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  1. Article ; Online: Stress-Induced Phenoptosis: Mechanistic Insights and Evolutionary Implications.

    Pandey, Taruna / Ma, Dengke K

    Biochemistry. Biokhimiia

    2023  Volume 87, Issue 12, Page(s) 1504–1511

    Abstract: Evolution by natural selection results in biological traits that enable organismic adaptation and survival under various stressful environments. External stresses can be sometimes too severe to overcome, leading to organismic death either because of ... ...

    Abstract Evolution by natural selection results in biological traits that enable organismic adaptation and survival under various stressful environments. External stresses can be sometimes too severe to overcome, leading to organismic death either because of failure in adapting to such stress, or alternatively, through a regulated form of organismic death (phenoptosis). While regulated cell deaths, including apoptosis, have been extensively studied, little is known about the molecular and cellular mechanisms underlying phenoptosis and its evolutionary significance for multicellular organisms. In this article, we review documented phenomena and mechanistic evidence emerging from studies of stress-induced phenoptosis in the multicellular organism C. elegans and stress-induced deaths at cellular levels in organisms ranging from bacteria to mammals, focusing on abiotic and pathogen stresses. Genes and signaling pathways involved in phenoptosis appear to promote organismic death during severe stress and aging, while conferring fitness and immune defense during mild stress and early life, consistent with their antagonistic pleiotropy actions. As cell apoptosis during development can shape tissues and organs, stress-induced phenoptosis may also contribute to possible benefits at the population level, through mechanisms including kin selection, abortive infection, and soma-to-germline resource allocation. Current models can generate experimentally testable predictions and conceptual frameworks with implications for understanding both stress-induced phenoptosis and natural aging.
    MeSH term(s) Animals ; Humans ; Caenorhabditis elegans/genetics ; Apoptosis ; Aging/genetics ; Bacteria ; Signal Transduction ; Biological Evolution ; Mammals
    Language English
    Publishing date 2023-01-31
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1109-5
    ISSN 1608-3040 ; 0006-2979 ; 0320-9717
    ISSN (online) 1608-3040
    ISSN 0006-2979 ; 0320-9717
    DOI 10.1134/S0006297922120082
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Fluorescent reporter of

    Vozdek, Roman / Wang, Bingying / Li, Kathy H / Pramstaller, Peter P / Hicks, Andrew A / Ma, Dengke K

    Open research Europe

    2023  Volume 2, Page(s) 23

    Abstract: Background: ...

    Abstract Background:
    Language English
    Publishing date 2023-09-15
    Publishing country Belgium
    Document type Journal Article
    ISSN 2732-5121
    ISSN (online) 2732-5121
    DOI 10.12688/openreseurope.14235.2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Bridge-Like Lipid Transfer Proteins (BLTPs) in

    Pandey, Taruna / Zhang, Jianxiu / Wang, Bingying / Ma, Dengke K

    Contact (Thousand Oaks (Ventura County, Calif.))

    2023  Volume 6, Page(s) 25152564231186489

    Abstract: In eukaryotic cells, lipid transfer can occur at membrane contact sites (MCS) to facilitate the exchange of various lipids between two adjacent cellular organelle membranes. Lipid transfer proteins (LTPs), including shuttle LTP or bridge-like LTP (BLTP), ...

    Abstract In eukaryotic cells, lipid transfer can occur at membrane contact sites (MCS) to facilitate the exchange of various lipids between two adjacent cellular organelle membranes. Lipid transfer proteins (LTPs), including shuttle LTP or bridge-like LTP (BLTP), transport lipids at MCS and are critical for diverse cellular processes, including lipid metabolism, membrane trafficking, and cell signaling. BLTPs (BLTP1-5, including the ATG2 and VPS13 family proteins) contain lipid-accommodating hydrophobic repeating β-groove (RBG) domains that allow the bulk transfer of lipids through MCS. Compared with vesicular lipid transfer and shuttle LTP, BLTPs have been only recently identified. Their functions and regulatory mechanisms are currently being unraveled in various model organisms and by diverse approaches. In this review, we summarize the genetics, structural features, and biological functions of BLTP in the genetically tractable model organism
    Language English
    Publishing date 2023-07-12
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2964312-0
    ISSN 2515-2564 ; 2515-2564
    ISSN (online) 2515-2564
    ISSN 2515-2564
    DOI 10.1177/25152564231186489
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Bridge-Like Lipid Transfer Proteins (BLTPs) in

    Taruna Pandey / Jianxiu Zhang / Bingying Wang / Dengke K. Ma

    Contact, Vol

    From Genetics to Structures and Functions

    2023  Volume 6

    Abstract: In eukaryotic cells, lipid transfer can occur at membrane contact sites (MCS) to facilitate the exchange of various lipids between two adjacent cellular organelle membranes. Lipid transfer proteins (LTPs), including shuttle LTP or bridge-like LTP (BLTP), ...

