Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Autophagy01:27

Autophagy

5.6K
Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...
5.6K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

4.6K
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...
4.6K
Autophagic Cell Death01:18

Autophagic Cell Death

4.3K
Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
4.3K
Mechanisms of Retrovirus-induced Cancers01:51

Mechanisms of Retrovirus-induced Cancers

6.8K
Retroviruses are RNA viruses that have been shown to cause cancers in diverse species, including chickens, mice, cats, and monkeys. The RNA genomes of these viruses are first reverse-transcribed into single and then double-stranded DNA (dsDNA) copies. This dsDNA called proviral DNA then integrates into the host genome. Subsequently, the host cell transcribes the proviral DNA in concert with the chromosomal DNA. This leads to the production of viral RNA and proteins that assemble at the host...
6.8K
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

2.7K
Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR...
2.7K
Experimental RNAi02:15

Experimental RNAi

7.2K
RNA interference (RNAi) is a cellular mechanism that inhibits gene expression by suppressing its transcription or activating the RNA degradation process. The mechanism was discovered by Andrew Fire and Craig Mello in 1998 in plants. Today, it is observed in almost all eukaryotes, including protozoa, flies, nematodes, insects, parasites, and mammals. This precise cellular mechanism of gene silencing has been developed into a technique that provides an efficient way to identify and determine the...
7.2K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Bridging the diagnostic gap: the role of culture methods in the era of syndromic panels for central nervous system infections.

Frontiers in cellular and infection microbiology·2026
Same author

<i>YoyoMut</i>: Interactive Exploration of SARS-CoV-2 Mutation Fixation and Reversion Through Time.

Life (Basel, Switzerland)·2026
Same author

Evaluation of a Novel Multiplex PCR Assay for Vesicular Viruses.

International journal of molecular sciences·2026
Same author

TTV Viremia and Immune Responses Following Vaccination Against Mpox and Dengue Viruses.

Vaccines·2026
Same author

TTV virome marks immune exhaustion, α7nAChR alteration, and mortality in elderly patients with severe COPD.

GeroScience·2026
Same author

Risk of Developing Low-Level Viral Rebound Among People With HIV Receiving 2- or 3-Drug Regimens: A Case-Control Study Nested in the ICONA Cohort.

Open forum infectious diseases·2026

Related Experiment Video

Updated: Jan 8, 2026

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells
09:10

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells

Published on: October 28, 2019

7.7K

The monkeypox virus suppresses autophagy by modulating Rubicon expression.

Giulia Refolo1, Cosmina Mija2, Fabiola Ciccosanti1

  • 1Laboratory of Cellular Biology and Electron Microscopy, National Institute for Infectious Diseases "Lazzaro Spallanzani" -IRCCS, Rome, Italy.

Cell Death Discovery
|December 23, 2025
PubMed
Summary
This summary is machine-generated.

Monkeypox virus (MPXV) impairs cellular autophagy by increasing Rubicon. Silencing Rubicon restores autophagy and reduces MPXV replication, suggesting autophagy activation as a potential therapy.

More Related Videos

A Primary Human Trophoblast Model to Study the Effect of Inflammation Associated with Maternal Obesity on Regulation of Autophagy in the Placenta
11:44

A Primary Human Trophoblast Model to Study the Effect of Inflammation Associated with Maternal Obesity on Regulation of Autophagy in the Placenta

Published on: September 27, 2017

11.8K
Tyramide Signal Amplification for the Immunofluorescent Staining of ZBP1-Dependent Phosphorylation of RIPK3 and MLKL After HSV-1 Infection in Human Cells
09:15

Tyramide Signal Amplification for the Immunofluorescent Staining of ZBP1-Dependent Phosphorylation of RIPK3 and MLKL After HSV-1 Infection in Human Cells

Published on: October 20, 2022

2.7K

Related Experiment Videos

Last Updated: Jan 8, 2026

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells
09:10

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells

Published on: October 28, 2019

7.7K
A Primary Human Trophoblast Model to Study the Effect of Inflammation Associated with Maternal Obesity on Regulation of Autophagy in the Placenta
11:44

A Primary Human Trophoblast Model to Study the Effect of Inflammation Associated with Maternal Obesity on Regulation of Autophagy in the Placenta

Published on: September 27, 2017

11.8K
Tyramide Signal Amplification for the Immunofluorescent Staining of ZBP1-Dependent Phosphorylation of RIPK3 and MLKL After HSV-1 Infection in Human Cells
09:15

Tyramide Signal Amplification for the Immunofluorescent Staining of ZBP1-Dependent Phosphorylation of RIPK3 and MLKL After HSV-1 Infection in Human Cells

Published on: October 20, 2022

2.7K

Area of Science:

  • Virology
  • Cellular Biology
  • Immunology

Background:

  • Monkeypox virus (MPXV) is a reemerging global health threat.
  • Autophagy is a cellular process with complex roles in viral infections.
  • The interaction between MPXV and autophagy is not well understood.

Purpose of the Study:

  • To investigate the interplay between MPXV and cellular autophagy.
  • To identify mechanisms by which MPXV affects autophagy.
  • To explore autophagy modulation as a therapeutic strategy against MPXV.

Main Methods:

  • Infection of Calu-3 cells with MPXV.
  • Analysis of autophagic flux.
  • Gene silencing of Rubicon.

Main Results:

  • MPXV infection significantly impairs autophagic flux in Calu-3 cells.
  • MPXV upregulates Rubicon, a negative regulator of autophagy.
  • Silencing Rubicon restored autophagic flux and reduced MPXV replication.

Conclusions:

  • MPXV inhibits autophagy through Rubicon upregulation.
  • Targeting Rubicon and activating autophagy presents a potential therapeutic avenue for MPXV infections.