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  1. Article ; Online: Voltage-gated Ca

    Cahalan, Michael D

    Science signaling

    2022  Volume 15, Issue 738, Page(s) eabq5594

    Abstract: ... Calcium ( ... ...

    Abstract Calcium (Ca
    MeSH term(s) Calcium/metabolism ; Ion Channels/metabolism ; Signal Transduction ; T-Lymphocytes/metabolism
    Chemical Substances Ion Channels ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2022-06-14
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 2417226-1
    ISSN 1937-9145 ; 1945-0877
    ISSN (online) 1937-9145
    ISSN 1945-0877
    DOI 10.1126/scisignal.abq5594
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Photoswitching alters fluorescence readout of jGCaMP8 Ca

    Dynes, Joseph L / Yeromin, Andriy V / Cahalan, Michael D

    Proceedings of the National Academy of Sciences of the United States of America

    2023  Volume 120, Issue 39, Page(s) e2309328120

    Abstract: We used electrophysiology and ... ...

    Abstract We used electrophysiology and Ca
    MeSH term(s) Fluorescent Dyes ; Heart Rate ; Ionophores ; Lighting ; Membrane Potentials
    Chemical Substances Fluorescent Dyes ; Ionophores
    Language English
    Publishing date 2023-09-20
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2309328120
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1148: Show issues Location:
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  3. Article ; Online: Calcium Imaging in T Lymphocytes: a Protocol for Use with Genetically Encoded or Chemical Ca

    Jairaman, Amit / Cahalan, Michael D

    Bio-protocol

    2021  Volume 11, Issue 19, Page(s) e4170

    Abstract: Elevations in cytosolic calcium ( ... ...

    Abstract Elevations in cytosolic calcium (Ca
    Language English
    Publishing date 2021-10-05
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2833269-6
    ISSN 2331-8325 ; 2331-8325
    ISSN (online) 2331-8325
    ISSN 2331-8325
    DOI 10.21769/BioProtoc.4170
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  4. Article ; Online: Cell-wide mapping of Orai1 channel activity reveals functional heterogeneity in STIM1-Orai1 puncta.

    Dynes, Joseph L / Yeromin, Andriy V / Cahalan, Michael D

    The Journal of general physiology

    2020  Volume 152, Issue 9

    Abstract: Upon Ca2+ store depletion, Orai1 channels cluster and open at endoplasmic reticulum-plasma membrane (ER-PM) junctions in signaling complexes called puncta. Little is known about whether and how Orai1 channel activity may vary between individual puncta. ... ...

    Abstract Upon Ca2+ store depletion, Orai1 channels cluster and open at endoplasmic reticulum-plasma membrane (ER-PM) junctions in signaling complexes called puncta. Little is known about whether and how Orai1 channel activity may vary between individual puncta. Previously, we developed and validated optical recording of Orai channel activity, using genetically encoded Ca2+ indicators fused to Orai1 or Orai3 N or C termini. We have now combined total internal reflection fluorescence microscopy with whole-cell recording to map functional properties of channels at individual puncta. After Ca2+ store depletion in HEK cells cotransfected with mCherry-STIM1 and Orai1-GCaMP6f, Orai1-GCaMP6f fluorescence increased progressively with increasingly negative test potentials and robust responses could be recorded from individual puncta. Cell-wide fluorescence half-rise and -fall times during steps to -100 mV test potential indicated probe response times of <50 ms. The in situ Orai1-GCaMP6f affinity for Ca2+ was 620 nM, assessed by monitoring fluorescence using buffered Ca2+ solutions in "unroofed" cells. Channel activity and temporal activation profile were tracked in individual puncta using image maps and automated puncta identification and recording. Simultaneous measurement of mCherry-STIM1 fluorescence uncovered an unexpected gradient in STIM1/Orai1 ratio that extends across the cell surface. Orai1-GCaMP6f channel activity was found to vary across the cell, with inactive channels occurring in the corners of cells where the STIM1/Orai1 ratio was lowest; low-activity channels typically at edges displayed a slow activation phase lasting hundreds of milliseconds. Puncta with high STIM1/Orai1 ratios exhibited a range of channel activity that appeared unrelated to the stoichiometric requirements for gating. These findings demonstrate functional heterogeneity of Orai1 channel activity between individual puncta and establish a new experimental platform that facilitates systematic comparisons between puncta composition and activity.
    MeSH term(s) Calcium/metabolism ; Cell Membrane/metabolism ; Endoplasmic Reticulum/metabolism ; HEK293 Cells ; Humans ; Neoplasm Proteins ; ORAI1 Protein/metabolism ; Stromal Interaction Molecule 1/metabolism
    Chemical Substances Neoplasm Proteins ; ORAI1 Protein ; ORAI1 protein, human ; STIM1 protein, human ; Stromal Interaction Molecule 1 ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2020-07-15
    Publishing country United States
    Document type 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.201812239
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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.150: Show issues Location:
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  5. Article ; Online: Imaging transplant rejection: a new view.

