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  1. Article ; Online: Hypoxia Hits Glucose Metabolism in the Guts.

    Taylor, Cormac T

    Cellular and molecular gastroenterology and hepatology

    2022  Volume 13, Issue 4, Page(s) 1263–1264

    MeSH term(s) Gastrointestinal Microbiome ; Glucose ; Humans ; Hypoxia
    Chemical Substances Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2022-02-12
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 2819778-1
    ISSN 2352-345X ; 2352-345X
    ISSN (online) 2352-345X
    ISSN 2352-345X
    DOI 10.1016/j.jcmgh.2022.01.021
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  2. Article: Hypoxia research, where to now?

    Ortmann, Brian M / Taylor, Cormac T / Rocha, Sonia

    Trends in biochemical sciences

    2024  

    Abstract: Investigating how cells and organisms sense and respond to ... ...

    Abstract Investigating how cells and organisms sense and respond to O
    Language English
    Publishing date 2024-04-09
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 194216-5
    ISSN 1362-4326 ; 0968-0004 ; 0376-5067
    ISSN (online) 1362-4326
    ISSN 0968-0004 ; 0376-5067
    DOI 10.1016/j.tibs.2024.03.008
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  3. Article ; Online: Hypoxia-inducible factor-driven glycolytic adaptations in host-microbe interactions.

    DeMichele, Emily / Buret, Andre G / Taylor, Cormac T

    Pflugers Archiv : European journal of physiology

    2024  

    Abstract: Mammalian cells utilize glucose as a primary carbon source to produce energy for most cellular functions. However, the bioenergetic homeostasis of cells can be perturbed by environmental alterations, such as changes in oxygen levels which can be ... ...

    Abstract Mammalian cells utilize glucose as a primary carbon source to produce energy for most cellular functions. However, the bioenergetic homeostasis of cells can be perturbed by environmental alterations, such as changes in oxygen levels which can be associated with bacterial infection. Reduction in oxygen availability leads to a state of hypoxia, inducing numerous cellular responses that aim to combat this stress. Importantly, hypoxia strongly augments cellular glycolysis in most cell types to compensate for the loss of aerobic respiration. Understanding how this host cell metabolic adaptation to hypoxia impacts the course of bacterial infection will identify new anti-microbial targets. This review will highlight developments in our understanding of glycolytic substrate channeling and spatiotemporal enzymatic organization in response to hypoxia, shedding light on the integral role of the hypoxia-inducible factor (HIF) during host-pathogen interactions. Furthermore, the ability of intracellular and extracellular bacteria (pathogens and commensals alike) to modulate host cellular glucose metabolism will be discussed.
    Language English
    Publishing date 2024-04-04
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 6380-0
    ISSN 1432-2013 ; 0031-6768
    ISSN (online) 1432-2013
    ISSN 0031-6768
    DOI 10.1007/s00424-024-02953-w
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  4. Article: Hypoxia in the Gut.

    Taylor, Cormac T

    Cellular and molecular gastroenterology and hepatology

    2017  Volume 5, Issue 1, Page(s) 61–62

    Language English
    Publishing date 2017-09-19
    Publishing country United States
    Document type Editorial
    ISSN 2352-345X
    ISSN 2352-345X
    DOI 10.1016/j.jcmgh.2017.09.005
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  5. Article ; Online: The effect of HIF on metabolism and immunity.

    Taylor, Cormac T / Scholz, Carsten C

    Nature reviews. Nephrology

    2022  Volume 18, Issue 9, Page(s) 573–587

    Abstract: Cellular hypoxia occurs when the demand for sufficient molecular oxygen needed to produce the levels of ATP required to perform physiological functions exceeds the vascular supply, thereby leading to a state of oxygen depletion with the associated risk ... ...

    Abstract Cellular hypoxia occurs when the demand for sufficient molecular oxygen needed to produce the levels of ATP required to perform physiological functions exceeds the vascular supply, thereby leading to a state of oxygen depletion with the associated risk of bioenergetic crisis. To protect against the threat of hypoxia, eukaryotic cells have evolved the capacity to elicit oxygen-sensitive adaptive transcriptional responses driven primarily (although not exclusively) by the hypoxia-inducible factor (HIF) pathway. In addition to the canonical regulation of HIF by oxygen-dependent hydroxylases, multiple other input signals, including gasotransmitters, non-coding RNAs, histone modifiers and post-translational modifications, modulate the nature of the HIF response in discreet cell types and contexts. Activation of HIF induces various effector pathways that mitigate the effects of hypoxia, including metabolic reprogramming and the production of erythropoietin. Drugs that target the HIF pathway to induce erythropoietin production are now approved for the treatment of chronic kidney disease-related anaemia. However, HIF-dependent changes in cell metabolism also have profound implications for functional responses in innate and adaptive immune cells, and thereby heavily influence immunity and the inflammatory response. Preclinical studies indicate a potential use of HIF therapeutics to treat inflammatory diseases, such as inflammatory bowel disease. Understanding the links between HIF, cellular metabolism and immunity is key to unlocking the full therapeutic potential of drugs that target the HIF pathway.
    MeSH term(s) Cell Hypoxia ; Erythropoietin/metabolism ; Erythropoietin/therapeutic use ; Humans ; Hypoxia/metabolism ; Kidney/metabolism ; Oxygen/metabolism
    Chemical Substances Erythropoietin (11096-26-7) ; Oxygen (S88TT14065)
    Language English
    Publishing date 2022-06-20
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2490366-8
    ISSN 1759-507X ; 1759-5061
    ISSN (online) 1759-507X
    ISSN 1759-5061
    DOI 10.1038/s41581-022-00587-8
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  6. Article ; Online: Intracellular energy production and distribution in hypoxia.

