Related Experiment Video

Updated: Mar 31, 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

10.2K

Sp100A is a tumor suppressor that activates p53-dependent transcription and counteracts E1A/E1B-55K-mediated

J Berscheminski1, J Brun1, T Speiseder1

  • 1Department of Viral Transformation, Heinrich Pette Institute, Leibniz Institute for Experimental Virology, Hamburg, Germany.

Oncogene
|October 20, 2015
PubMed

Insights

Human adenoviruses use oncoproteins E1A and E1B-55K for oncogenic transformation. The viral E1B-55K protein interacts with Sp100A, inhibiting its tumor-suppressive activity and promoting cell cycle progression.

Area of Science:

  • Oncology
  • Virology
  • Molecular Biology

Background:

  • Human adenoviruses (HAdV) are models for studying cancer development.
  • Viral oncoproteins E1A and E1B-55K are crucial for oncogenic transformation.
  • These oncoproteins accelerate cell cycle progression and inhibit tumor suppressors like p53.

Purpose of the Study:

  • To investigate the role of E1B-55K binding to Sp100A in adenovirus-mediated transformation.
  • To elucidate the mechanism by which Sp100A regulates p53 activity and tumor suppression.
  • To understand how E1B-55K counteracts Sp100A's tumor-suppressive functions.

Main Methods:

  • Studying the interaction between viral oncoprotein E1B-55K and PML-NB component Sp100A.
  • Analyzing the effect of the E1B-55K/Sp100A complex on p53 transcriptional activity.
  • Investigating Sp100A SUMOylation and cellular localization induced by E1B-55K.

Main Results:

  • E1B-55K binding to Sp100A is essential for adenovirus-driven transformation.
  • The E1B-55K/Sp100A complex inhibits Sp100A-mediated p53 activation.
  • Sp100A exhibits tumor-suppressive activity by stabilizing p53 and hindering transformation.
  • E1B-55K counteracts Sp100A's suppression via SUMOylation and altered localization.

Conclusions:

  • Sp100A acts as a tumor suppressor by modulating p53 activity.
  • E1B-55K manipulates Sp100A to promote viral oncogenesis and lytic infection.
  • These findings offer new insights into viral oncoprotein strategies for cellular control.

More Related Videos

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence04:56

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence

Published on: December 30, 2025

328
Purification of Ubiquitinated p53 Proteins from Mammalian Cells10:55

Purification of Ubiquitinated p53 Proteins from Mammalian Cells

Published on: March 21, 2022

2.9K

Related Concept Videos

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...
5.4K
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
6.3K
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

2.1K
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...
10.1K
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

3.0K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
9.2K