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  1. Article ; Online: Plasma membrane integrity: implications for health and disease.

    Ammendolia, Dustin A / Bement, William M / Brumell, John H

    BMC biology

    2021  Volume 19, Issue 1, Page(s) 71

    Abstract: Plasma membrane integrity is essential for cellular homeostasis. In vivo, cells experience plasma membrane damage from a multitude of stressors in the extra- and intra-cellular environment. To avoid lethal consequences, cells are equipped with repair ... ...

    Abstract Plasma membrane integrity is essential for cellular homeostasis. In vivo, cells experience plasma membrane damage from a multitude of stressors in the extra- and intra-cellular environment. To avoid lethal consequences, cells are equipped with repair pathways to restore membrane integrity. Here, we assess plasma membrane damage and repair from a whole-body perspective. We highlight the role of tissue-specific stressors in health and disease and examine membrane repair pathways across diverse cell types. Furthermore, we outline the impact of genetic and environmental factors on plasma membrane integrity and how these contribute to disease pathogenesis in different tissues.
    MeSH term(s) Cell Membrane ; Homeostasis
    Language English
    Publishing date 2021-04-13
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ISSN 1741-7007
    ISSN (online) 1741-7007
    DOI 10.1186/s12915-021-00972-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Listeriolysin O: from bazooka to Swiss army knife.

    Osborne, Suzanne E / Brumell, John H

    Philosophical transactions of the Royal Society of London. Series B, Biological sciences

    2017  Volume 372, Issue 1726

    Abstract: ... Listeria ... ...

    Abstract Listeria monocytogenes
    MeSH term(s) Animals ; Bacterial Proteins/chemistry ; Bacterial Toxins/chemistry ; Heat-Shock Proteins/chemistry ; Hemolysin Proteins/chemistry ; Listeria monocytogenes/chemistry ; Listeriosis/microbiology ; Virulence Factors/chemistry
    Chemical Substances Bacterial Proteins ; Bacterial Toxins ; Heat-Shock Proteins ; Hemolysin Proteins ; Virulence Factors ; hlyA protein, Listeria monocytogenes (R06ZRQ1YX9)
    Language English
    Publishing date 2017-06-19
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 208382-6
    ISSN 1471-2970 ; 0080-4622 ; 0264-3839 ; 0962-8436
    ISSN (online) 1471-2970
    ISSN 0080-4622 ; 0264-3839 ; 0962-8436
    DOI 10.1098/rstb.2016.0222
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: An autophagy-independent role for ATG16L1: promoting lysosome-mediated plasma membrane repair.

    Tan, Joel M J / Mellouk, Nora / Brumell, John H

    Autophagy

    2019  Volume 15, Issue 5, Page(s) 932–933

    Abstract: There is growing evidence in the literature for unconventional roles of autophagy-related (ATG) proteins, outside of their function in canonical autophagy. Here we discuss our recent study that revealed a novel ATG16L1-dependent pathway that promotes ... ...

    Abstract There is growing evidence in the literature for unconventional roles of autophagy-related (ATG) proteins, outside of their function in canonical autophagy. Here we discuss our recent study that revealed a novel ATG16L1-dependent pathway that promotes plasma membrane repair upon bacterial pore-forming toxin damage. Disruption of the ATG16L1-dependent pathway leads to an accumulation of cholesterol in lysosomes, which affects lysosomal exocytosis required for efficient membrane repair. Our study provides insights into the role of ATG16L1 in cholesterol homeostasis and plasma membrane integrity.
    MeSH term(s) Autophagy ; Autophagy-Related Proteins ; Carrier Proteins ; Cell Membrane ; Lysosomes
    Chemical Substances Autophagy-Related Proteins ; Carrier Proteins
    Language English
    Publishing date 2019-02-27
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2019.1586261
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  4. Article ; Online: Salmonella exploits membrane reservoirs for invasion of host cells.