    Abstract In eukaryotic cells, lipid transfer can occur at membrane contact sites (MCS) to facilitate the exchange of various lipids between two adjacent cellular organelle membranes. Lipid transfer proteins (LTPs), including shuttle LTP or bridge-like LTP (BLTP), transport lipids at MCS and are critical for diverse cellular processes, including lipid metabolism, membrane trafficking, and cell signaling. BLTPs (BLTP1-5, including the ATG2 and VPS13 family proteins) contain lipid-accommodating hydrophobic repeating β-groove (RBG) domains that allow the bulk transfer of lipids through MCS. Compared with vesicular lipid transfer and shuttle LTP, BLTPs have been only recently identified. Their functions and regulatory mechanisms are currently being unraveled in various model organisms and by diverse approaches. In this review, we summarize the genetics, structural features, and biological functions of BLTP in the genetically tractable model organism C. elegans . We discuss our recent studies and findings on C. elegans LPD-3, a prototypical megaprotein ortholog of BLTP1, with identified lipid transfer functions that are evolutionarily conserved in multicellular organisms and in human cells. We also highlight areas for future research of BLTP using C. elegans and complementary model systems and approaches. Given the emerging links of BLTP to several human diseases, including Parkinson's disease and Alkuraya-Kučinskas syndrome, discovering evolutionarily conserved roles of BLTPs and their mechanisms of regulation and action should contribute to new advances in basic cell biology and potential therapeutic development for related human disorders.
    Keywords Biology (General) ; QH301-705.5 ; Biochemistry ; QD415-436
    Subject code 571 ; 572
    Language English
    Publishing date 2023-07-01T00:00:00Z
    Publisher SAGE Publishing
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article: Suppressing mortality and curbing cellular damage by targeting VHL.

    Jiang, Wei I / Cao, Yiming / Xue, Yue / Ji, Yichun / Winer, Benjamin Y / Zhang, Mengqi / Singhal, Neel S / Pierce, Jonathan T / Chen, Song / Ma, Dengke K

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Mortality rate increases with age and can accelerate upon extrinsic or intrinsic damage to individuals. Identifying factors and mechanisms that curb population mortality rate has wide-ranging implications. Here, we show that targeting the VHL-1 (Von ... ...

    Abstract Mortality rate increases with age and can accelerate upon extrinsic or intrinsic damage to individuals. Identifying factors and mechanisms that curb population mortality rate has wide-ranging implications. Here, we show that targeting the VHL-1 (Von Hippel-Lindau) protein suppresses
    Language English
    Publishing date 2024-03-03
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.02.28.582664
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Acquired stress resilience through bacteria-to-nematode horizontal gene transfer.

    Pandey, Taruna / Kalluraya, Chinmay / Wang, Bingying / Xu, Ting / Huang, Xinya / Guang, Shouhong / Daugherty, Matthew D / Ma, Dengke K

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Natural selection drives acquisition of organismal resilience traits to protect against adverse environments. Horizontal gene transfer (HGT) is an important evolutionary mechanism for the acquisition of novel traits, including metazoan acquisition of ... ...

    Abstract Natural selection drives acquisition of organismal resilience traits to protect against adverse environments. Horizontal gene transfer (HGT) is an important evolutionary mechanism for the acquisition of novel traits, including metazoan acquisition of functions in immunity, metabolism, and reproduction via interdomain HGT (iHGT) from bacteria. We report that the nematode gene
    Language English
    Publishing date 2023-08-21
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.08.20.554039
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Neuronal GDPGP1 and glycogen metabolism: friend or foe?

    Singhal, Neel S / Lee, Evan M / Ma, Dengke K

    The Journal of cell biology

    2020  Volume 219, Issue 2

    Abstract: The adult brain consumes glucose for energy needs and stores glucose as glycogen mainly in astrocytes. Schulz et al. (2020. J. Cell Biol.https://doi.org/10.1083/jcb.201807127) identify the stress-regulated metabolic enzyme GDPGP1 that promotes neuronal ... ...

    Abstract The adult brain consumes glucose for energy needs and stores glucose as glycogen mainly in astrocytes. Schulz et al. (2020. J. Cell Biol.https://doi.org/10.1083/jcb.201807127) identify the stress-regulated metabolic enzyme GDPGP1 that promotes neuronal survival likely through glycogen reserves in mouse and C. elegans neurons.
    MeSH term(s) Animals ; Astrocytes ; Brain ; Caenorhabditis elegans ; Glycogen ; Mice ; Neurons
    Chemical Substances Glycogen (9005-79-2)
    Language English
    Publishing date 2020-01-23
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 218154-x
    ISSN 1540-8140 ; 0021-9525
    ISSN (online) 1540-8140
    ISSN 0021-9525
    DOI 10.1083/jcb.202001006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Early-life stress triggers long-lasting organismal resilience and longevity via tetraspanin.

