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Related Concept Videos

Protein Digestion01:02

Protein Digestion

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Protein digestion begins in the stomach, where the highly acidic environment can easily disrupt protein structure by exposing the peptide bonds of polypeptide chains. After polypeptide chains are broken into individual amino acids by a series of digestive enzymes, the amino acids are transported to the liver via the bloodstream to produce energy.
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Protein Absorption01:12

Protein Absorption

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Proteins in the gastrointestinal tract typically come from food, but they can also originate from disintegrated cells or secreted enzymes. In the stomach, the enzyme pepsin breaks down these proteins into polypeptides. The fragments then move into the duodenum as a semi-fluid mass called chyme. Pancreatic proteases, such as trypsin and chymotrypsin, and intestinal brush border enzymes like carboxypeptidases further dismantle the polypeptides into tripeptides, dipeptides, and free amino acids.
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Physiology of the Gastrointestinal System II: Digestion and Absorption01:22

Physiology of the Gastrointestinal System II: Digestion and Absorption

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The gastrointestinal (GI) tract, extending from the mouth to the anus, plays a pivotal role in the digestion and absorption of nutrients. This process involves both mechanical and chemical actions facilitated by various enzymes.
Digestion begins in the mouth, where food undergoes mechanical breakdown by chewing and combines with saliva. Salivary amylase, an enzyme in saliva, starts the breakdown of starches into maltose. The food then travels down the esophagus to the stomach.
In the stomach, a...
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Accessory Organs01:31

Accessory Organs

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Accessory organs are those that participate in the digestion of food but do not come into direct contact with it like the mouth, stomach, or intestine do. Accessory organs secrete enzymes into the digestive tract to facilitate the breakdown of food.
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Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors01:24

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

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Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI)  tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.
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Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

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Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
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Evaluation of Protein–Protein Interactions using an On-Membrane Digestion Technique
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Evaluation of Protein–Protein Interactions using an On-Membrane Digestion Technique

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ADAM Proteases and Gastrointestinal Function.

Jennifer C Jones1,2, Shelly Rustagi2, Peter J Dempsey1,2

  • 1Cell Biology, Stem Cells, and Development Program and.

Annual Review of Physiology
|December 16, 2015
PubMed
Summary
This summary is machine-generated.

A disintegrin and metalloproteinases (ADAMs) are crucial proteases regulating cell functions and communication in the gut. Aberrant ADAM activity is linked to intestinal inflammation, cancer, and tumorigenesis.

Keywords:
ADAM10ADAM17EGFRNotchTNFαintestinal stem cells

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Area of Science:

  • Biochemistry and Molecular Biology
  • Gastroenterology
  • Cell Biology

Background:

  • A disintegrin and metalloproteinases (ADAMs) are cell surface proteases involved in diverse cellular functions.
  • ADAMs mediate ectodomain shedding, modulating cell signaling and intercellular communication.
  • ADAM10 and ADAM17 are key ADAMs in the gastrointestinal tract, influencing intestinal development and stem cell maintenance.

Purpose of the Study:

  • To explore the role of ADAMs in intestinal biology.
  • To understand how ADAMs regulate signaling pathways involved in inflammation and repair.
  • To investigate the link between dysregulated ADAM activity and gastrointestinal diseases.

Main Methods:

  • Review of literature on ADAM family proteases in the gastrointestinal tract.
  • Analysis of ADAM-mediated ectodomain shedding of key signaling molecules (e.g., EGFR, TNFα receptors).
  • Examination of the role of ADAMs in intestinal development, stem cell function, and inflammatory responses.

Main Results:

  • ADAMs are critical regulators of intestinal development, cell fate, and stem cell populations.
  • ADAM-mediated shedding of EGFR/ErbB and TNFR family members influences intestinal inflammation and injury/repair.
  • Aberrant ADAM expression or activity is associated with chronic inflammation and gastrointestinal tumorigenesis.

Conclusions:

  • ADAM proteases play a central role in maintaining intestinal homeostasis.
  • Dysregulation of ADAMs contributes to the pathogenesis of inflammatory bowel disease and associated cancers.
  • Targeting ADAMs may offer therapeutic strategies for gastrointestinal disorders.