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  1. Article ; Online: Critical Amino Acid Residues Regulating TRPA1 Zn

    Matsubara, Masaki / Muraki, Yukiko / Suzuki, Hiroka / Hatano, Noriyuki / Muraki, Katsuhiko

    The Journal of biological chemistry

    2024  , Page(s) 107302

    Abstract: Cellular zinc ions ( ... ...

    Abstract Cellular zinc ions (Zn
    Language English
    Publishing date 2024-04-18
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1016/j.jbc.2024.107302
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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.108: Show issues Location:
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  2. Article ; Online: Potent Activation of Human but Not Mouse TRPA1 by JT010.

    Matsubara, Masaki / Muraki, Yukiko / Hatano, Noriyuki / Suzuki, Hiroka / Muraki, Katsuhiko

    International journal of molecular sciences

    2022  Volume 23, Issue 22

    Abstract: Transient receptor potential (TRP) ankyrin repeat 1 (TRPA1), which is involved in inflammatory pain sensation, is activated by endogenous factors, such as intracellular ... ...

    Abstract Transient receptor potential (TRP) ankyrin repeat 1 (TRPA1), which is involved in inflammatory pain sensation, is activated by endogenous factors, such as intracellular Zn
    MeSH term(s) Humans ; Transient Receptor Potential Channels/genetics ; Calcium Channels/genetics ; TRPA1 Cation Channel/genetics ; Cysteine ; Calcium/metabolism ; Methionine
    Chemical Substances Transient Receptor Potential Channels ; Calcium Channels ; TRPA1 Cation Channel ; JT010 ; Cysteine (K848JZ4886) ; Calcium (SY7Q814VUP) ; Methionine (AE28F7PNPL) ; TRPA1 protein, human
    Language English
    Publishing date 2022-11-18
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms232214297
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  3. Article ; Online: HIF-1α Dependent Upregulation of ZIP8, ZIP14, and TRPA1 Modify Intracellular Zn

    Hatano, Noriyuki / Matsubara, Masaki / Suzuki, Hiroka / Muraki, Yukiko / Muraki, Katsuhiko

    International journal of molecular sciences

    2021  Volume 22, Issue 12

    Abstract: Intracellular free zinc ([ ... ...

    Abstract Intracellular free zinc ([Zn
    MeSH term(s) Cation Transport Proteins/genetics ; Cation Transport Proteins/metabolism ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Inflammation/genetics ; Inflammation/pathology ; Intracellular Space/metabolism ; Synoviocytes/metabolism ; Synoviocytes/pathology ; TRPA1 Cation Channel/genetics ; TRPA1 Cation Channel/metabolism ; Up-Regulation/genetics ; Zinc/metabolism
    Chemical Substances Cation Transport Proteins ; Hypoxia-Inducible Factor 1, alpha Subunit ; SLC39A14 protein, human ; SLC39A8 protein, human ; TRPA1 Cation Channel ; TRPA1 protein, human ; Zinc (J41CSQ7QDS)
    Language English
    Publishing date 2021-06-14
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms22126349
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  4. Article ; Online: HIF-1α Dependent Upregulation of ZIP8, ZIP14, and TRPA1 Modify Intracellular Zn 2+ Accumulation in Inflammatory Synoviocytes

    Noriyuki Hatano / Masaki Matsubara / Hiroka Suzuki / Yukiko Muraki / Katsuhiko Muraki

    International Journal of Molecular Sciences, Vol 22, Iss 6349, p

    2021  Volume 6349

    Abstract: Intracellular free zinc ([Zn 2+ ] i ) is mobilized in neuronal and non-neuronal cells under physiological and/or pathophysiological conditions; therefore, [Zn 2+ ] i is a component of cellular signal transduction in biological systems. Although several ... ...