    Flood, Darragh / Lee, Eun Sang / Taylor, Cormac T

    The Journal of biological chemistry

    2023  Volume 299, Issue 9, Page(s) 105103

    Abstract: The hydrolysis of ATP is the primary source of metabolic energy for eukaryotic cells. Under physiological conditions, cells generally produce more than sufficient levels of ATP to fuel the active biological processes necessary to maintain homeostasis. ... ...

    Abstract The hydrolysis of ATP is the primary source of metabolic energy for eukaryotic cells. Under physiological conditions, cells generally produce more than sufficient levels of ATP to fuel the active biological processes necessary to maintain homeostasis. However, mechanisms underpinning the distribution of ATP to subcellular microenvironments with high local demand remain poorly understood. Intracellular distribution of ATP in normal physiological conditions has been proposed to rely on passive diffusion across concentration gradients generated by ATP producing systems such as the mitochondria and the glycolytic pathway. However, subcellular microenvironments can develop with ATP deficiency due to increases in local ATP consumption. Alternatively, ATP production can be reduced during bioenergetic stress during hypoxia. Mammalian cells therefore need to have the capacity to alter their metabolism and energy distribution strategies to compensate for local ATP deficits while also controlling ATP production. It is highly likely that satisfying the bioenergetic requirements of the cell involves the regulated distribution of ATP producing systems to areas of high ATP demand within the cell. Recently, the distribution (both spatially and temporally) of ATP-producing systems has become an area of intense investigation. Here, we review what is known (and unknown) about intracellular energy production and distribution and explore potential mechanisms through which this targeted distribution can be altered in hypoxia, with the aim of stimulating investigation in this important, yet poorly understood field of research.
    MeSH term(s) Animals ; Humans ; Adenosine Triphosphate/biosynthesis ; Adenosine Triphosphate/metabolism ; Energy Metabolism ; Mitochondria/metabolism ; Cell Hypoxia/physiology ; Adaptation, Physiological
    Chemical Substances Adenosine Triphosphate (8L70Q75FXE)
    Language English
    Publishing date 2023-07-26
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1016/j.jbc.2023.105103
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  7. Article ; Online: SUMOylation indirectly suppresses activity of the HIF-1α pathway in intestinal epithelial cells.

    Malkov, Mykyta I / Flood, Darragh / Taylor, Cormac T

    The Journal of biological chemistry

    2023  Volume 299, Issue 11, Page(s) 105280

    Abstract: The hypoxia-inducible factor (HIF) is a master regulator of the cellular transcriptional response to hypoxia. While the oxygen-sensitive regulation of HIF-1α subunit stability via the ubiquitin-proteasome pathway has been well described, less is known ... ...

