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Related Concept Videos

Endoplasmic Reticulum01:39

Endoplasmic Reticulum

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The Endoplasmic Reticulum (ER) in eukaryotic cells is a substantial network of interconnected membranes with diverse functions, from calcium storage to biomolecule synthesis. A primary component of the endomembrane system, the ER manufactures phospholipids critical for membrane function throughout the cell. Additionally, the two distinct regions of the ER specialize in the manufacture of specific lipids and proteins.
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The Endoplasmic Reticulum01:43

The Endoplasmic Reticulum

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The endoplasmic reticulum or ER makes up for more than half of the membranes in a cell and accounts for 10% of total cell volume. It is also the primary protein and lipid synthesis factory for most cell organelles, such as the Golgi apparatus, lysosomes, secretory vesicles, and the plasma membrane. Despite being the most extensive and functionally complex subcellular organelle, ER was the last to be discovered. After years of deliberation, Keith Porter and George Palade in the year 1954,...
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Smooth Endoplasmic Reticulum01:21

Smooth Endoplasmic Reticulum

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Smooth endoplasmic reticulum or smooth ER is a sub-organelle with specialized functions in animal cells and plant cells. It is often associated with the tubule morphology of the endoplasmic reticulum.
The ER provides optimal conditions for synthesizing steroid hormones and lipids, such as phospholipids and triglycerides. Traditionally, lipid metabolism was considered to be a smooth ER function. However, there is no direct evidence to prove that rough ER is completely excluded from lipid...
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Directing Proteins to the Rough Endoplasmic Reticulum01:34

Directing Proteins to the Rough Endoplasmic Reticulum

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The organelle-specific signaling sequences direct proteins synthesized in the cytosol to their final destination like ER, mitochondria, peroxisomes, etc. Some of the proteins directed to ER are then trafficked via vesicles to other organelles within the cell or the extracellular environment through the Golgi complex. For example, the rough ER synthesizes soluble proteins for transportation to the lysosomes or secretion out of the cell. It can also synthesize transmembrane proteins that can...
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Autophagy01:27

Autophagy

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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,...
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C4 Pathway and CAM01:27

C4 Pathway and CAM

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Most plants use the C3 pathway for carbon fixation. However, some plants, such as sugar cane, corn, and cacti that grow in hot conditions, use alternative pathways to fix carbon and conserve energy loss due to photorespiration. Photorespiration is the process that occurs when the oxygen concentration is high. Under such conditions, the rubisco enzyme in the Calvin cycle binds O2 instead of CO2, which halts photosynthesis and consumes energy.
C4 Pathway
The C4 pathway is used by plants such as...
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Molecular Modulation by Lentivirus-Delivered Specific shRNAs in Endoplasmic Reticulum Stressed Neurons
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Coxsackievirus B3 Infection Triggers Autophagy through 3 Pathways of Endoplasmic Reticulum Stress.

Xiao Nuan Luo1, Hai Lan Yao2, Juan Song1

  • 1State Key Laboratory of Infectious Disease Prevention and Control, Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, National Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention, Beijing 102206, China.

Biomedical and Environmental Sciences : BES
|January 15, 2019
PubMed
Summary

Coxsackievirus B3 infection triggers autophagy via endoplasmic reticulum stress in HeLa cells. This process involves key ER stress sensors and may inhibit the mTOR signaling pathway, impacting viral replication.

Keywords:
AutophagyCoxsackievirus B3 (CVB3)Endoplasmic reticulum (ER) stressUnfolded protein response (UPR)

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Visualization of Endoplasmic Reticulum Subdomains in Cultured Cells
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Area of Science:

  • Cell Biology
  • Virology
  • Molecular Biology

Background:

  • Autophagy is a crucial cellular process for degrading damaged components.
  • Picornaviruses, including coxsackievirus B3 (CVB3), often manipulate autophagy for their replication.
  • The precise mechanisms by which viruses induce autophagy remain incompletely understood.

Purpose of the Study:

  • To investigate if coxsackievirus B3 (CVB3) infection induces autophagy through endoplasmic reticulum (ER) stress.
  • To identify the specific ER stress pathways involved in CVB3-induced autophagy.

Main Methods:

  • Utilized Western blotting, RT-PCR, and confocal microscopy to detect ER stress and autophagy markers in CVB3-infected HeLa cells.
  • Employed inhibitors for key ER stress sensors: PKR-like ER protein kinase (PERK), inositol-requiring protein-1 (IRE1), and activating transcription factor-6 (ATF6).
  • Assessed the impact of these inhibitors on autophagy by measuring microtubule-associated protein light chain 3 (LC3) conversion.

Main Results:

  • CVB3 infection activated ER stress sensors PERK, IRE1, and ATF6.
  • Increased accumulation of GFP-LC3 puncta and conversion of LC3-I to LC3-II indicated autophagy induction.
  • CVB3 infection led to decreased mammalian target of rapamycin (mTOR) and p-mTOR expression.
  • Inhibiting PERK, IRE1, or ATF6 significantly reduced the LC3-II/LC3-I ratio in infected cells.

Conclusions:

  • CVB3 infection induces autophagy in HeLa cells via ER stress.
  • The PERK, IRE1, and ATF6 pathways are integral to regulating this autophagy induction.
  • ER stress likely inhibits the mTOR signaling pathway, promoting autophagy during CVB3 infection.