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CRKL mediates p110β-dependent PI3K signaling in PTEN-deficient cancer cells
The p110β isoform of PI3K is preferentially activated in many tumors deficient in the phosphatase and tensin homolog (PTEN). However, the mechanism(s) linking PTEN loss to p110β activation remain(s) mysterious. Here we identify CRKL as a member of the class of PI3Kβ interacting proteins. Silencing C...
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| Vydáno v: | Cell Rep |
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| Hlavní autoři: | , , , , , , , |
| Médium: | Artigo |
| Jazyk: | Inglês |
| Vydáno: |
2017
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| Témata: | |
| On-line přístup: | https://ncbi.nlm.nih.gov/pmc/articles/PMC5704918/ https://ncbi.nlm.nih.gov/pubmed/28723560 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1016/j.celrep.2017.06.054 |
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