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March 22, 2024Cancer Research

Tribbles 1 Pseudokinase Complex Formation and Akt Activation in Glioblastoma

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Authors

KSKarnika SinghCHChunhua HanHMHeather R. Manring

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Overview

Preclinical study reveals TRIB1 pseudokinase binds and activates Akt in glioblastoma cells, suggesting targeting this complex may circumvent direct Akt inhibitor toxicity.

Key Points

  • Elevated TRIB1 pseudokinase expression activates Akt signaling to drive therapy resistance, with binding mapped specifically to amino acids 90 to 160.
  • Co-immunoprecipitation and Western blotting across patient-derived xenograft glioblastoma cell lines revealed distinct isoform-specific TRIB1 interactions.
  • Targeting TRIB1-mediated Akt activation may suppress glioblastoma oncogenesis while avoiding inhibitor toxicity; preclinical cell models require validation.

Cite This Study

Singh et al. (2024) studied this question.

synapsesocial.com/papers/68e72f4bb6db6435876a885ehttps://doi.org/10.1158/1538-7445.am2024-3358
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Abstract 4616: TBK1 and GSK3 mediated TRAF2 phosphorylation confers resistance to PI3K-AKT inhibition in breast cancer cells2024
  2. 2Abstract 2985: TRIB2 as a therapeutic vulnerability in ALK-rearranged non-small cell lung cancer2026
  3. 3Glucose‑driven TRIB3 enhances the tumorigenic potential of colon cancer via the PI3K/AKT pathway2026
  4. 4Abstract 5959: Targeting TRIM11 is a potential therapeutic strategy for malignant gliomas2024
  5. 5Abstract 406: Discovery of potent and selective TRIB2 inhibitors with therapeutic efficacy in therapy-resistant neuroendocrine prostate cancer.2026