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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...
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Proteins can undergo many types of post-translational modifications, often in response to changes in their environment. These modifications play an important role in the function and stability of these proteins. Covalently linked molecules include functional groups, such as methyl, acetyl, and phosphate groups, and also small proteins, such as ubiquitin. There are around 200 different types of covalent regulators that have been identified.
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Related Experiment Video

Updated: Oct 22, 2025

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

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TP53 isoform junction reads based analysis in malignant and normal contexts.

Suleyman Vural1,2, Lun-Ching Chang3, Laura M Yee1

  • 1National Cancer Institute, Division of Cancer Treatment and Diagnosis, Biometric Research Program, Rockville, MD, 20850, USA.

Scientific Reports
|August 27, 2021
PubMed
Summary
This summary is machine-generated.

The TP53 gene

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Area of Science:

  • Oncology
  • Genetics
  • Molecular Biology

Background:

  • The TP53 gene is frequently altered in cancer, with NM_000546.6 being the predominant isoform.
  • Alternative TP53 isoforms exist at lower expression levels and may have altered tumor suppressor activity.

Purpose of the Study:

  • To investigate the expression patterns of TP53 alternative isoforms in cancer and normal tissues.
  • To determine if TP53 C-terminal alternative isoforms increase in tumors with wild-type TP53.

Main Methods:

  • Analysis of exon-exon junction reads from RNA-seq data.
  • Utilized datasets from The Cancer Genome Atlas (TCGA), Cancer Cell Line Encyclopedia (CCLE), and Genotype-Tissue Expression (GTEx) projects.

Main Results:

  • Observed no substantial increase in the fraction of TP53 C-terminal alternative isoforms in TCGA tumors and CCLE cell lines with wild-type TP53.
  • Contrary to expectations, TP53 C-terminal alternative isoforms did not significantly increase in tumors with wild-type TP53.

Conclusions:

  • TP53 C-terminal alternative isoforms, which have reduced tumor suppressor activity, are not significantly selected for during tumor progression.
  • The expression of TP53 alternative isoforms may not be a reliable indicator for tumor progression in wild-type TP53 cancers.