Related Experiment Video

Updated: Aug 8, 2026

Preparation of Cell-lines for Conditional Knockdown of Gene Expression and Measurement of the Knockdown Effects on E4orf4-Induced Cell Death
13:54

Preparation of Cell-lines for Conditional Knockdown of Gene Expression and Measurement of the Knockdown Effects on E4orf4-Induced Cell Death

Published on: October 21, 2012

p202, an interferon-inducible negative regulator of cell growth, is a target of the adenovirus E1A protein

H Xin1, S D'Souza, L Fang

  • 1Department of Radiation Oncology, Stritch School of Medicine, Loyola University Medical Center, 2160 South First Avenue, Building No. 1, Maywood, Illinois, IL 60153, USA.

Oncogene
|November 1, 2001
PubMed

Insights

Adenovirus E1A protein promotes cell growth by targeting the p202 protein, an inhibitor of cell division. This interaction relieves E2F pathway inhibition, promoting cell proliferation and counteracting p202

Area of Science:

  • Molecular Biology
  • Virology
  • Cancer Research

Background:

  • Human adenovirus E1A protein promotes cell proliferation by interacting with negative growth regulators.
  • Retinoblastoma tumor suppressor protein (pRb) and interferon (IFN)-inducible p202 are key negative regulators of cell growth.
  • p202 functions partly through the pRb/E2F pathway.

Purpose of the Study:

  • To investigate if adenovirus E1A protein targets p202 for functional inactivation.
  • To determine if E1A/p202 interaction affects cell proliferation and the pRb/E2F pathway.

Main Methods:

  • Expression of E1A protein in cells.
  • Assessing cell growth inhibition by p202.
  • Measuring E2F transcriptional activity and DNA-binding activity.
  • In vitro and in vivo binding assays for E1A and p202.
  • Analyzing E1A-mediated apoptosis with ectopic p202 expression.

Main Results:

  • E1A expression overcame p202-mediated cell growth inhibition.
  • E1A alleviated p202's inhibition of E2F transcriptional activity and DNA-binding.
  • E1A directly bound to p202 in vitro and in vivo.
  • A specific deletion in E1A CR2 reduced p202 binding.
  • Ectopic p202 expression reduced E1A-mediated apoptosis.

Conclusions:

  • Adenovirus E1A protein and p202 functionally counteract each other.
  • E1A targets p202 to promote cell proliferation.
  • This interaction offers insights into viral oncogenesis and cell cycle regulation.

More Related Videos

Adenoviral Transduction of Naive CD4 T Cells to Study Treg Differentiation15:33

Adenoviral Transduction of Naive CD4 T Cells to Study Treg Differentiation

Published on: August 13, 2013

Isolation of Viral Replication Compartment-enriched Sub-nuclear Fractions from Adenovirus-infected Normal Human Cells10:22

Isolation of Viral Replication Compartment-enriched Sub-nuclear Fractions from Adenovirus-infected Normal Human Cells

Published on: November 12, 2015

Related Concept Videos

Negative Regulator Molecules01:23

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
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...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

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...