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Related Concept Videos

Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
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Initiating translation is complex because it involves multiple molecules. Initiator tRNA, ribosomal subunits, and eukaryotic initiation factors (eIFs) are all required to assemble on the initiation codon of mRNA. This process consists of several steps that are mediated by different eIFs.
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Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
Transducer Mechanism: Enzyme-Linked Receptors01:27

Transducer Mechanism: Enzyme-Linked Receptors

Enzyme-linked receptors are cell-surface receptors acting as an enzyme or associating with an enzyme intracellularly. They make excellent drug targets. Drugs can bind to the extracellular ligand-binding domain or directly affect their enzymatic domain and alter their activity.
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Related Experiment Video

Updated: Jul 7, 2026

Monitoring eIF4F Assembly by Measuring eIF4E-eIF4G Interaction in Live Cells
08:47

Monitoring eIF4F Assembly by Measuring eIF4E-eIF4G Interaction in Live Cells

Published on: May 1, 2020

MNK, EIF4E and targeting translation for therapy.

Ricardo L A Silva1, Hans Guido Wendel

  • 1Cancer Biology & Genetics Program, Memorial Sloan-Kettering Cancer Center, New York, New York 10021, USA.

Cell Cycle (Georgetown, Tex.)
|February 8, 2008
PubMed
Summary
This summary is machine-generated.

Cancer cells require specific protein translation pathways for growth, driven by AKT signaling. This study finds that MNK1/2 kinases are essential for the oncogenic activity of eIF4E, offering a potential cancer therapy target.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Protein translation is frequently deregulated in cancer, often linked to AKT pathway activation.
  • The translation initiation factor eIF4E has demonstrated in vivo oncogenic activity downstream of AKT and mTOR signaling.
  • MNK1/2 kinases are known regulators of protein synthesis and cellular processes.

Purpose of the Study:

  • To investigate the role of MNK1/2 kinases in the oncogenic function of eIF4E.
  • To determine if Ser209 phosphorylation of eIF4E by MNK1/2 is critical for its oncogenic activity.
  • To explore the therapeutic potential of targeting MNK1/2 kinases in cancer.

Main Methods:

  • Utilizing molecular biology techniques to study protein-protein interactions and phosphorylation events.
  • Employing cell-based assays to assess oncogenic activity and translational regulation.
  • Investigating the in vivo relevance of the identified pathway in cancer models.

Main Results:

  • Identified an absolute requirement for Ser209 phosphorylation of eIF4E by MNK1/2 kinases for its oncogenic action.
  • Demonstrated that MNK1/2 kinases are dispensable for normal mammalian development, unlike their role in cancer.
  • Established a direct link between AKT/mTOR signaling, MNK1/2 activity, and eIF4E phosphorylation in cancer.

Conclusions:

  • MNK1/2-mediated phosphorylation of eIF4E at Ser209 is essential for its oncogenic activity.
  • The differential requirement for MNK1/2 kinases in cancer versus normal cells presents a potential therapeutic window.
  • Targeting MNK1/2 kinases could be a viable strategy for cancer treatment by inhibiting critical translational machinery.