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

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Inhibition of CDK Activity02:34

Inhibition of CDK Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...
Cell Specific Gene Expression01:58

Cell Specific Gene Expression

Multicellular organisms contain a variety of structurally and functionally distinct cell types, but the DNA in all the cells originated from the same parent cells. The differences in the cells can be attributed to the differential gene expression. Liver cells, whose functions include detoxification of blood, production of bile to metabolize fats, and synthesis of proteins essential for metabolism, must express a specific set of genes to perform their functions. Gene expression also varies with...
Positive Regulator Molecules02:39

Positive Regulator Molecules

Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.
Positive Regulator Molecules01:45

Positive Regulator Molecules

To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated.

You might also read

Related Articles

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

Sort by
Same author

Sex-dependent effects of maternal high-fat diet during lactation in the offspring of adult THY-Tau22 mice.

Brain : a journal of neurology·2025
Same author

Beta-cell adaptation unveiled: The role of myokines in insulin-resistant mice.

Cell reports·2025
Same author

IL-34 is expressed in the pancreas and regulates local inflammation.

Translational research : the journal of laboratory and clinical medicine·2025
Same author

Tumor-instructed glutamine synthesis in cancer-associated fibroblasts promotes pro-tumor macrophages.

The Journal of experimental medicine·2025
Same author

Mechanical and functional characterisation of a 3D porous biomimetic extracellular matrix to study insulin secretion from pancreatic β-cell lines.

In vitro models·2025
Same author

CDK4 inactivation inhibits apoptosis via mitochondria-ER contact remodeling in triple-negative breast cancer.

Nature communications·2025
Same journal

The roles and clinical significance of LINC01140 in human cancers in the real world.

Cell division·2026
Same journal

Transcription factor FOXA1 suppresses ferroptosis of cervical cancer cells by upregulating SLC7A11 expression.

Cell division·2026
Same journal

p53 overexpression counteracts the pro-survival effect of Bcl-2 by restoring MAMs function in cutaneous squamous cell carcinoma.

Cell division·2026
Same journal

Esculentoside A suppresses the malignant progression of hepatocellular carcinoma by promoting RORB.

Cell division·2026
Same journal

Linalool targets NR3C2 to inhibit NF-κB-mediated gastric cancer progression.

Cell division·2026
Same journal

The adipogenesis-related gene CEBPD as a prognostic biomarker and functional tumor suppressor in breast cancer.

Cell division·2026
See all related articles

Related Experiment Video

Updated: Jun 15, 2026

Efficient Differentiation of Pluripotent Stem Cells to NKX6-1+ Pancreatic Progenitors
09:23

Efficient Differentiation of Pluripotent Stem Cells to NKX6-1+ Pancreatic Progenitors

Published on: March 7, 2017

CDK4, pRB and E2F1: connected to insulin.

Lluis Fajas1, Emilie Blanchet, Jean-Sébastien Annicotte

  • 1IRCM, Institut de Recherche en Cancérologie de Montpellier, Montpellier, F-34298, France. lluis.fajas@inserm.fr.

Cell Division
|February 26, 2010
PubMed
Summary
This summary is machine-generated.

The study reveals that E2F1 controls insulin secretion by regulating Kir6.2 expression in pancreatic beta-cells, impacting glucose homeostasis and offering new avenues for type 2 diabetes treatment.

More Related Videos

A High-content In Vitro Pancreatic Islet β-cell Replication Discovery Platform
09:35

A High-content In Vitro Pancreatic Islet β-cell Replication Discovery Platform

Published on: July 16, 2016

Related Experiment Videos

Last Updated: Jun 15, 2026

Efficient Differentiation of Pluripotent Stem Cells to NKX6-1+ Pancreatic Progenitors
09:23

Efficient Differentiation of Pluripotent Stem Cells to NKX6-1+ Pancreatic Progenitors

Published on: March 7, 2017

A High-content In Vitro Pancreatic Islet β-cell Replication Discovery Platform
09:35

A High-content In Vitro Pancreatic Islet β-cell Replication Discovery Platform

Published on: July 16, 2016

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Metabolic Diseases

Background:

  • Pancreatic beta-cells are crucial for glucose homeostasis and insulin secretion.
  • Dysregulation of these processes is linked to type 2 diabetes.
  • E2F1's role in pancreatic beta-cell function was previously unexplored.

Discussion:

  • E2F1 directly regulates Kir6.2, a key component of the KATP channel essential for glucose-induced insulin secretion.
  • Loss of Kir6.2 expression in E2F1-deficient mice leads to impaired insulin secretion.
  • The CDK4-retinoblastoma protein (pRB)-E2F1 pathway is implicated in this regulation.

Key Insights:

  • E2F1 is highly expressed in non-proliferating pancreatic beta-cells.
  • E2F1 controls insulin secretion by modulating Kir6.2 expression.
  • Glucose and insulin regulate E2F1 activity via CDK4-dependent pRB inactivation.

Outlook:

  • The CDK4-pRB-E2F1 pathway is a novel target for treating metabolic diseases.
  • Understanding this pathway opens new therapeutic strategies for type 2 diabetes.
  • Further research can explore the therapeutic potential of modulating this pathway.