in sur-6 mutants. We identify the kinase PAR-1 as a negative regulator of vulval induction and show that it acts in opposition to SUR-6 and KSR-1. In addition to their roles in Ras signaling, SUR-6/PR55 and LET-92/PP2A-C cooperate to control mitotic progression during early embryogenesis.
Nyckelord
- Animals
- Animals; Genetically Modified
- Caenorhabditis elegans/embryology/*enzymology/genetics
- Caenorhabditis elegans Proteins/metabolism
- Drosophila Proteins
- Female
- Mutation
- Phosphoprotein Phosphatase/genetics/*metabolism
- Phosphorylation
- Protein-Serine-Threonine Kinases/metabolism
- Protein-Tyrosine-Phosphatase/metabolism
- Proto-Oncogene Proteins/*metabolism
- Proto-Oncogene Proteins c-akt
- Proto-Oncogene Proteins c-raf/*metabolism
- Vulva/embryology
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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