    Zhu, Hongxian / Sydor, Andrew M / Boddy, Kirsten C / Coyaud, Etienne / Laurent, Estelle M N / Au, Aaron / Tan, Joel M J / Yan, Bing-Ru / Moffat, Jason / Muise, Aleixo M / Yip, Christopher M / Grinstein, Sergio / Raught, Brian / Brumell, John H

    Nature communications

    2024  Volume 15, Issue 1, Page(s) 3120

    Abstract: Salmonella utilizes a type 3 secretion system to translocate virulence proteins (effectors) into host cells during ... ...

    Abstract Salmonella utilizes a type 3 secretion system to translocate virulence proteins (effectors) into host cells during infection
    MeSH term(s) Humans ; Salmonella typhimurium/metabolism ; Bacterial Proteins/genetics ; Bacterial Proteins/metabolism ; Salmonella Infections/microbiology ; Cell Membrane/metabolism ; Membranes/metabolism ; HeLa Cells
    Chemical Substances Bacterial Proteins
    Language English
    Publishing date 2024-04-10
    Publishing country England
    Document type Journal Article
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-024-47183-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Rab5 regulates macropinocytosis by recruiting the inositol 5-phosphatases OCRL and Inpp5b that hydrolyse PtdIns(4,5)P2.

    Maxson, Michelle E / Sarantis, Helen / Volchuk, Allen / Brumell, John H / Grinstein, Sergio

    Journal of cell science

    2021  Volume 134, Issue 7

    Abstract: Rab5 is required for macropinosome formation, but its site and mode of action remain unknown. We report that Rab5 acts at the plasma membrane, downstream of ruffling, to promote macropinosome sealing and scission. Dominant-negative Rab5, which ... ...

    Abstract Rab5 is required for macropinosome formation, but its site and mode of action remain unknown. We report that Rab5 acts at the plasma membrane, downstream of ruffling, to promote macropinosome sealing and scission. Dominant-negative Rab5, which obliterates macropinocytosis, had no effect on the development of membrane ruffles. However, Rab5-containing vesicles were recruited to circular membrane ruffles, and soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE)-dependent endomembrane fusion was necessary for the completion of macropinocytosis. This fusion event coincided with the disappearance of PtdIns(4,5)P2 that accompanies macropinosome closure. Counteracting the depletion of PtdIns(4,5)P2 by expression of phosphatidylinositol-4-phosphate 5-kinase impaired macropinosome formation. Importantly, we found that the removal of PtdIns(4,5)P2 is dependent on Rab5, through the Rab5-mediated recruitment of the inositol 5-phosphatases OCRL and Inpp5b, via APPL1. Knockdown of OCRL and Inpp5b, or APPL1, prevented macropinosome closure without affecting ruffling. We therefore propose that Rab5 is essential for the clearance of PtdIns(4,5)P2 needed to complete the scission of macropinosomes or to prevent their back-fusion with the plasmalemma.
    Language English
    Publishing date 2021-04-15
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2993-2
    ISSN 1477-9137 ; 0021-9533
    ISSN (online) 1477-9137
    ISSN 0021-9533
    DOI 10.1242/jcs.252411
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  6. Article: Communication Between Autophagy and Insulin Action: At the Crux of Insulin Action-Insulin Resistance?

    Frendo-Cumbo, Scott / Tokarz, Victoria L / Bilan, Philip J / Brumell, John H / Klip, Amira

    Frontiers in cell and developmental biology

    2021  Volume 9, Page(s) 708431

    Abstract: Insulin is a paramount anabolic hormone that promotes energy-storage in adipose tissue, skeletal muscle and liver, and these responses are significantly attenuated in insulin resistance leading to type 2 diabetes. Contrasting with insulin's function, ... ...

    Abstract Insulin is a paramount anabolic hormone that promotes energy-storage in adipose tissue, skeletal muscle and liver, and these responses are significantly attenuated in insulin resistance leading to type 2 diabetes. Contrasting with insulin's function, macroautophagy/autophagy is a physiological mechanism geared to the degradation of intracellular components for the purpose of energy production, building-block recycling or tissue remodeling. Given that both insulin action and autophagy are dynamic phenomena susceptible to the influence of nutrient availability, it is perhaps not surprising that there is significant interaction between these two major regulatory mechanisms. This review examines the crosstalk between autophagy and insulin action, with specific focus on dysregulated autophagy as a cause or consequence of insulin resistance.
    Language English
    Publishing date 2021-07-15
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2021.708431
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  7. Article ; Online: Plasma membrane integrity

    Dustin A. Ammendolia / William M. Bement / John H. Brumell

    BMC Biology, Vol 19, Iss 1, Pp 1-

    implications for health and disease

    2021  Volume 29

    Abstract: Abstract Plasma membrane integrity is essential for cellular homeostasis. In vivo, cells experience plasma membrane damage from a multitude of stressors in the extra- and intra-cellular environment. To avoid lethal consequences, cells are equipped with ... ...