    Abstract The hypoxia-inducible factor (HIF) is a master regulator of the cellular transcriptional response to hypoxia. While the oxygen-sensitive regulation of HIF-1α subunit stability via the ubiquitin-proteasome pathway has been well described, less is known about how other oxygen-independent post-translational modifications impact the HIF pathway. SUMOylation, the attachment of SUMO (small ubiquitin-like modifier) proteins to a target protein, regulates the HIF pathway, although the impact of SUMO on HIF activity remains controversial. Here, we examined the effects of SUMOylation on the expression pattern of HIF-1α in response to pan-hydroxylase inhibitor dimethyloxalylglycine (DMOG) in intestinal epithelial cells. We evaluated the effects of SUMO-1, SUMO-2, and SUMO-3 overexpression and inhibition of SUMOylation using a novel selective inhibitor of the SUMO pathway, TAK-981, on the sensitivity of HIF-1α in Caco-2 intestinal epithelial cells. Our findings demonstrate that treatment with TAK-981 decreases global SUMO-1 and SUMO-2/3 modification and enhances HIF-1α protein levels, whereas SUMO-1 and SUMO-2/3 overexpression results in decreased HIF-1α protein levels in response to DMOG. Reporter assay analysis demonstrates reduced HIF-1α transcriptional activity in cells overexpressing SUMO-1 and SUMO-2/3, whereas pretreatment with TAK-981 increased HIF-1α transcriptional activity in response to DMOG. In addition, HIF-1α nuclear accumulation was decreased in cells overexpressing SUMO-1. Importantly, we showed that HIF-1α is not directly SUMOylated, but that SUMOylation affects HIF-1α stability and activity indirectly. Taken together, our results indicate that SUMOylation indirectly suppresses HIF-1α protein stability, transcriptional activity, and nuclear accumulation in intestinal epithelial cells.
    MeSH term(s) Humans ; Caco-2 Cells ; Epithelial Cells/metabolism ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Sumoylation/drug effects ; Intestinal Mucosa/cytology ; Intestinal Mucosa/metabolism ; Gene Expression Regulation/drug effects ; Enzyme Inhibitors/pharmacology ; Small Ubiquitin-Related Modifier Proteins/genetics ; Small Ubiquitin-Related Modifier Proteins/metabolism
    Chemical Substances Hypoxia-Inducible Factor 1, alpha Subunit ; oxalylglycine (VVW38EB8YS) ; Enzyme Inhibitors ; Small Ubiquitin-Related Modifier Proteins
    Language English
    Publishing date 2023-09-22
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1016/j.jbc.2023.105280
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  8. Article: Controlling pericellular oxygen tension in cell culture reveals distinct breast cancer responses to low oxygen tensions.

    Rogers, Zachary J / Colombani, Thibault / Khan, Saad / Bhatt, Khushbu / Nukovic, Alexandra / Zhou, Guanyu / Woolston, Benjamin M / Taylor, Cormac T / Gilkes, Daniele M / Slavov, Nikolai / Bencherif, Sidi A

    bioRxiv : the preprint server for biology

    2023  

    Abstract: ... Oxygen ( ... ...

    Abstract Oxygen (O
    Language English
    Publishing date 2023-10-03
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.10.02.560369
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  9. Article: HIF1α-Dependent Induction of

    Fagundes, Raphael R / Bourgonje, Arno R / Hu, Shixian / Barbieri, Ruggero / Jansen, Bernadien H / Sinnema, Nienke / Blokzijl, Tjasso / Taylor, Cormac T / Weersma, Rinse K / Faber, Klaas Nico / Dijkstra, Gerard

    Frontiers in physiology

    2022  Volume 13, Page(s) 889091

    Abstract: Background and Aims: ...

    Abstract Background and Aims:
    Language English
    Publishing date 2022-06-08
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2022.889091
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  10. Article ; Online: Hypoxia-inducible factor as a bridge between healthy barrier function, wound healing, and fibrosis.

    Steiner, Calen A / Cartwright, Ian M / Taylor, Cormac T / Colgan, Sean P

    American journal of physiology. Cell physiology

    2022  Volume 323, Issue 3, Page(s) C866–C878

    Abstract: The healthy mammalian intestine is lined by a single layer of epithelial cells. These cells provide a selectively permeable barrier to luminal contents and normally do so in an efficient and effective manner. Barrier function in the healthy mucosa is ... ...

    Abstract The healthy mammalian intestine is lined by a single layer of epithelial cells. These cells provide a selectively permeable barrier to luminal contents and normally do so in an efficient and effective manner. Barrier function in the healthy mucosa is provided via several mechanisms including epithelial junctional complexes, mucus production, as well as mucosal-derived antimicrobial proteins. As tissue metabolism is central to the maintenance of homeostasis in the mucosa, intestinal [Formula: see text] levels are uniquely low due to counter-current blood flow and the presence of the microbiota, resulting in the stabilization of the transcription factor hypoxia-inducible factor (HIF). Ongoing studies have revealed that HIF molds normal intestinal metabolism and is central to the coordination of barrier regulation during both homeostasis and active disease. During acute inflammation, HIF is central to controlling the rapid restitution of the epithelium consistent with normal wound healing responses. In contrast, HIF may also contribute to the fibrostenotic response associated with chronic, nonresolving inflammation. As such, HIF may function as a double-edged sword in the overall course of the inflammatory response. Here, we review recent literature on the contribution of HIF to mucosal barrier function, wound healing, and fibrosis.
    MeSH term(s) Animals ; Fibrosis ; Humans ; Hypoxia/metabolism ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Inflammation/metabolism ; Intestinal Mucosa/metabolism ; Mammals ; Wound Healing
    Chemical Substances Hypoxia-Inducible Factor 1, alpha Subunit
    Language English
    Publishing date 2022-08-01
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 392098-7
    ISSN 1522-1563 ; 0363-6143
    ISSN (online) 1522-1563
    ISSN 0363-6143
    DOI 10.1152/ajpcell.00227.2022
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