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Related Concept Videos

Autophagy01:27

Autophagy

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,...
Delivery Pathways to the Lysosome01:36

Delivery Pathways to the Lysosome

Eukaryotic cells use different mechanisms to eliminate toxic waste obsolete and worn-out substances. Lysosomes play a pivotal role in this, and hence, these substances are carried to the lysosome from other parts of the cell and extracellular space through different pathways. The most elaborately studied pathways to the lysosome are the endocytic pathways.
Endocytosis
In endocytosis, the cell membrane takes up macromolecules and particles from the surrounding medium. Clathrin-mediated...
Autophagic Cell Death01:18

Autophagic Cell Death

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 pro-apoptotic...
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...
The Unfolded Protein Response01:37

The Unfolded Protein Response

The ER is the hub of protein synthesis in a cell. It has robust systems to quality control protein folding and also for degradation of terminally misfolded proteins. Under normal conditions, a small proportion of misfolded proteins that cannot be salvaged need to be transported to the cytoplasm by the ER-associated degradation or ERAD pathways. However, if the ERAD cannot handle the misfolded proteins, the cell activates the unfolded protein response or UPR to adjust the protein folding...

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Study of Protein-protein Interactions in Autophagy Research
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Study of Protein-protein Interactions in Autophagy Research

Published on: September 9, 2017

DRAM-1 encodes multiple isoforms that regulate autophagy.

Li Yen Mah1, Jim O'Prey, Alice D Baudot

  • 1Tumour Cell Death Laboratory, Beatson Institute for Cancer Research, Glasgow, Scotland, UK.

Autophagy
|November 16, 2011
PubMed
Summary
This summary is machine-generated.

This study identifies novel splice variants of the DRAM-1 gene, regulated by the tumor suppressor p53. These variants modulate autophagy, a key cellular process, offering new insights into cancer protection mechanisms.

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Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Autophagy is a crucial cellular degradation process that maintains integrity and protects against diseases like cancer.
  • The tumor suppressor p53 influences autophagy, including inducing it via the Damage-Regulated Autophagy Modulator (DRAM-1) gene.

Purpose of the Study:

  • To investigate the existence and function of novel p53-inducible splice variants of DRAM-1.
  • To determine the cellular localization and autophagy-modulating capabilities of these new variants.

Main Methods:

  • Analysis of p53-inducible splice variants of DRAM-1 in human and mouse cell lines.
  • Subcellular localization studies of DRAM-1 splice variants using specific markers.
  • Assessment of the impact of splice variants on autophagy and programmed cell death.

Main Results:

  • DRAM-1 encodes multiple p53-inducible splice variants, with SV4 and SV5 being mature mRNA species.
  • Unlike full-length DRAM-1 (SV1), SV4 and SV5 exhibit distinct subcellular localizations, including peroxisomes, autophagosomes, and the endoplasmic reticulum.
  • SV4 and SV5 modulate autophagy but do not appear to induce programmed cell death.

Conclusions:

  • Discovery of novel DRAM-1 splice variants (SV4, SV5) that regulate autophagy downstream of p53.
  • These variants represent new players in the intricate control of autophagy, with implications for understanding cellular integrity and disease.
  • Findings provide a deeper understanding of p53-mediated autophagy regulation and its role in cancer biology.