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

mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
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...
Translocation of Proteins into the Mitochondria01:19

Translocation of Proteins into the Mitochondria

Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
Sorting of outer membrane proteins:
Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...
Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
Regulation of Metabolism01:19

Regulation of Metabolism

Cellular needs and conditions vary from cell to cell and change within individual cells over time. For example, the required enzymes and energetic demands of stomach cells are different from those of fat storage cells, skin cells, blood cells, and nerve cells. Furthermore, a digestive cell works much harder to process and break down nutrients during the time that closely follows a meal compared with many hours after a meal. As these cellular demands and conditions vary, so do the amounts and...

You might also read

Related Articles

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

Sort by
Same author

Pharmacological profiling of intravenous MP-04: sustained NAD<sup>+</sup> augmentation, immune modulation, and renal protection in preclinical models.

Frontiers in pharmacology·2026
Same author

Comprehensive Metabolomic Analysis of Saliva Using SWATH-DIA Reveals Systemic Metabolic Adaptations to Exercise.

ACS omega·2026
Same author

Dose-Dependent Effects of Dihydronicotinamide Riboside on Human Engineered Skeletal Muscle Development.

ACS biomaterials science & engineering·2026
Same author

Mechanistic insights into the association and activation of the SARS-CoV-2 2'-O-Methyltransferase (NSP16).

bioRxiv : the preprint server for biology·2026
Same author

Discovery of molecular glues that bind FKBP12 and structurally distinct targets using DNA-encoded libraries.

Nature communications·2026
Same author

Computational microbiology: Where is artificial intelligence addressing the barriers to large-scale simulations of bacterial cell envelopes?

Current opinion in structural biology·2026
Same journal

Chemotactic self-organization captures the dynamics of mammalian hair follicle patterning.

Proceedings of the National Academy of Sciences of the United States of America·2026
Same journal

Tomographic imaging of superconducting order using particle-hole interference.

Proceedings of the National Academy of Sciences of the United States of America·2026
Same journal

Inhibitory potential of autologous neutralizing antibodies sets quantitative limits on the rebound-competent HIV-1 reservoir.

Proceedings of the National Academy of Sciences of the United States of America·2026
Same journal

Inferring epidemiological parameters under an infectious phylogeography model with visitor dynamics.

Proceedings of the National Academy of Sciences of the United States of America·2026
Same journal

Analytical modeling for suction cup designs for skin-interfaced wearable devices.

Proceedings of the National Academy of Sciences of the United States of America·2026
Same journal

Improving cell-free metabolism through direct integration of artificial respiratory chains.

Proceedings of the National Academy of Sciences of the United States of America·2026
See all related articles

Related Experiment Video

Updated: Jun 17, 2026

Isolation of Primary Mouse Hepatocytes for Nascent Protein Synthesis Analysis by Non-radioactive L-azidohomoalanine Labeling Method
08:04

Isolation of Primary Mouse Hepatocytes for Nascent Protein Synthesis Analysis by Non-radioactive L-azidohomoalanine Labeling Method

Published on: October 23, 2018

Direct control of mitochondrial function by mTOR.

Arvind Ramanathan1, Stuart L Schreiber

  • 1Chemical Biology Program, Broad Institute of Harvard and Massachusetts Institute of Technology, 7 Cambridge Center, Cambridge, MA 02142, USA.

Proceedings of the National Academy of Sciences of the United States of America
|January 19, 2010
PubMed
Summary
This summary is machine-generated.

The mechanistic target of rapamycin (mTOR) pathway rapidly influences cellular metabolism in leukemia. Inhibiting mTOR boosts aerobic glycolysis and increases leukemic cell dependence on this pathway for survival.

More Related Videos

Experimental Approaches to Study Mitochondrial Localization and Function of a Nuclear Cell Cycle Kinase, Cdk1
13:15

Experimental Approaches to Study Mitochondrial Localization and Function of a Nuclear Cell Cycle Kinase, Cdk1

Published on: February 25, 2016

Isolation and Functional Analysis of Mitochondria from Cultured Cells and Mouse Tissue
09:27

Isolation and Functional Analysis of Mitochondria from Cultured Cells and Mouse Tissue

Published on: March 23, 2015

Related Experiment Videos

Last Updated: Jun 17, 2026

Isolation of Primary Mouse Hepatocytes for Nascent Protein Synthesis Analysis by Non-radioactive L-azidohomoalanine Labeling Method
08:04

Isolation of Primary Mouse Hepatocytes for Nascent Protein Synthesis Analysis by Non-radioactive L-azidohomoalanine Labeling Method

Published on: October 23, 2018

Experimental Approaches to Study Mitochondrial Localization and Function of a Nuclear Cell Cycle Kinase, Cdk1
13:15

Experimental Approaches to Study Mitochondrial Localization and Function of a Nuclear Cell Cycle Kinase, Cdk1

Published on: February 25, 2016

Isolation and Functional Analysis of Mitochondria from Cultured Cells and Mouse Tissue
09:27

Isolation and Functional Analysis of Mitochondria from Cultured Cells and Mouse Tissue

Published on: March 23, 2015

Area of Science:

  • Cellular Metabolism
  • Cancer Biology
  • Molecular Signaling

Background:

  • The mechanistic target of rapamycin (mTOR) is a key regulator of cell growth and metabolism.
  • Understanding mTOR's rapid regulatory mechanisms in cancer is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the immediate effects of mTOR inhibition on cellular metabolism in leukemic cells.
  • To explore the role of posttranslational modifications in mTOR-mediated metabolic control.
  • To identify molecular interactions of mTOR within cellular compartments relevant to metabolism.

Main Methods:

  • Metabolic profiling of leukemic cells.
  • Application of small-molecule inhibitors, including rapamycin.
  • In vitro kinase assays.
  • Analysis of protein-protein interactions (mTOR, Bcl-xl, VDAC1).

Main Results:

  • Inhibition of the FKBP12/rapamycin-sensitive mTOR subset rapidly enhanced aerobic glycolysis and decreased mitochondrial respiration in leukemic cells.
  • mTOR forms a complex with Bcl-xl and VDAC1; Bcl-xl is a direct kinase substrate of mTOR.
  • mTOR regulates the association of Bcl-xl within the mTOR complex.
  • mTOR inhibition induced leukemic cell dependence on aerobic glycolysis, potentiated by 2-deoxyglucose.

Conclusions:

  • mTOR exerts rapid, posttranslational control over cellular metabolism, particularly aerobic glycolysis, in leukemic cells.
  • The mTOR-Bcl-xl interaction is a key component of this rapid metabolic regulation.
  • Targeting mTOR and glycolysis simultaneously may represent a viable therapeutic strategy for leukemia.