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Related Concept Videos

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...
Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
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GPCRs Regulate Adenylyl Cylase Activity01:09

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
Two...
Selectins01:25

Selectins

Cell adhesion is  an essential aspect of multicellularity. While stable cell interactions usually occur between cells of the same type, transient cell interactions occur between cells of different tissue types, such as between neutrophils and endothelial cells. Selectins are one class of cell adhesion molecules (CAMs) that bind carbohydrate ligands to form transient cell adhesion. They are rod-like proteins with a long extracellular part of variable length ending with the lectin domain, which...
Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
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Related Experiment Videos

Galectin-8 Modulates Membrane CD44v Localization and Tempers STAT3 Signaling in Gastric Metaplasia.

Xiaobo Lin, Xuemei Liu, Gabriel Nicolazzi

    Biorxiv : the Preprint Server for Biology
    |June 22, 2026
    PubMed
    Summary
    This summary is machine-generated.

    Galectin-8 is crucial for localizing CD44 variants in gastric metaplasia. Its absence leads to increased STAT3 signaling, potentially explaining poor prognosis in gastric cancer.

    Related Experiment Videos

    Area of Science:

    • Biochemistry
    • Molecular Biology
    • Gastroenterology

    Background:

    • Galectin-8 binds specific glycotopes, including those on CD44 variants (CD44v).
    • CD44v are biomarkers for metaplasia and cancer, modulating STAT3 signaling.
    • Gastric metaplasia involves changes in cell surface glycoproteins and signaling pathways.

    Purpose of the Study:

    • To investigate the role of galectin-8 in gastric metaplasia.
    • To determine if galectin-8 interacts with CD44v.
    • To assess the impact of galectin-8 on STAT3 signaling in metaplasia.

    Main Methods:

    • Utilized a chemically induced murine model for gastric spasmolytic polypeptide expressing metaplasia (SPEM).
    • Compared wild-type mice with galectin-8 knockout (Lgals8 -/-) mice.
    • Analyzed membrane localization of CD44v and STAT3 phosphorylation (pSTAT3) in metaplastic glands.

    Main Results:

    • Galectin-8 is essential for CD44v membrane localization on SPEM cells.
    • Absence of galectin-8 resulted in increased nuclear pSTAT3 in metaplastic glands.
    • STAT3 signaling was derepressed in galectin-8 deficient mice, particularly in the gland neck.

    Conclusions:

    • Galectin-8 restrains CD44v-mediated STAT3 signaling in gastric metaplasia.
    • The interaction between galectin-8 and CD44v is critical for regulating this pathway.
    • Low galectin-8 levels may correlate with a worse prognosis in gastric cancer due to STAT3 pathway dysregulation.