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Related Concept Videos

Hedgehog Signaling Pathway02:33

Hedgehog Signaling Pathway

The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...
Hedgehog Signaling Pathway02:33

Hedgehog Signaling Pathway

The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...
Hormones Secreted by the Stomach01:25

Hormones Secreted by the Stomach

Enteroendocrine cells, accounting for only 1% of stomach epithelial cells, play a significant role in digestion and are classified by their digestive hormone secretions.
Each of these hormones secreted by different enteroendocrine cells plays a unique role in digestion. Here are a few examples:
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.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...

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Related Experiment Video

Updated: Jun 26, 2026

Quantitative PCR-based Assay to Measure Sonic Hedgehog Signaling in Cellular Model of Ciliogenesis
07:26

Quantitative PCR-based Assay to Measure Sonic Hedgehog Signaling in Cellular Model of Ciliogenesis

Published on: January 31, 2025

Sonic hedgehog and CDX2 expression in the stomach.

Akiko Shiotani1, Tomoari Kamada, Yoshiyuki Yamanaka

  • 1Department of Internal Medicine, Kawasaki Medical School, Kurashiki City, Okayama, Japan. shiotani@med.kawasaki-m.ac.jp

Journal of Gastroenterology and Hepatology
|January 6, 2009
PubMed
Summary

Sonic hedgehog (Shh) and CDX2 are key in development and linked to cellular differentiation. Their roles in H. pylori-associated gastritis and gastric cancer progression, particularly intestinal transformation, require further investigation.

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Area of Science:

  • Developmental biology
  • Gastroenterology
  • Oncology

Background:

  • Sonic hedgehog (Shh) regulates developmental patterning, while CDX proteins are crucial for intestinal development.
  • Shh and CDX2 signaling pathways are interconnected with cellular differentiation.
  • Aberrant Shh signaling and CDX2 expression are implicated in gastric pathologies, including H. pylori-associated gastritis and gastric cancer.

Purpose of the Study:

  • To elucidate the interdependent roles of Shh and CDX2 in intestinal transformation and gastric carcinogenesis.
  • To investigate the impact of H. pylori eradication on Shh and CDX2 expression in atrophic gastritis.
  • To understand how Shh and CDX2 signaling contributes to the progression of gastric cancer.

Main Methods:

  • Analysis of Shh and CDX2 expression patterns in gastric tissues.
  • Investigation of signaling cascades involving Shh and CDX2.
  • Correlation of protein expression with disease stage and patient outcomes.

Main Results:

  • Shh and CDX2 are interdependent regulators of cellular differentiation.
  • H. pylori eradication can modify Shh loss and CDX2 aberrant expression in atrophic gastritis.
  • Abnormal Shh signaling is linked to gastric cancer proliferation, while CDX2 expression correlates with better outcomes in early carcinogenesis.

Conclusions:

  • Shh and CDX2 play critical, interconnected roles in intestinal development and differentiation.
  • Understanding their interplay is vital for addressing H. pylori-associated gastritis and gastric cancer.
  • Further research is needed to fully delineate their involvement in intestinal transformation and carcinogenesis.