Hypoxia Inducible Factors
Hypoxia Inducible Factors - Related Videos
02:54
Hypoxia-Induced Climbing Behavior of Drosophila melanogaster
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2026
Source:Siddarth Gunnala1, Nafisa M. Jadavji2,3,41Department of Biomedical Sciences, Midwestern University, Glendale, AZ, USA2Division of Integrative and Molecular Physiology, Department of Biomedical Sciences, Southern University of Illinois, Carbondale, IL, USA3Department of Child Health, College of Medicine Phoenix, University of Arizona, Phoenix, AZ, USA4Department of Neuroscience, Carleton University, Ottawa, ON, CanadaThis video demonstrates hypoxia-induced climbing behavior in Drosophila...
02:42
Inducing Thrombotic Stroke Through Hypoxia and Ischemia in a Mouse Model
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2025
This video demonstrates the procedure of replicating a thrombotic stroke in a mouse model by blocking the right common carotid artery and exposing the mouse to a low-oxygen environment. This process reduces blood and oxygen flow to the brain, causing blood clot formation and brain damage.
06:43
Imaging Brain Damage Induced by Cerebral Hypoxia-Ischemia in a Mouse Model
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2025
Source: Ouyang, Y., et al. Simultaneous PET/MRI Imaging During Mouse Cerebral Hypoxia-ischemia. J. Vis. Exp. (2015)This video demonstrates a technique to assess cerebral hypoxia injury via simultaneous positron-emission tomography (PET) and magnetic resonance imaging (MRI). An anesthetized mouse undergoes common carotid artery (CCA) ligation, reducing blood flow to one brain hemisphere and predisposing it to hypoxia-induced injury. PET and MRI imaging evaluate glucose metabolism and structural...
07:01
Induction and Testing of Hypoxia in Cell Culture
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Cited by 247 •
2011
Here we propose simple methods to induce hypoxia in cell cultures and simple tests to evaluate the hypoxic status of the cultures.
10:41
A Hypoxia-Reoxygenation Injury Model in Self-Assembling Human Cardioids
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2026
Self-assembling human cardiac organoids (hCOs) are an emerging system for modeling human cardiac development and disease. Here, a methodology for generating and injuring hCOs with hypoxia-reoxygenation and details of expected histological and functional outcomes after injury are provided.
FAQs
Prolyl hydroxylation acts as an oxygen-dependent marking step. When oxygen is available, this modification enables recognition of HIF-alpha by the von Hippel-Lindau protein, which leads to degradation of the subunit. When oxygen becomes limited, hydroxylation decreases, so HIF-alpha is no longer efficiently targeted for removal and can accumulate to transmit a hypoxic response.
Stabilized HIF-alpha pairs with HIF-beta to form a functional transcription-factor complex. This complex binds hypoxia-response elements, specialized DNA regulatory sequences associated with oxygen-sensitive gene control. Binding changes transcription of selected target genes, linking the initial oxygen-sensing event to coordinated cellular responses rather than to an isolated change in one protein.
Hypoxia Inducible Factors coordinate several programs that help cells function when oxygen is scarce. Their target genes can promote glycolysis, support angiogenesis, stimulate erythropoiesis, and enhance cellular survival. Together, these outputs address energy production, blood-vessel growth, oxygen transport, and resistance to low-oxygen stress, illustrating how one signaling system produces multiple adaptive effects.
Hypoxia-response elements provide the DNA sites through which the HIF-alpha and HIF-beta complex selects regulated genes. Their role connects transcription-factor stabilization to specific biological outputs, including metabolic, vascular, blood-forming, and survival responses. Consequently, HIF activity depends not only on alpha-subunit stability but also on successful DNA binding at these regulatory sequences.
A useful conceptual workflow follows the pathway from oxygen availability to outcome. First, compare normal oxygen with hypoxic conditions; then examine prolyl hydroxylation, HIF-alpha recognition by von Hippel-Lindau protein, alpha-subunit stability, dimerization with HIF-beta, DNA binding, and downstream gene regulation. This sequence helps connect molecular events with physiological adaptation or disease-related changes.
HIF research provides a framework for examining how oxygen-sensitive regulation contributes to cancer, ischemia, and anemia. In these contexts, investigators can relate altered oxygen conditions or signaling to changes in glycolysis, angiogenesis, erythropoiesis, and cellular survival. The resulting knowledge supports investigation of oxygen-sensing pathways as potential targets for therapies that modulate HIF-related responses.