    Cahalan, Michael D

    Nature medicine

    2011  Volume 17, Issue 6, Page(s) 662–663

    MeSH term(s) Animals ; Graft Rejection/immunology ; Graft Survival/immunology ; Mice ; Models, Immunological ; Skin Transplantation/immunology ; T-Lymphocytes/immunology
    Language English
    Publishing date 2011-06-06
    Publishing country United States
    Document type Comment ; News
    ZDB-ID 1220066-9
    ISSN 1546-170X ; 1078-8956
    ISSN (online) 1546-170X
    ISSN 1078-8956
    DOI 10.1038/nm0611-662
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    Zs.A 4212: Show issues Location:
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  6. Article ; Online: Cell biology. How to STIMulate calcium channels.

    Cahalan, Michael D

    Science (New York, N.Y.)

    2010  Volume 330, Issue 6000, Page(s) 43–44

    MeSH term(s) Animals ; Calcium/metabolism ; Calcium Channel Blockers/metabolism ; Calcium Channels/metabolism ; Calcium Channels, L-Type/chemistry ; Calcium Channels, L-Type/metabolism ; Calcium Signaling ; Cell Membrane/metabolism ; Endoplasmic Reticulum/metabolism ; Humans ; Lymphocytes/metabolism ; Membrane Glycoproteins/chemistry ; Membrane Glycoproteins/metabolism ; Membrane Proteins/chemistry ; Membrane Proteins/metabolism ; Neoplasm Proteins/chemistry ; Neoplasm Proteins/metabolism ; Neurons/metabolism ; ORAI1 Protein ; Protein Structure, Tertiary ; Rats ; Stromal Interaction Molecule 1
    Chemical Substances Calcium Channel Blockers ; Calcium Channels ; Calcium Channels, L-Type ; L-type calcium channel alpha(1C) ; Membrane Glycoproteins ; Membrane Proteins ; Neoplasm Proteins ; ORAI1 Protein ; Orai1 protein, rat ; STIM1 protein, human ; Stim1 protein, rat ; Stromal Interaction Molecule 1 ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2010-09-21
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.1196348
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    Zs.A 27: Show issues Location:
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    Zs.MG 77: Show issues

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  7. Article ; Online: STIMulating store-operated Ca(2+) entry.

    Cahalan, Michael D

    Nature cell biology

    2009  Volume 11, Issue 6, Page(s) 669–677

    Abstract: Calcium influx through plasma membrane store-operated Ca(2+) (SOC) channels is triggered when the endoplasmic reticulum (ER) Ca(2+) store is depleted - a homeostatic Ca(2+) signalling mechanism that remained enigmatic for more than two decades. RNA- ... ...