    Jiang, Wei I / De Belly, Henry / Wang, Bingying / Wong, Andrew / Kim, Minseo / Oh, Fiona / DeGeorge, Jason / Huang, Xinya / Guang, Shouhong / Weiner, Orion D / Ma, Dengke K

    Science advances

    2024  Volume 10, Issue 4, Page(s) eadj3880

    Abstract: Early-life stress experiences can produce lasting impacts on organismal adaptation and fitness. How transient stress elicits memory-like physiological effects is largely unknown. Here, we show that early-life thermal stress strongly up- ... ...

    Abstract Early-life stress experiences can produce lasting impacts on organismal adaptation and fitness. How transient stress elicits memory-like physiological effects is largely unknown. Here, we show that early-life thermal stress strongly up-regulates
    MeSH term(s) Adult ; Humans ; Animals ; Longevity ; Thrombospondin 1 ; Adverse Childhood Experiences ; Caenorhabditis elegans ; Resilience, Psychological ; Tetraspanins/genetics ; Transcription Factors ; Caenorhabditis elegans Proteins/genetics ; Histone Acetyltransferases
    Chemical Substances Thrombospondin 1 ; Tetraspanins ; CBP-1 protein, C elegans (EC 2.3.1.48) ; Transcription Factors ; Caenorhabditis elegans Proteins ; Histone Acetyltransferases (EC 2.3.1.48)
    Language English
    Publishing date 2024-01-24
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.adj3880
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: LPD-3 as a megaprotein brake for aging and insulin-mTOR signaling in C. elegans.

    Pandey, Taruna / Wang, Bingying / Wang, Changnan / Zu, Jenny / Deng, Huichao / Shen, Kang / do Vale, Goncalo Dias / McDonald, Jeffrey G / Ma, Dengke K

    Cell reports

    2024  Volume 43, Issue 3, Page(s) 113899

    Abstract: Insulin-mechanistic target of rapamycin (mTOR) signaling drives anabolic growth during organismal development; its late-life dysregulation contributes to aging and limits lifespans. Age-related regulatory mechanisms and functional consequences of insulin- ...

    Abstract Insulin-mechanistic target of rapamycin (mTOR) signaling drives anabolic growth during organismal development; its late-life dysregulation contributes to aging and limits lifespans. Age-related regulatory mechanisms and functional consequences of insulin-mTOR remain incompletely understood. Here, we identify LPD-3 as a megaprotein that orchestrates the tempo of insulin-mTOR signaling during C. elegans aging. We find that an agonist insulin, INS-7, is drastically overproduced from early life and shortens lifespan in lpd-3 mutants. LPD-3 forms a bridge-like tunnel megaprotein to facilitate non-vesicular cellular lipid trafficking. Lipidomic profiling reveals increased hexaceramide species in lpd-3 mutants, accompanied by up-regulation of hexaceramide biosynthetic enzymes, including HYL-1. Reducing the abundance of HYL-1, insulin receptor/DAF-2 or mTOR/LET-363, normalizes INS-7 levels and rescues the lifespan of lpd-3 mutants. LPD-3 antagonizes SINH-1, a key mTORC2 component, and decreases expression with age. We propose that LPD-3 acts as a megaprotein brake for organismal aging and that its age-dependent decline restricts lifespan through the sphingolipid-hexaceramide and insulin-mTOR pathways.
    MeSH term(s) Animals ; Aging ; Caenorhabditis elegans/metabolism ; Caenorhabditis elegans Proteins/metabolism ; Forkhead Transcription Factors/metabolism ; Insulin/metabolism ; Longevity/physiology ; TOR Serine-Threonine Kinases/metabolism
    Chemical Substances Caenorhabditis elegans Proteins ; Forkhead Transcription Factors ; Insulin ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; lpd-3 protein, C elegans
    Language English
    Publishing date 2024-03-05
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2024.113899
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: LPD-3 as a megaprotein brake for aging and insulin-mTOR signaling in

    Pandey, Taruna / Wang, Bingying / Wang, Changnan / Zu, Jenny / Deng, Huichao / Shen, Kang / do Vale, Goncalo Dias / McDonald, Jeffrey G / Ma, Dengke K

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Insulin-mTOR signaling drives anabolic growth during organismal development, while its late-life dysregulation may detrimentally contribute to aging and limit lifespans. Age-related regulatory mechanisms and functional consequences of insulin-mTOR remain ...

    Abstract Insulin-mTOR signaling drives anabolic growth during organismal development, while its late-life dysregulation may detrimentally contribute to aging and limit lifespans. Age-related regulatory mechanisms and functional consequences of insulin-mTOR remain incompletely understood. Here we identify LPD-3 as a megaprotein that orchestrates the tempo of insulin-mTOR signaling during
    Language English
    Publishing date 2023-07-17
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.02.14.528431
    Database MEDical Literature Analysis and Retrieval System OnLINE

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