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  1. Article ; Online: The road not taken en route to T cell exhaustion.

    Dash, Barsha / Hogan, Patrick G

    Nature immunology

    2023  Volume 24, Issue 9, Page(s) 1402–1404

    MeSH term(s) T-Cell Exhaustion ; CD8-Positive T-Lymphocytes
    Language English
    Publishing date 2023-08-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/s41590-023-01596-w
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  2. Article ; Online: The Reappraisal of the Reappraisal-CRAC Channels Are Activated by L-Type Ca

    Trebak, Mohamed / Machaca, Khaled / Hogan, Patrick G

    Function (Oxford, England)

    2024  Volume 5, Issue 2, Page(s) zqae007

    MeSH term(s) Humans ; Calcium Release Activated Calcium Channels ; Calcium Channels ; Calcium Channel Blockers/pharmacology ; Heart Failure
    Chemical Substances Calcium Release Activated Calcium Channels ; Calcium Channels ; Calcium Channel Blockers
    Language English
    Publishing date 2024-02-02
    Publishing country England
    Document type Journal Article ; Comment
    ISSN 2633-8823
    ISSN (online) 2633-8823
    DOI 10.1093/function/zqae007
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  3. Article ; Online: TET2, tumor control, and CAR T cell hyperproliferation.

    Dash, Barsha / Hogan, Patrick G

    Trends in cancer

    2023  Volume 9, Issue 7, Page(s) 521–523

    Abstract: A recent study by Jain et al. published in Nature followed up on evidence suggesting that depletion of 5-methylcytosine dioxygenase TET2 in chimeric antigen receptor CAR T cells could enhance their expansion, persistence, and antitumor efficacy. Their ... ...

    Abstract A recent study by Jain et al. published in Nature followed up on evidence suggesting that depletion of 5-methylcytosine dioxygenase TET2 in chimeric antigen receptor CAR T cells could enhance their expansion, persistence, and antitumor efficacy. Their findings are cautionary, but offer hope of a path forward.
    MeSH term(s) Humans ; T-Lymphocytes ; Receptors, Chimeric Antigen/genetics ; Immunotherapy, Adoptive ; Neoplasms/therapy ; Cell Proliferation ; DNA-Binding Proteins/genetics ; Dioxygenases
    Chemical Substances Receptors, Chimeric Antigen ; TET2 protein, human (EC 1.13.11.-) ; DNA-Binding Proteins ; Dioxygenases (EC 1.13.11.-)
    Language English
    Publishing date 2023-05-11
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 2852626-0
    ISSN 2405-8025 ; 2405-8033 ; 2405-8033
    ISSN (online) 2405-8025 ; 2405-8033
    ISSN 2405-8033
    DOI 10.1016/j.trecan.2023.04.009
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  4. Article ; Online: TET Enzymes in the Immune System: From DNA Demethylation to Immunotherapy, Inflammation, and Cancer.

    López-Moyado, Isaac F / Ko, Myunggon / Hogan, Patrick G / Rao, Anjana

    Annual review of immunology

    2024  

    Abstract: Ten-eleven translocation (TET) proteins are iron-dependent and α-ketoglutarate-dependent dioxygenases that sequentially oxidize the methyl group of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC) and 5-carboxylcytosine ( ... ...

    Abstract Ten-eleven translocation (TET) proteins are iron-dependent and α-ketoglutarate-dependent dioxygenases that sequentially oxidize the methyl group of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC), 5-formylcytosine (5fC) and 5-carboxylcytosine (5caC). All three epigenetic modifications are intermediates in DNA demethylation. TET proteins are recruited by transcription factors and by RNA polymerase II to modify 5mC at enhancers and gene bodies, thereby regulating gene expression during development, cell lineage specification, and cell activation. It is not yet clear, however, how the established biochemical activities of TET enzymes in oxidizing 5mC and mediating DNA demethylation relate to the known association of TET deficiency with inflammation, clonal hematopoiesis, and cancer. There are hints that the ability of TET deficiency to promote cell proliferation in a signal-dependent manner may be harnessed for cancer immunotherapy. In this review, we draw upon recent findings in cells of the immune system to illustrate established as well as emerging ideas of how TET proteins influence cellular function. Expected final online publication date for the
    Language English
    Publishing date 2024-02-15
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 604953-9
    ISSN 1545-3278 ; 0732-0582
    ISSN (online) 1545-3278
    ISSN 0732-0582
    DOI 10.1146/annurev-immunol-080223-044610
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    Se 849: Show issues Location:
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  5. Article ; Online: Calcineurin: A star is reborn.

