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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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MAPK Signaling Cascades01:07

MAPK Signaling Cascades

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Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
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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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Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

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Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
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Related Experiment Video

Updated: Jan 28, 2026

Visualization of Endoplasmic Reticulum Subdomains in Cultured Cells
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After Traumatic Brain Injury, EPHA4 Enhances Endoplasmic Reticulum Stress to Promote M1 Microglial Polarization

Yang Tan1, Jing Xia1, Mingwei Liu2

  • 1Emergency Medicine, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, China, kmmc.cn.

Mediators of Inflammation
|January 26, 2026
PubMed
Summary

Ephrin receptor A4 (EPHA4) promotes microglial M1 polarization after traumatic brain injury (TBI) by enhancing endoplasmic reticulum stress via the MAPK signaling pathway. Inhibiting EPHA4 may offer a therapeutic strategy for TBI treatment.

Keywords:
EPHA4M1 polarization of microgliaMAPK signaling pathwaysMI-5595023endoplasmic reticulum stresstraumatic brain injury

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Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Traumatic brain injury (TBI) is a leading cause of global disability and mortality.
  • Neuroinflammation, driven by M1-type microglia, is a critical factor in TBI pathogenesis.
  • The precise mechanisms regulating M1 microglia polarization post-TBI remain incompletely understood.

Purpose of the Study:

  • To investigate the role of ephrin receptor A4 (EPHA4) in M1 microglia polarization following TBI.
  • To elucidate the molecular mechanisms underlying EPHA4-mediated microglial activation in TBI.

Main Methods:

  • Established a TBI rat model using controlled cortical impact (CCI).
  • Induced M1 microglia polarization in vitro using lipopolysaccharide (LPS).
  • Utilized transcriptome sequencing, RT-qPCR, Western blot, ELISA, immunofluorescence, HE staining, and Evans blue staining to assess molecular and tissue changes.

Main Results:

  • EPHA4 expression was upregulated in TBI rat brains.
  • Inhibition of EPHA4 with KYL peptide ameliorated TBI progression, reduced pro-inflammatory cytokines, and suppressed M1 microglia polarization.
  • EPHA4 was found to promote M1 microglia polarization by enhancing endoplasmic reticulum stress (ERS) and activating the MAPK signaling pathway.

Conclusions:

  • The EPHA4/MAPK signaling axis is a key regulator of microglial M1 polarization in TBI.
  • Targeting the EPHA4/MAPK pathway presents a potential therapeutic strategy for TBI management.