Related Experiment Video

Updated: May 31, 2026

Inducible, Cell Type-Specific Expression in Arabidopsis thaliana Through LhGR-Mediated Trans-Activation
09:31

Inducible, Cell Type-Specific Expression in Arabidopsis thaliana Through LhGR-Mediated Trans-Activation

Published on: April 19, 2019

Glucocorticoid elevation of dexamethasone-induced gene 2 (Dig2/RTP801/REDD1) protein mediates autophagy in

Jason K Molitoris1, Karen S McColl, Sarah Swerdlow

  • 1Department of Medicine, Case Western Reserve University and University Hospitals of Cleveland, Cleveland, Ohio 44106, USA.

The Journal of Biological Chemistry
|July 8, 2011
PubMed

Insights

Dexamethasone, a glucocorticoid, triggers autophagy in lymphocytes via REDD1 protein induction. Suppressing REDD1 reduces autophagy and increases cell death, suggesting REDD1-mediated autophagy promotes lymphocyte survival during chemotherapy.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Immunology

Background:

  • Glucocorticoids like dexamethasone induce apoptosis in lymphocytes, used in treating hematologic malignancies.
  • Dexamethasone also induces autophagy in lymphocytes, but the underlying mechanism requires elucidation.

Purpose of the Study:

  • To investigate the role of the stress response protein Dig2/RTP801/REDD1 in dexamethasone-induced autophagy in lymphocytes.
  • To determine if REDD1 mediates autophagy via mammalian target of rapamycin (mTOR) signaling inhibition.

Main Methods:

  • Gene expression analysis to identify dexamethasone-induced genes.
  • RNA interference (RNAi) to suppress Dig2/RTP801/REDD1 expression.
  • Analysis of mTOR signaling and autophagy markers.
  • Experiments using Dig2/Rtp801/Redd1 knock-out murine thymocytes.

Main Results:

  • Dexamethasone treatment elevates Dig2/RTP801/REDD1 expression in lymphocytes.
  • Suppression of Dig2/RTP801/REDD1 inhibits dexamethasone-induced mTOR signaling and autophagy.
  • Similar results were observed in knock-out murine thymocytes.
  • Knockdown of Dig2/RTP801/REDD1 enhanced dexamethasone-induced lymphocyte cell death.

Conclusions:

  • Elevation of Dig2/RTP801/REDD1 is a key contributor to dexamethasone-induced autophagy in lymphocytes.
  • The study suggests that Dig2/RTP801/REDD1-mediated autophagy promotes lymphocyte survival, potentially impacting chemotherapy efficacy.

More Related Videos

A Simple and Efficient Method for Testing Immunomodulatory Agents for Generation of Tolerogenic Dendritic Cells from Human CD14+ Monocytes11:34

A Simple and Efficient Method for Testing Immunomodulatory Agents for Generation of Tolerogenic Dendritic Cells from Human CD14+ Monocytes

Published on: April 11, 2025

siRNA Electroporation to Modulate Autophagy in Herpes Simplex Virus Type 1-Infected Monocyte-Derived Dendritic Cells09:10

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

Published on: October 28, 2019

Related Concept Videos

Exon Recombination02:32

Exon Recombination

The evolution of new genes is critical for speciation. Exon recombination, also known as exon shuffling or domain shuffling, is an important means of new gene formation. It is observed across vertebrates, invertebrates, and in some plants such as potatoes and sunflowers. During exon recombination, exons from the same or different genes recombine and produce new exon-intron combinations, which might evolve into new genes. 
Exon shuffling follows “splice frame rules.” Each exon has three reading...
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

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 activation may...
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...