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Related Concept Videos

Hypoxia01:23

Hypoxia

Hypoxia is a medical condition characterized by an inadequate oxygen supply to body tissues. It typically manifests as a bluish discoloration of the skin and mucosae, especially in fair-skinned individuals, when hemoglobin (Hb) saturation drops below 75%.
Types of Hypoxia
There are four primary types of hypoxia, each resulting from a different cause:
1. Anemic hypoxia: This type occurs due to insufficient oxygen delivery caused by a lack of red blood cells (RBCs) or RBCs with abnormal or...
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...
Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...

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Related Experiment Video

Updated: May 27, 2026

Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells
06:23

Modeling Hypoxia/Reoxygenation Injury in Proximal Tubular Epithelial Cells

Published on: November 21, 2025

mTOR activity under hypoxia.

Douangsone D Vadysirisack1, Leif W Ellisen

  • 1Massachusetts General Hospital Cancer Center, Harvard Medical School, Boston, MA, USA.

Methods in Molecular Biology (Clifton, N.J.)
|November 30, 2011
PubMed
Summary

Hypoxia, or low oxygen, inhibits protein translation by decreasing mammalian target of rapamycin complex 1 (mTORC1) activity. The protein REDD1 is essential for this hypoxia-induced mTORC1 inhibition, with detailed molecular mechanisms now elucidated.

Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Hypoxia triggers adaptive cellular responses, including the inhibition of energy-intensive processes like protein translation.
  • Mammalian target of rapamycin complex 1 (mTORC1) is a key regulator of protein translation, and its activity decreases during hypoxia.
  • The precise molecular mechanisms underlying hypoxia-induced mTORC1 inhibition were not fully understood.

Purpose of the Study:

  • To elucidate the role of the stress-induced protein REDD1 in hypoxia-mediated mTORC1 inhibition.
  • To define the molecular mechanism by which REDD1 represses mTORC1 activity under hypoxic conditions.
  • To provide biochemical methodologies for assessing mTORC1 activity and related signaling pathways in hypoxic stress.

Main Methods:

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Oxygen-Independent Assays to Measure Mitochondrial Function in Mammals

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Co-immunoprecipitation Assay Using Endogenous Nuclear Proteins from Cells Cultured Under Hypoxic Conditions
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Co-immunoprecipitation Assay Using Endogenous Nuclear Proteins from Cells Cultured Under Hypoxic Conditions

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  • Biochemical assays to measure kinase activity of mTORC1.
  • Western blotting to monitor signaling components upstream and downstream of mTORC1.
  • Cellular studies using REDD1 as a model system to investigate hypoxic stress response.

    • Main Results:

    • Demonstrated that the stress-induced protein REDD1 is essential for regulating mTORC1 activity during hypoxia.
    • Elucidated the molecular mechanism through which REDD1 represses mTORC1 activity under hypoxic stress.
    • Established methodologies to assess mTORC1 signaling in the context of hypoxic stress.

    Conclusions:

    • REDD1 plays a critical role in the adaptive response to hypoxia by inhibiting mTORC1.
    • Understanding the REDD1-mTORC1 axis provides insight into cellular adaptation to low oxygen.
    • The described biochemical methods are valuable tools for studying mTORC1 dysregulation in hypoxic conditions.