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Related Concept Videos

Translation01:31

Translation

Lesson: Translation
Translation is the process of synthesizing proteins from the genetic information carried by messenger RNA (mRNA). Following transcription, it constitutes the final step in the expression of genes. This process is carried out by ribosomes, complexes of protein and specialized RNA molecules. Ribosomes, transfer RNA (tRNA), and other proteins produce a chain of amino acids—the polypeptide—as the end product of translation.
Translation Produces the Building Blocks of Life
Translation01:31

Translation

Lesson: Translation
Translation is the process of synthesizing proteins from the genetic information carried by messenger RNA (mRNA). Following transcription, it constitutes the final step in the expression of genes. This process is carried out by ribosomes, complexes of protein and specialized RNA molecules. Ribosomes, transfer RNA (tRNA), and other proteins produce a chain of amino acids—the polypeptide—as the end product of translation.
Translation Produces the Building Blocks of Life
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
Initiation of Translation02:33

Initiation of Translation

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.
First, the initiator tRNA must be selected from the pool of elongator tRNAs by eukaryotic initiation factor 2 (eIF2). The initiator tRNA (Met-tRNAi) has conserved sequence elements including modified bases at...
Improving Translational Accuracy02:07

Improving Translational Accuracy

Base complementarity between the three base pairs of mRNA codon and the tRNA anticodon is not a failsafe mechanism. Inaccuracies can range from a single mismatch to no correct base pairing at all. The free energy difference between the correct and nearly correct base pairs can be as small as 3 kcal/ mol. With complementarity being the only proofreading step, the estimated error frequency would be one wrong amino acid in every 100 amino acids incorporated. However, error frequencies observed in...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...

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Related Experiment Video

Updated: Jun 19, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

TP53 cancerous mutations exhibit selection for translation efficiency.

Yedael Y Waldman1, Tamir Tuller, Roded Sharan

  • 1Department of Molecular Microbiology and Biotechnology, Blavatnik School of Computer Science, Tel Aviv University, Ramat Aviv, Israel.

Cancer Research
|November 6, 2009
PubMed
Summary

TP53 mutations, common in cancer, may be selected to increase translation efficiency (TE). This study reveals increased TE in mutated TP53, correlating with mutation frequency and oncogenic effects, suggesting TE influences cancer development.

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Assessment of Selective mRNA Translation in Mammalian Cells by Polysome Profiling
10:00

Assessment of Selective mRNA Translation in Mammalian Cells by Polysome Profiling

Published on: October 28, 2014

Area of Science:

  • Molecular Biology
  • Genetics
  • Cancer Research

Background:

  • The TP53 gene is a critical tumor suppressor, frequently mutated in human cancers.
  • TP53 mutations can gain oncogenic functions, including dominant-negative effects on wild-type TP53.
  • Selection pressures may favor TP53 mutations that enhance translation efficiency (TE) in cancer cells.

Purpose of the Study:

  • To investigate the role of translation efficiency (TE) in the selection of TP53 mutations during cancer development.
  • To analyze the correlation between TE and the frequency and oncogenic effects of TP53 mutations.
  • To explore how TE influences mutation location, outcome, and progression.

Main Methods:

  • Large-scale analysis of TE in human cancer mutated TP53 variants.
  • Correlation analysis between TE and TP53 mutation frequency and known oncogenic effects.
  • Investigation of codon-specific TE and selection pressures.
  • Comparison of TE increase in progressive versus primary tumors.
  • Analysis of TP53 NCI-60 cell lines for coadaptation with tRNA pools.

Main Results:

  • A significant increase in TE was identified in mutated TP53 variants, correlating with mutation frequency.
  • TP53 mutations with known oncogenic effects showed significantly higher TE increases.
  • Codons with lower TE exhibited stronger selection for nonsynonymous mutations.
  • Frequent mutations demonstrated a greater TE increase compared to less frequent ones.
  • Progressive tumors showed a higher TE increase in TP53 mutations than primary tumors.
  • Evidence of coadaptation between TP53 mutations and tRNA pools was observed, enhancing overall TE.

Conclusions:

  • Translation efficiency (TE) plays a significant role in the selection of TP53 mutations in cancer.
  • TE influences the location and functional outcome of TP53 mutations.
  • The findings suggest TE is a crucial factor in oncogenesis driven by TP53 mutations.