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Updated: Jun 1, 2026

Co-immunoprecipitation Assay Using Endogenous Nuclear Proteins from Cells Cultured Under Hypoxic Conditions
Published on: August 2, 2018
Hypoxia-driven cell motility reflects the interplay between JMY and HIF-1α
A S Coutts1, I M Pires, L Weston
1Laboratory of Cancer Biology, Department of Oncology, University of Oxford, Oxon, UK.
Abstract:
Junction-mediating and regulatory protein (JMY) is a novel p53 cofactor that regulates p53 activity during stress. JMY interacts with p300/CBP, which are ubiquitous transcriptional co-activators that interact with a variety of sequence-specific transcription factors, including hypoxia-inducible factor-1α (HIF-1α). In addition, JMY is an actin-nucleating protein, which, through its WH2 domains, stimulates cell motility. In this study, we show that JMY is upregulated during hypoxia in a HIF-1α-dependent manner. The JMY gene contains HIF-responsive elements in its promoter region and HIF-1α is recruited to its promoter during hypoxia. HIF-1α drives transcription of JMY, which accounts for its induction under hypoxia. Moreover, the enhanced cell motility and invasion that occurs during hypoxia requires JMY, as depleting JMY under hypoxic conditions causes decreased cell motility. Our results establish the interplay between JMY and HIF-1α as a new mechanism that controls cell motility under hypoxic stress.
Insights
Junction-mediating and regulatory protein (JMY) is upregulated by hypoxia-inducible factor-1α (HIF-1α). This interaction is crucial for enhancing cell motility and invasion during hypoxic stress.
Area of Science:
- Molecular Biology
- Cell Biology
- Biochemistry
Background:
- Junction-mediating and regulatory protein (JMY) is a p53 cofactor regulating p53 activity during stress.
- JMY interacts with p300/CBP, transcriptional co-activators involved with factors like hypoxia-inducible factor-1α (HIF-1α).
- JMY functions as an actin-nucleating protein, promoting cell motility via its WH2 domains.
Purpose of the Study:
- To investigate the regulation of JMY during hypoxia.
- To determine the role of JMY in hypoxia-induced cell motility and invasion.
- To elucidate the interplay between JMY and HIF-1α in cellular responses to hypoxic stress.
Main Methods:
- Analyzing JMY gene promoter for HIF-responsive elements.
- Assessing HIF-1α recruitment to the JMY promoter under hypoxia.
- Measuring JMY expression levels during hypoxic conditions.
- Evaluating cell motility and invasion upon JMY depletion under hypoxia.
Main Results:
- JMY is upregulated during hypoxia in a HIF-1α-dependent manner.
- HIF-1α binds to the JMY promoter, driving its transcription.
- Hypoxia-induced cell motility and invasion are dependent on JMY.
- Depletion of JMY significantly reduces cell motility under hypoxic conditions.
Conclusions:
- Establishes a novel mechanism where JMY and HIF-1α interplay to control cell motility under hypoxic stress.
- Highlights JMY as a key mediator of cellular adaptation to hypoxia.
- Provides insights into the regulation of cell motility in response to environmental stress.
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