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TGF-β promotes PI3K...
TGF-β promotes PI3K-AKT signaling and prostate cancer cell migration through the TRAF6-mediated ubiquitylation of p85α
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- Hamidi, Anahita (författare)
- Uppsala universitet,Science for Life Laboratory, SciLifeLab,Ludwiginstitutet för cancerforskning
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- Song, Jie, 1984- (författare)
- Umeå universitet,Patologi,Marene Landstrom,Umea Univ, Dept Med Biosci, Unit Pathol, SE-90185 Umea, Sweden
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- Thakur, Noopur (författare)
- Uppsala universitet,Science for Life Laboratory, SciLifeLab,Ludwiginstitutet för cancerforskning
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- Itoh, Susumu (författare)
- Showa Pharmaceut Univ, Biochem Lab, Tokyo 1948543, Japan
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- Marcusson, Anders (författare)
- Uppsala universitet,Ludwiginstitutet för cancerforskning,Science for Life Laboratory, SciLifeLab
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- Bergh, Anders (författare)
- Umeå universitet,Patologi,Anders Bergh,Umea Univ, Dept Med Biosci, Unit Pathol, SE-90185 Umea, Sweden
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- Heldin, Carl-Henrik, 1952- (författare)
- Uppsala universitet,Science for Life Laboratory, SciLifeLab,Ludwiginstitutet för cancerforskning
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- Landström, Maréne (författare)
- Uppsala universitet,Umeå universitet,Patologi,Ludwig Institute for Cancer Research, Science for Life Laboratory, Uppsala University, Uppsala, Sweden,Marene Landström,Science for Life Laboratory, SciLifeLab,Ludwiginstitutet för cancerforskning,Umea Univ, Dept Med Biosci, Unit Pathol, SE-90185 Umea, Sweden
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(creator_code:org_t)
- American Association for the Advancement of Science, 2017
- 2017
- Engelska.
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Ingår i: Science Signaling. - : American Association for the Advancement of Science. - 1945-0877 .- 1937-9145. ; 10:486
- Relaterad länk:
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https://urn.kb.se/re...
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https://doi.org/10.1...
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https://urn.kb.se/re...
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Abstract
Ämnesord
Stäng
- TGF-β signaling stimulates various intracellular pathways that can promote migration in tumor cells. These pathways are generally thought to be either dependent or independent of transcription factors called SMADs. One of the SMAD-independent pathways (PI3K-AKT) is mediated by a direct interaction between PI3K and the TGF-β type I receptor. However, Hamidi et al. found that the TGF-β–induced activation of PI3K depends on another ubiquitin ligase–mediated mechanism and a SMAD protein but is independent of the kinase function of TβRI. The binding of TGF-β to its receptor triggered the recruitment of PI3K and the ubiquitin ligase TRAF6, which polyubiquitylated the regulatory PI3K subunit p85α, thus enabling phosphorylation of the catalytic PI3K subunit p110, but only in the presence of SMAD7. The abundance of ubiquitylated p85α correlated with migration in cultured cells and prostate tumor grade in patient samples. TRAF6 mediates activation of the other “SMAD-independent” (JNK) pathway. These data suggest that, although distinct, the TGF-β signaling pathways are not as insulated from each other as was once thought.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Cell- och molekylärbiologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Cell and Molecular Biology (hsv//eng)
- NATURVETENSKAP -- Biologi -- Biokemi och molekylärbiologi (hsv//swe)
- NATURAL SCIENCES -- Biological Sciences -- Biochemistry and Molecular Biology (hsv//eng)
Nyckelord
- TRAF6
- AKT
- p85
Publikations- och innehållstyp
- vet (ämneskategori)
- art (ämneskategori)
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