Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Allosteric Regulation01:08

Allosteric Regulation

58.1K
Allosteric regulation of enzymes occurs when the binding of an effector molecule to a site that is different from the active site causes a change in the enzymatic activity. This alternate site is called an allosteric site, and an enzyme can contain more than one of these sites. Allosteric regulation can either be positive or negative, resulting in an increase or decrease in enzyme activity. Most enzymes that display allosteric regulation are metabolic enzymes involved in the degradation or...
58.1K
Insulin: Biosynthesis, Chemistry, and Preparation01:25

Insulin: Biosynthesis, Chemistry, and Preparation

393
The endoplasmic reticulum (ER) of pancreatic β-cells synthesizes preproinsulin, which consists of a signal peptide, A and B chains, and a C-peptide. Preproinsulin is then cleaved and folded into proinsulin, which translocates to the Golgi apparatus for sorting and packaging into secretory granules. In these granules, enzymatic clipping generates insulin and C-peptide.
Damage or functional impairment of β-cells inhibits insulin production, leading to diabetes. Diabetes treatment...
393
Glucagon-like Receptor Agonists01:24

Glucagon-like Receptor Agonists

334
Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by...
334
Insulin: The Receptor and Signaling Pathways01:28

Insulin: The Receptor and Signaling Pathways

1.2K
Insulin action is mediated through a receptor tyrosine kinase, akin to the IGF-1 receptor. The number of receptors per cell varies significantly, from 40 on erythrocytes to 300,000 on adipocytes and hepatocytes. The insulin receptor consists of linked α/β subunit dimers, forming a heterotetramer glycoprotein with two extracellular α subunits and two β subunits spanning the membrane. The α subunits inhibit the inherent tyrosine kinase activity of the β subunits, but...
1.2K
Enzyme Inhibition01:30

Enzyme Inhibition

78.5K
Inhibitors are molecules that reduce enzyme activity by binding to the enzyme. In a normally functioning cell, enzymes are regulated by a variety of inhibitors. Drugs and other toxins can also inhibit enzymes. Some inhibitors bind to the enzyme’s active site, while others inhibit enzymatic activity by binding to other sites on the protein structure.
78.5K
Glucose Homeostasis: Pancreatic Islets and Insulin Secretion01:27

Glucose Homeostasis: Pancreatic Islets and Insulin Secretion

1.3K
The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
Insulin and C-peptide are...
1.3K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Switching to aflibercept 8 mg in neovascular age-related macular degeneration: real-world outcomes according to switch indication.

Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie·2026
Same author

Pachy-reticular pseudodrusen associated with pachyvitelliform maculopathy.

Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie·2026
Same author

OCT predictors discerning progression to neovascular vs atrophic age-related macular degeneration.

Eye (London, England)·2026
Same author

Memantine prevents acute stress-induced memory deficits by reversing sex-dependent pathophysiological glutamatergic alterations in the dorsal hippocampus.

British journal of pharmacology·2026
Same author

Schlaegel lines: History, etiology, multimodal imaging, and differential diagnosis of curvilinear streaks in chorioretinal disorders.

Survey of ophthalmology·2026
Same author

Prognostic Imaging Biomarkers in Diabetic Macular Edema Treated with Anti-VEGF: A Multicenter AI Perspective.

Ophthalmology and therapy·2026

Related Experiment Video

Updated: Jul 12, 2025

An In Ovo Model for Testing Insulin-mimetic Compounds
06:09

An In Ovo Model for Testing Insulin-mimetic Compounds

Published on: April 23, 2018

10.7K

The Insulin-Degrading Enzyme from Structure to Allosteric Modulation: New Perspectives for Drug Design.

Grazia Raffaella Tundo1, Giuseppe Grasso2, Marco Persico3

  • 1Department of Clinical Science and Traslational Medicine, University of Rome Tor Vergata, Via Della Ricerca Scientifica 1, 00133 Rome, Italy.

Biomolecules
|October 28, 2023
PubMed
Summary

The insulin-degrading enzyme (IDE) degrades insulin and amyloid peptides. Understanding its structure and diverse functions could unlock new treatments for diabetes and Alzheimer's disease.

Keywords:
Alzheimer’s diseaseallosterydiabetesinsulininsulin-degrading enzymeproteasome

More Related Videos

Homogeneous Time-resolved Förster Resonance Energy Transfer-based Assay for Detection of Insulin Secretion
07:30

Homogeneous Time-resolved Förster Resonance Energy Transfer-based Assay for Detection of Insulin Secretion

Published on: May 10, 2018

9.3K
Screening Traditional Chinese Medicine Compounds for Inhibiting UCHL3 Activity Based on Molecular Docking and Deubiquitinating Enzyme Probe Technology
10:25

Screening Traditional Chinese Medicine Compounds for Inhibiting UCHL3 Activity Based on Molecular Docking and Deubiquitinating Enzyme Probe Technology

Published on: November 22, 2024

312

Related Experiment Videos

Last Updated: Jul 12, 2025

An In Ovo Model for Testing Insulin-mimetic Compounds
06:09

An In Ovo Model for Testing Insulin-mimetic Compounds

Published on: April 23, 2018

10.7K
Homogeneous Time-resolved Förster Resonance Energy Transfer-based Assay for Detection of Insulin Secretion
07:30

Homogeneous Time-resolved Förster Resonance Energy Transfer-based Assay for Detection of Insulin Secretion

Published on: May 10, 2018

9.3K
Screening Traditional Chinese Medicine Compounds for Inhibiting UCHL3 Activity Based on Molecular Docking and Deubiquitinating Enzyme Probe Technology
10:25

Screening Traditional Chinese Medicine Compounds for Inhibiting UCHL3 Activity Based on Molecular Docking and Deubiquitinating Enzyme Probe Technology

Published on: November 22, 2024

312

Area of Science:

  • Biochemistry
  • Enzymology
  • Neuroscience

Background:

  • The insulin-degrading enzyme (IDE) is a zinc-dependent metallopeptidase.
  • IDE was initially identified for its role in insulin degradation.
  • IDE also degrades amyloidogenic peptides, including amyloid-beta (Aβ).

Purpose of the Study:

  • To elucidate the structure-function relationship of IDE.
  • To clarify IDE's role in amyloidogenic protein degradation.
  • To explore novel non-proteolytic functions of IDE.

Main Methods:

  • Structural analysis of IDE.
  • Enzymatic assays for peptide degradation.
  • Investigation of non-proteolytic functions.

Main Results:

  • IDE possesses an atypical clamshell structure.
  • IDE's role in amyloidogenic protein degradation requires further definition.
  • Emerging evidence suggests non-proteolytic functions for IDE.

Conclusions:

  • Understanding IDE's unique structure and multifunctional activities is crucial.
  • Further research into IDE's structure-function relationship may resolve biological paradoxes.
  • Novel therapeutic strategies targeting IDE may emerge from its multifaceted roles.