    Li, Huiming / Hogan, Patrick G

    Cell calcium

    2021  Volume 94, Page(s) 102324

    Abstract: The protein phosphatase calcineurin has long been familiar to the calcium community, but the definition of its physiological substrates has been far from complete. A new study rectifies this deficiency and sets the stage for new insights into the role of ...

    Abstract The protein phosphatase calcineurin has long been familiar to the calcium community, but the definition of its physiological substrates has been far from complete. A new study rectifies this deficiency and sets the stage for new insights into the role of calcineurin in diverse cellular processes.
    MeSH term(s) Animals ; Calcineurin/chemistry ; Calcineurin/metabolism ; Humans ; NFATC Transcription Factors/metabolism ; Signal Transduction ; Substrate Specificity
    Chemical Substances NFATC Transcription Factors ; Calcineurin (EC 3.1.3.16)
    Language English
    Publishing date 2021-01-12
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 757687-0
    ISSN 1532-1991 ; 0143-4160
    ISSN (online) 1532-1991
    ISSN 0143-4160
    DOI 10.1016/j.ceca.2020.102324
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  6. Article ; Online: Calcium-NFAT transcriptional signalling in T cell activation and T cell exhaustion.

    Hogan, Patrick G

    Cell calcium

    2017  Volume 63, Page(s) 66–69

    Abstract: A cornerstone of the adaptive immune response is the T cell receptor (TcR)-calcium-calcineurin signalling pathway leading to T cell activation. The 'nuclear factor of activated T cells' proteins NFAT1, NFAT2, and NFAT4 are transcription factors that ... ...

    Abstract A cornerstone of the adaptive immune response is the T cell receptor (TcR)-calcium-calcineurin signalling pathway leading to T cell activation. The 'nuclear factor of activated T cells' proteins NFAT1, NFAT2, and NFAT4 are transcription factors that promote expression of a panel of genes required for activation. It has become apparent that these same NFAT transcription factors underlie an alternative transcriptional program in T cells that serves to limit the immune response. This duality in NFAT transcriptional functions raises the possibility that NFAT transcriptional complexes could be targeted therapeutically to alter the relative strength of the effector and alternative transcriptional programs, thereby modulating immune responses.
    MeSH term(s) Animals ; Calcium/metabolism ; Calcium Signaling/physiology ; Humans ; Lymphocyte Activation ; NFATC Transcription Factors/physiology ; T-Lymphocytes/immunology ; Transcriptional Activation
    Chemical Substances NFATC Transcription Factors ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2017-01-28
    Publishing country Netherlands
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 757687-0
    ISSN 1532-1991 ; 0143-4160
    ISSN (online) 1532-1991
    ISSN 0143-4160
    DOI 10.1016/j.ceca.2017.01.014
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    Zs.A 1596: Show issues Location:
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  7. Article ; Online: Time-motion observations to characterize the developmental environment in a paediatric post-acute care hospital.

    Hogan, Patrick G / Wallace, Claire E / Schaffer-Nay, Nanette R / Al-Zubeidi, Duha / Holekamp, Nicholas A

    Child: care, health and development

    2023  Volume 50, Issue 1, Page(s) e13179

    Abstract: Background: Chronically hospitalized children are at risk for neurodevelopmental delay, compounded by restricted social interactions, movement and environmental stimulation. We measured patients' movements and interactions to characterize ... ...

    Abstract Background: Chronically hospitalized children are at risk for neurodevelopmental delay, compounded by restricted social interactions, movement and environmental stimulation. We measured patients' movements and interactions to characterize developmentally relevant aspects of our inpatient environment and identify opportunities for developmental enrichment.
    Methods: As part of a quality improvement initiative to inform neurodevelopmental programming for children with medical complexity at our paediatric post-acute care specialty hospital, we conducted >232 hours of time-motion observations. Trained observers followed 0- to 5-year-old inpatients from 7 am to 7 pm on weekdays, categorizing observations within five domains: Where, With, Position, State and Environment. Observations were collected continuously utilizing REDCap on iPads. A change in any domain initiated a new observation.
    Results: Patients were median 1 year and 8 months of age (range 2 months to 3 years 9 months) with a median length of hospitalization of 514 days (range 66-1298). In total, 2636 unique observations (or median 134 observations per patient-day [range 95-210]) were collected. Patients left their rooms up to 4 times per day for median 1 h and 34 min (range 41 min to 4 h:30 min). Patients spent 4 h:6 min (2 h:57 min to 6 h:30 min) interacting with someone and 3 h:51 min (57 min to 6 h:36 min) out of bed each day. Patients were simultaneously out of their beds, interacting with someone and awake for 2 h:21 min (51 min to 4 h:19 min) each day.
    Conclusions: Despite a care model prioritizing time out of bed and social interaction, time-motion observations indicate patients spent many of their waking hours in bed and alone. Quantifying our inpatients developmental opportunities will inform neurodevelopmental programming initiatives.
    MeSH term(s) Child ; Humans ; Infant, Newborn ; Infant ; Child, Preschool ; Subacute Care ; Hospitalization ; Child, Hospitalized ; Environment ; Hospitals, Pediatric
    Language English
    Publishing date 2023-09-25
    Publishing country England
    Document type Journal Article
    ZDB-ID 223039-2
    ISSN 1365-2214 ; 0305-1862
    ISSN (online) 1365-2214
    ISSN 0305-1862
    DOI 10.1111/cch.13179
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  8. Article ; Online: Sphingomyelin, ORAI1 channels, and cellular Ca2+ signaling.

