mTOR kinase inhibition causes feedback-dependent biphasic regulation of AKT signaling Academic Article uri icon

Overview

MeSH Major

  • Proteins
  • Proto-Oncogene Proteins c-akt
  • Signal Transduction
  • Transcription Factors

abstract

  • The results of this study show the adaptive capabilities of oncogenic signaling networks, as AKT signaling becomes reactivated through a feedback-induced AKT species phosphorylated on T308 but lacking S473. The addition of RTK inhibitors can prevent this reactivation of AKT signaling and cause profound cell death and tumor regression in vivo, highlighting the possible need for combinatorial approaches to block feedback-regulated pathways.

publication date

  • August 2011

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed Central ID

  • PMC3227125

Digital Object Identifier (DOI)

  • 10.1158/2159-8290.CD-11-0085

PubMed ID

  • 22140653

Additional Document Info

start page

  • 248

end page

  • 59

volume

  • 1

number

  • 3