Related Experiment Video

Updated: Jan 23, 2026

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
07:15

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

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Beyond growth signaling: apoptotic sensor MERTK activates AKT by a novel mechanism

Yanqiong Zhang1,2, H Shelton Earp1,3, Pengda Liu1,2

  • 1UNC Lineberger Comprehensive Cancer Center, The University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.

Molecular & Cellular Oncology
|June 19, 2019
PubMed

Insights

Tumor apoptotic materials activate the oncogenic AKT kinase via MERTK, promoting drug resistance. This novel pathway bypasses traditional growth signals, offering new therapeutic targets.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • The oncogenic kinase AKT is typically activated by growth signals.
  • Understanding alternative AKT activation pathways is crucial for cancer therapy.

Purpose of the Study:

  • To investigate a novel mechanism of AKT activation involving apoptotic materials.
  • To explore the role of MERTK and SAV1 in AKT regulation.

Main Methods:

  • Investigated the interaction between apoptotic materials, MERTK, and AKT.
  • Analyzed the phosphorylation of AKT at Y26.
  • Assessed the impact of SAV1 binding on AKT activity.

Main Results:

  • Apoptotic materials stimulate MERTK, leading to AKT phosphorylation at Y26.
  • Phosphorylation at Y26 disrupts the binding of the AKT inhibitor SAV1.
  • This mechanism enhances AKT responsiveness to growth signals, potentially contributing to drug resistance.

Conclusions:

  • A novel pathway for AKT activation by apoptotic materials, mediated by MERTK and SAV1, has been identified.
  • This mechanism may play a significant role in cancer progression and drug resistance.
Keywords:
AktKidney cancerMERTKSAV1drug resistance

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