    Abstract Calcium influx through plasma membrane store-operated Ca(2+) (SOC) channels is triggered when the endoplasmic reticulum (ER) Ca(2+) store is depleted - a homeostatic Ca(2+) signalling mechanism that remained enigmatic for more than two decades. RNA-interference (RNAi) screening and molecular and cellular physiological analysis recently identified STIM1 as the mechanistic 'missing link' between the ER and the plasma membrane. STIM proteins sense the depletion of Ca(2+) from the ER, oligomerize, translocate to junctions adjacent to the plasma membrane, organize Orai or TRPC (transient receptor potential cation) channels into clusters and open these channels to bring about SOC entry.
    MeSH term(s) Animals ; Calcium/metabolism ; Calcium Channels/genetics ; Calcium Channels/metabolism ; Calcium Signaling/physiology ; Cell Membrane/metabolism ; Endoplasmic Reticulum/metabolism ; Gene Knockdown Techniques ; Humans ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Models, Biological ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; ORAI1 Protein ; Protein Subunits/metabolism ; Stromal Interaction Molecule 1 ; TRPC Cation Channels/genetics ; TRPC Cation Channels/metabolism
    Chemical Substances Calcium Channels ; Membrane Proteins ; Neoplasm Proteins ; ORAI1 Protein ; ORAI1 protein, human ; Protein Subunits ; STIM1 protein, human ; Stromal Interaction Molecule 1 ; TRPC Cation Channels ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2009-06-02
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1474722-4
    ISSN 1476-4679 ; 1465-7392
    ISSN (online) 1476-4679
    ISSN 1465-7392
    DOI 10.1038/ncb0609-669
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    Zs.A 5169: Show issues Location:
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  8. Article ; Online: Piezo1 channels restrain regulatory T cells but are dispensable for effector CD4

    Jairaman, Amit / Othy, Shivashankar / Dynes, Joseph L / Yeromin, Andriy V / Zavala, Angel / Greenberg, Milton L / Nourse, Jamison L / Holt, Jesse R / Cahalan, Stuart M / Marangoni, Francesco / Parker, Ian / Pathak, Medha M / Cahalan, Michael D

    Science advances

    2021  Volume 7, Issue 28

    Abstract: T lymphocytes encounter complex mechanical cues during an immune response. The mechanosensitive ion channel, Piezo1, drives inflammatory responses to bacterial infections, wound healing, and cancer; however, its role in helper T cell function remains ... ...

    Abstract T lymphocytes encounter complex mechanical cues during an immune response. The mechanosensitive ion channel, Piezo1, drives inflammatory responses to bacterial infections, wound healing, and cancer; however, its role in helper T cell function remains unclear. In an animal model for multiple sclerosis, experimental autoimmune encephalomyelitis (EAE), we found that mice with genetic deletion of Piezo1 in T cells showed diminished disease severity. Unexpectedly, Piezo1 was not essential for lymph node homing, interstitial motility, Ca
    MeSH term(s) Animals ; Cell Differentiation ; Encephalomyelitis, Autoimmune, Experimental/pathology ; Ion Channels/genetics ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Multiple Sclerosis ; T-Lymphocytes, Regulatory ; Th1 Cells
    Chemical Substances Ion Channels ; Piezo1 protein, mouse
    Language English
    Publishing date 2021-07-07
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.abg5859
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  9. Article ; Online: Biotin Supplementation Ameliorates Murine Colitis by Preventing NF-κB Activation.

    Skupsky, Jonathan / Sabui, Subrata / Hwang, Michael / Nakasaki, Manando / Cahalan, Michael D / Said, Hamid M

    Cellular and molecular gastroenterology and hepatology

    2019  Volume 9, Issue 4, Page(s) 557–567

    Abstract: Background & aims: Biotin is a water-soluble vitamin that is indispensable for human health. Biotin deficiency can cause failure-to-thrive, immunodeficiency, alopecia, dermatitis, and conjunctivitis. We previously reported that biotin deficiency also ... ...

