Related Experiment Video

Updated: Jul 9, 2026

Lentiviral Vector Preparation for Efficient Gene and MicroRNA Modulation of Peritoneal Cavity Tissue-Resident Macrophages In Vivo in Mice
06:33

Lentiviral Vector Preparation for Efficient Gene and MicroRNA Modulation of Peritoneal Cavity Tissue-Resident Macrophages In Vivo in Mice

Published on: February 16, 2024

Expression of murine leukemia virus envelope protein is sufficient for the induction of apoptosis

Xiaoqing Zhao1, Fayth K Yoshimura

  • 1Department of Immunology and Microbiology, Wayne State University, 540 E. Canfield Ave., Detroit, MI 48201, USA.

Journal of Virology
|December 14, 2007
PubMed

Insights

Murine leukemia viruses (MLVs) cause cell damage and thymic lymphoma. High levels of a viral envelope precursor protein (gPr80(env)) induce apoptosis by causing endoplasmic reticulum stress.

Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • Murine leukemia viruses (MLVs) can cause cytopathic effects and thymic lymphoma.
  • The mechanisms linking viral infection to cellular apoptosis and oncogenesis are not fully understood.

Purpose of the Study:

  • To investigate the molecular mechanisms by which mink cell focus-forming (MCF) MLV induces apoptosis in mink epithelial cells.
  • To determine the role of viral DNA and envelope protein accumulation in MLV-induced cytopathic effects.

Main Methods:

  • Infection of mink epithelial cells with MCF MLV and NZB-9 MLV.
  • Analysis of unintegrated viral DNA and envelope precursor polyprotein (gPr80(env)) levels.
  • Comparison of env gene expression from plasmid clones of different MLV strains.
  • Assessment of endoplasmic reticulum stress markers.

Main Results:

  • MCF MLV infection led to high levels of unintegrated viral DNA and gPr80(env).
  • Accumulation of MCF13 gPr80(env) was sufficient to induce apoptosis.
  • MCF13 gPr80(env) accumulation caused endoplasmic reticulum stress.

Conclusions:

  • The accumulation of gPr80(env) is a key factor in MLV-induced apoptosis.
  • Endoplasmic reticulum stress triggered by viral protein accumulation contributes to cytopathic effects.
  • Understanding these mechanisms may inform strategies against MLV-induced diseases.

More Related Videos

Evaluation of Caspase Activation to Assess Innate Immune Cell Death10:23

Evaluation of Caspase Activation to Assess Innate Immune Cell Death

Published on: January 20, 2023

Highly Efficient Transfection of Primary Macrophages with In Vitro Transcribed mRNA06:46

Highly Efficient Transfection of Primary Macrophages with In Vitro Transcribed mRNA

Published on: November 9, 2019

Related Concept Videos

The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
Leaky Scanning02:28

Leaky Scanning

During most eukaryotic translation processes, the small 40S ribosome subunit scans an mRNA from its 5' end until it encounters the first start AUG codon. The large 60S ribosomal subunit then joins the smaller one to initiate protein synthesis. The location of the translation initiation is largely determined by the nucleotides near the start codon as there may be multiple translation initiation sites present on the mRNA.  Marilyn Kozak discovered that the sequence RCCAUGG (where R stands for...
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...