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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

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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.
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Directing Proteins to the Rough Endoplasmic Reticulum01:34

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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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Destabilization of Microtubules01:45

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The destabilization of microtubules can occur during different stages of the microtubule lifecycle, such as nucleation or elongation. It can take place at either end of the microtubule or in the microtubule lattices as a whole. The lifespan of individual microtubules within a cell varies according to the cell type and stage of the cell cycle. During interphase, the lifespan of the microtubule is about 30 minutes, while during cell division, it is about 15 minutes. In axonal microtubules of...
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Drugs that Destabilize Microtubules01:10

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Microtubules are dynamic structures and can be regulated by microtubule targeting agents (MTAs). Microtubule destabilizing drugs are a class of MTAs that destabilize and prevent microtubules' polymerization. Both natural and synthetic chemicals can be found under this class of drugs. Vincristine and vinblastine, two vinca alkaloids, and colchicine were among the first to be discovered. These drugs can affect cells in various ways, either by inducing a change in cell morphology, preventing...
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Visualization of Endoplasmic Reticulum Subdomains in Cultured Cells
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MARCH6 Confers Protection Against Endoplasmic Reticulum Autophagy in Gliomas by Destabilizing FAM134B.

Yeming Zhou1, Rui Chen2, Guokun Liu3

  • 1Department of Emergency, The Fourth Affiliated Hospital of Nanjing Medical University, Nanjing, China.

Neurochemical Research
|February 9, 2026
PubMed
Summary

MARCH6 destabilizes FAM134B, inhibiting endoplasmic reticulum autophagy (ER-phagy) and promoting glioma development. Lower MARCH6 and higher FAM134B levels correlate with glioma, while MARCH6 knockdown reverses these effects.

Keywords:
Endoplasmic reticulum autophagyEndoplasmic reticulum stress responseFAM134BGliomaMARCH6Ubiquitination

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Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • Glioma development involves complex cellular mechanisms, including endoplasmic reticulum stress and autophagy.
  • Endoplasmic reticulum autophagy (ER-phagy) plays a role in cellular homeostasis and disease progression.
  • The precise regulatory mechanisms of ER-phagy in glioma remain to be fully elucidated.

Purpose of the Study:

  • To investigate the role of MARCH6 in ER-phagy during glioma development.
  • To determine how MARCH6 regulates the stability of FAM134B, a key ER-phagy receptor.
  • To explore the therapeutic potential of targeting the MARCH6-FAM134B axis in glioma.

Main Methods:

  • Expression analysis of MARCH6 and FAM134B in glioma tissues and cells.
  • Gene knockdown experiments to assess the impact on cell viability, apoptosis, and ER stress markers.
  • Examination of autophagy-related proteins, autophagosome formation, and protein ubiquitination.
  • In vivo validation using a mouse glioma model.

Main Results:

  • MARCH6 expression was inversely correlated with FAM134B expression in glioma tissues.
  • MARCH6 induced FAM134B ubiquitination and degradation, reducing its stability.
  • FAM134B knockdown suppressed glioma cell survival, ER stress, and ER-phagy, while promoting apoptosis.
  • MARCH6 knockdown reversed the effects of FAM134B knockdown, and in vivo, FAM134B knockdown suppressed tumorigenesis.

Conclusions:

  • MARCH6 destabilizes FAM134B, thereby suppressing ER stress responses and ER-phagy in glioma cells.
  • The MARCH6-FAM134B interaction represents a potential therapeutic target for glioma treatment.
  • Understanding this mechanism provides insights into glioma pathogenesis and ER-phagy regulation.