    Abstract Background & aims: Biotin is a water-soluble vitamin that is indispensable for human health. Biotin deficiency can cause failure-to-thrive, immunodeficiency, alopecia, dermatitis, and conjunctivitis. We previously reported that biotin deficiency also can lead to severe colitis in mice, which is completely reversed with supplementation. Our aim in this study was to determine if high-dose biotin supplementation can provide a therapeutic benefit in a preclinical model for inflammatory bowel disease (IBD) and to identify the molecular mechanism by which this occurs.
    Methods: Mice were challenged with dextran sodium sulfate to induce colitis and were treated with 1 mmol/L biotin to induce or maintain remission. Clinical response was monitored by the Disease Activity Index and fecal calprotectin levels. The colon tissue was investigated for histology, length, as well as expression of inflammatory cytokines (interleukin 6, tumor necrosis factor-α, interleukin 1β), intestinal permeability, tight junctions (zonula occludens-1 and claudin-2), and the transcription factor nuclear factor-κB (NF-κB).
    Results: Biotin therapy led to delayed onset and severity of colitis as well as accelerated healing. There was improvement in the Disease Activity Index, fecal calprotectin levels, colon length, and histology. In addition, biotin-treated mice had reduced expression of inflammatory cytokines, reduced intestinal permeability, and reduced activation of NF-κB.
    Conclusions: Oral supplementation with biotin provides benefit for maintenance and induction of remission in the dextran sodium sulfate preclinical model for IBD. Biotin does this by reducing the activation of NF-κB, which prevents the production of inflammatory cytokines and helps maintain the integrity of the intestinal barrier. Clinically, the NF-κB pathway is important in the development of IBD and this finding suggests that biotin may have therapeutic potential for patients with IBD.
    MeSH term(s) Animals ; Biotin/pharmacology ; Biotin/therapeutic use ; Colitis/chemically induced ; Colitis/drug therapy ; Dextran Sulfate ; Dietary Supplements ; Humans ; Kruppel-Like Transcription Factors ; Mice ; Mice, Inbred C57BL ; NF-kappa B/metabolism ; Regeneration ; Signal Transduction ; Stem Cells/metabolism
    Chemical Substances Kruppel-Like Transcription Factors ; NF-kappa B ; Biotin (6SO6U10H04) ; Dextran Sulfate (9042-14-2)
    Language English
    Publishing date 2019-11-29
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Comment
    ISSN 2352-345X
    ISSN (online) 2352-345X
    DOI 10.1016/j.jcmgh.2019.11.011
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  10. Article ; Online: TREM2 regulates purinergic receptor-mediated calcium signaling and motility in human iPSC-derived microglia.

    Jairaman, Amit / McQuade, Amanda / Granzotto, Alberto / Kang, You Jung / Chadarevian, Jean Paul / Gandhi, Sunil / Parker, Ian / Smith, Ian / Cho, Hansang / Sensi, Stefano L / Othy, Shivashankar / Blurton-Jones, Mathew / Cahalan, Michael D

    eLife

    2022  Volume 11

    Abstract: The membrane protein TREM2 (Triggering Receptor Expressed on Myeloid cells 2) regulates key microglial functions including phagocytosis and chemotaxis. Loss-of-function variants of TREM2 are associated with increased risk of Alzheimer's disease (AD). ... ...

    Abstract The membrane protein TREM2 (Triggering Receptor Expressed on Myeloid cells 2) regulates key microglial functions including phagocytosis and chemotaxis. Loss-of-function variants of TREM2 are associated with increased risk of Alzheimer's disease (AD). Because abnormalities in Ca
    MeSH term(s) Adenosine Diphosphate/metabolism ; Alzheimer Disease/metabolism ; Calcium/metabolism ; Calcium Signaling ; Humans ; Induced Pluripotent Stem Cells/metabolism ; Membrane Glycoproteins/genetics ; Membrane Glycoproteins/metabolism ; Microglia/metabolism ; Receptors, Immunologic/metabolism ; Receptors, Purinergic/metabolism
    Chemical Substances Membrane Glycoproteins ; Receptors, Immunologic ; Receptors, Purinergic ; TREM2 protein, human ; Adenosine Diphosphate (61D2G4IYVH) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2022-02-22
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2687154-3
    ISSN 2050-084X ; 2050-084X
    ISSN (online) 2050-084X
    ISSN 2050-084X
    DOI 10.7554/eLife.73021
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