    Abstract Abstract Plasma membrane integrity is essential for cellular homeostasis. In vivo, cells experience plasma membrane damage from a multitude of stressors in the extra- and intra-cellular environment. To avoid lethal consequences, cells are equipped with repair pathways to restore membrane integrity. Here, we assess plasma membrane damage and repair from a whole-body perspective. We highlight the role of tissue-specific stressors in health and disease and examine membrane repair pathways across diverse cell types. Furthermore, we outline the impact of genetic and environmental factors on plasma membrane integrity and how these contribute to disease pathogenesis in different tissues.
    Keywords Plasma membrane ; Membrane damage ; Lipid peroxidation ; Pore formation ; Membrane repair ; Vesicle trafficking ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2021-04-01T00:00:00Z
    Publisher BMC
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: V-ATPase is a universal regulator of LC3-associated phagocytosis and non-canonical autophagy.

    Hooper, Kirsty M / Jacquin, Elise / Li, Taoyingnan / Goodwin, Jonathan M / Brumell, John H / Durgan, Joanne / Florey, Oliver

    The Journal of cell biology

    2022  Volume 221, Issue 6

    Abstract: Non-canonical autophagy is a key cellular pathway in immunity, cancer, and neurodegeneration, characterized by conjugation of ATG8 to endolysosomal single membranes (CASM). CASM is activated by engulfment (endocytosis, phagocytosis), agonists (STING, ... ...

    Abstract Non-canonical autophagy is a key cellular pathway in immunity, cancer, and neurodegeneration, characterized by conjugation of ATG8 to endolysosomal single membranes (CASM). CASM is activated by engulfment (endocytosis, phagocytosis), agonists (STING, TRPML1), and infection (influenza), dependent on K490 in the ATG16L1 WD40-domain. However, factors associated with non-canonical ATG16L1 recruitment and CASM induction remain unknown. Here, using pharmacological inhibitors, we investigate a role for V-ATPase during non-canonical autophagy. We report that increased V0-V1 engagement is associated with, and sufficient for, CASM activation. Upon V0-V1 binding, V-ATPase recruits ATG16L1, via K490, during LC3-associated phagocytosis (LAP), STING- and drug-induced CASM, indicating a common mechanism. Furthermore, during LAP, key molecular players, including NADPH oxidase/ROS, converge on V-ATPase. Finally, we show that LAP is sensitive to Salmonella SopF, which disrupts the V-ATPase-ATG16L1 axis and provide evidence that CASM contributes to the Salmonella host response. Together, these data identify V-ATPase as a universal regulator of CASM and indicate that SopF evolved in part to evade non-canonical autophagy.
    MeSH term(s) Autophagy ; Autophagy-Related Proteins/metabolism ; Cell Line ; Humans ; Microtubule-Associated Proteins/metabolism ; Phagocytosis ; Vacuolar Proton-Translocating ATPases/metabolism
    Chemical Substances ATG16L1 protein, human ; Autophagy-Related Proteins ; MAP1LC3A protein, human ; Microtubule-Associated Proteins ; Vacuolar Proton-Translocating ATPases (EC 3.6.1.-)
    Language English
    Publishing date 2022-05-05
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218154-x
    ISSN 1540-8140 ; 0021-9525
    ISSN (online) 1540-8140
    ISSN 0021-9525
    DOI 10.1083/jcb.202105112
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    Ub I Zs.190: Show issues Location:
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  9. Article ; Online: SLIT2/ROBO1 signaling suppresses mTORC1 for organelle control and bacterial killing.