    Hogan, Patrick G

    The Journal of general physiology

    2015  Volume 146, Issue 3, Page(s) 195–200

    MeSH term(s) Animals ; Bacterial Proteins/pharmacology ; Calcium Channels/metabolism ; Calcium Signaling/drug effects ; Humans ; Phosphoric Diester Hydrolases/pharmacology ; T-Lymphocytes/metabolism
    Chemical Substances Bacterial Proteins ; Calcium Channels ; Phosphoric Diester Hydrolases (EC 3.1.4.-)
    Language English
    Publishing date 2015-09
    Publishing country United States
    Document type Comment ; Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 3118-5
    ISSN 1540-7748 ; 0022-1295
    ISSN (online) 1540-7748
    ISSN 0022-1295
    DOI 10.1085/jgp.201511479
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  9. Article ; Online: The STIM1-ORAI1 microdomain.

    Hogan, Patrick G

    Cell calcium

    2015  Volume 58, Issue 4, Page(s) 357–367

    Abstract: The regulatory protein STIM1 controls gating of the Ca(2+) channel ORAI1 by a direct protein-protein interaction. Because STIM1 is anchored in the ER membrane and ORAI1 is in the plasma membrane, the STIM-ORAI pathway can support Ca(2+) influx only where ...

    Abstract The regulatory protein STIM1 controls gating of the Ca(2+) channel ORAI1 by a direct protein-protein interaction. Because STIM1 is anchored in the ER membrane and ORAI1 is in the plasma membrane, the STIM-ORAI pathway can support Ca(2+) influx only where the two membranes come into close apposition, effectively demarcating a microdomain for Ca(2+) signalling. This review begins with a brief summary of the STIM-ORAI pathway of store-operated Ca(2+) influx, then turns to the special geometry of the STIM-ORAI microdomain and the expected characteristics of the microdomain Ca(2+) signal. A final section of the review seeks to place the STIM-ORAI microdomain into a broader context of cellular Ca(2+) signalling.
    MeSH term(s) Animals ; Calcium/metabolism ; Calcium Channels/metabolism ; Calcium Signaling/physiology ; Cell Membrane/metabolism ; Endoplasmic Reticulum/metabolism ; Humans ; Membrane Proteins/metabolism ; Neoplasm Proteins/metabolism ; Stromal Interaction Molecule 1
    Chemical Substances Calcium Channels ; Membrane Proteins ; Neoplasm Proteins ; STIM1 protein, human ; Stromal Interaction Molecule 1 ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2015-10
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 757687-0
    ISSN 1532-1991 ; 0143-4160
    ISSN (online) 1532-1991
    ISSN 0143-4160
    DOI 10.1016/j.ceca.2015.07.001
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  10. Article: The STIM-Orai Pathway: Orai, the Pore-Forming Subunit of the CRAC Channel.

    Gudlur, Aparna / Hogan, Patrick G

    Advances in experimental medicine and biology

    2017  Volume 993, Page(s) 39–57

    Abstract: This chapter focuses on the Orai proteins, Orai1-Orai3, with special emphasis on Orai1, in humans and other mammals, and on the definitive evidence that Orai is the pore subunit of the CRAC channel. It begins by reviewing briefly the defining ... ...

    Abstract This chapter focuses on the Orai proteins, Orai1-Orai3, with special emphasis on Orai1, in humans and other mammals, and on the definitive evidence that Orai is the pore subunit of the CRAC channel. It begins by reviewing briefly the defining characteristics of the CRAC channel, then discusses the studies that implicated Orai as part of the store-operated Ca
    Language English
    Publishing date 2017
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ISSN 2214-8019 ; 0065-2598
    ISSN (online) 2214-8019
    ISSN 0065-2598
    DOI 10.1007/978-3-319-57732-6_3
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