    Bhosle, Vikrant K / Tan, Joel Mj / Li, Taoyingnan / Hua, Rong / Kwon, Hyunwoo / Li, Zhubing / Patel, Sajedabanu / Tessier-Lavigne, Marc / Robinson, Lisa A / Kim, Peter K / Brumell, John H

    Life science alliance

    2023  Volume 6, Issue 8

    Abstract: SLIT/ROBO signaling impacts many aspects of tissue development and homeostasis, in part, through the regulation of cell growth and proliferation. Recent studies have also linked SLIT/ROBO signaling to the regulation of diverse phagocyte functions. ... ...

    Abstract SLIT/ROBO signaling impacts many aspects of tissue development and homeostasis, in part, through the regulation of cell growth and proliferation. Recent studies have also linked SLIT/ROBO signaling to the regulation of diverse phagocyte functions. However, the mechanisms by which SLIT/ROBO signaling acts at the nexus of cellular growth control and innate immunity remain enigmatic. Here, we show that SLIT2-mediated activation of ROBO1 leads to inhibition of mTORC1 kinase activity in macrophages, leading to dephosphorylation of its downstream targets, including transcription factor EB and ULK1. Consequently, SLIT2 augments lysosome biogenesis, potently induces autophagy, and robustly promotes the killing of bacteria within phagosomes. Concordant with these results, we demonstrate decreased lysosomal content and accumulated peroxisomes in the spinal cords of embryos from
    MeSH term(s) Animals ; Mice ; Nerve Tissue Proteins/genetics ; Receptors, Immunologic/genetics ; Lysosomes ; Bacteria ; Mechanistic Target of Rapamycin Complex 1
    Chemical Substances Nerve Tissue Proteins ; Receptors, Immunologic ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
    Language English
    Publishing date 2023-06-13
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2575-1077
    ISSN (online) 2575-1077
    DOI 10.26508/lsa.202301964
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Loss of functional peroxisomes leads to increased mitochondrial biogenesis and reduced autophagy that preserve mitochondrial function.

    Chi, Lijun / Lee, Dorothy / Leung, Sharon / Hu, Guanlan / Wen, Bijun / Delgado-Olguin, Paul / Vissa, Miluska / Li, Ren / Brumell, John H / Kim, Peter K / Bandsma, Robert H J

    Cellular and molecular life sciences : CMLS

    2023  Volume 80, Issue 7, Page(s) 183

    Abstract: Peroxisomes are essential for mitochondrial health, as the absence of peroxisomes leads to altered mitochondria. However, it is unclear whether the changes in mitochondria are a function of preserving cellular function or a response to cellular damage ... ...

    Abstract Peroxisomes are essential for mitochondrial health, as the absence of peroxisomes leads to altered mitochondria. However, it is unclear whether the changes in mitochondria are a function of preserving cellular function or a response to cellular damage caused by the absence of peroxisomes. To address this, we developed conditional hepatocyte-specific Pex16 deficient (Pex16 KO) mice that develop peroxisome loss and subjected them to a low-protein diet to induce metabolic stress. Loss of PEX16 in hepatocytes led to increased biogenesis of small mitochondria and reduced autophagy flux but with preserved capacity for respiration and ATP capacity. Metabolic stress induced by low protein feeding led to mitochondrial dysfunction in Pex16 KO mice and impaired biogenesis. Activation of PPARα partially corrected these mitochondrial disturbances, despite the absence of peroxisomes. The findings of this study demonstrate that the absence of peroxisomes in hepatocytes results in a concerted effort to preserve mitochondrial function, including increased mitochondrial biogenesis, altered morphology, and modified autophagy activity. Our study underscores the relationship between peroxisomes and mitochondria in regulating the hepatic metabolic responses to nutritional stressors.
    MeSH term(s) Mice ; Animals ; Peroxisomes/metabolism ; Organelle Biogenesis ; Mitochondria/metabolism ; Liver/metabolism ; Autophagy
    Language English
    Publishing date 2023-06-20
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 1358415-7
    ISSN 1420-9071 ; 1420-682X
    ISSN (online) 1420-9071
    ISSN 1420-682X
    DOI 10.1007/s00018-023-04827-3
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