    Abstract Intracellular free zinc ([Zn 2+ ] i ) is mobilized in neuronal and non-neuronal cells under physiological and/or pathophysiological conditions; therefore, [Zn 2+ ] i is a component of cellular signal transduction in biological systems. Although several transporters and ion channels that carry Zn 2+ have been identified, proteins that are involved in Zn 2+ supply into cells and their expression are poorly understood, particularly under inflammatory conditions. Here, we show that the expression of Zn 2+ transporters ZIP8 and ZIP14 is increased via the activation of hypoxia-induced factor 1α (HIF-1α) in inflammation, leading to [Zn 2+ ] i accumulation, which intrinsically activates transient receptor potential ankyrin 1 (TRPA1) channel and elevates basal [Zn 2+ ] i . In human fibroblast-like synoviocytes (FLSs), treatment with inflammatory mediators, such as tumor necrosis factor-α (TNF-α) and interleukin-1α (IL-1α), evoked TRPA1-dependent intrinsic Ca 2+ oscillations. Assays with fluorescent Zn 2+ indicators revealed that the basal [Zn 2+ ] i concentration was significantly higher in TRPA1-expressing HEK cells and inflammatory FLSs. Moreover, TRPA1 activation induced an elevation of [Zn 2+ ] i level in the presence of 1 μM Zn 2+ in inflammatory FLSs. Among the 17 out of 24 known Zn 2+ transporters, FLSs that were treated with TNF-α and IL-1α exhibited a higher expression of ZIP8 and ZIP14 . Their expression levels were augmented by transfection with an active component of nuclear factor-κB P65 and HIF-1α expression vectors, and they could be abolished by pretreatment with the HIF-1α inhibitor echinomycin (Echi). The functional expression of ZIP8 and ZIP14 in HEK cells significantly increased the basal [Zn 2+ ] i level. Taken together, Zn 2+ carrier proteins, TRPA1, ZIP8, and ZIP14, induced under HIF-1α mediated inflammation can synergistically change [Zn 2+ ] i in inflammatory FLSs.
    Keywords TRPA1 ; ZIP8 ; ZIP14 ; intracellular Zn 2+ concentration ; synoviocytes ; inflammation ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 333
    Language English
    Publishing date 2021-06-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: The inflammatory regulation of TRPA1 expression in human A549 lung epithelial cells.

    Luostarinen, Samu / Hämäläinen, Mari / Hatano, Noriyuki / Muraki, Katsuhiko / Moilanen, Eeva

    Pulmonary pharmacology & therapeutics

    2021  Volume 70, Page(s) 102059

    Abstract: Transient receptor potential ankyrin-1 (TRPA1) is an ion channel mediating pain and cough signals in sensory neurons. We and others have shown that TRPA1 is also expressed in some non-neuronal cells and supports inflammatory responses. To address the ... ...

    Abstract Transient receptor potential ankyrin-1 (TRPA1) is an ion channel mediating pain and cough signals in sensory neurons. We and others have shown that TRPA1 is also expressed in some non-neuronal cells and supports inflammatory responses. To address the pathogenesis and to uncover potential targets for pharmacotherapy in inflammatory lung diseases, we set out to study the expression of TRPA1 in human A549 lung epithelial cells under inflammatory conditions. TRPA1 expression was determined by RT-qPCR and Western blotting at a mRNA and protein level, respectively and its function was studied by Fluo 3-AM intracellular Ca
    MeSH term(s) A549 Cells ; Cytokines ; Epithelial Cells ; Gene Expression ; Humans ; Lung ; TRPA1 Cation Channel/genetics ; Tumor Necrosis Factor-alpha
    Chemical Substances Cytokines ; TRPA1 Cation Channel ; TRPA1 protein, human ; Tumor Necrosis Factor-alpha
    Language English
    Publishing date 2021-07-21
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1399707-5
    ISSN 1522-9629 ; 1094-5539
    ISSN (online) 1522-9629
    ISSN 1094-5539
    DOI 10.1016/j.pupt.2021.102059
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2389: Show issues Location:
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  6. Article ; Online: Correction to: Characteristic MRI findings of shoulder, elbow, and wrist joints in wheelchair user.

    Sakai, Masafumi / Mutsuzaki, Hirotaka / Shimizu, Yukiyo / Okamoto, Yoshikazu / Yatabe, Katsuhiko / Muraki, Ichio / Nakajima, Kotaro

    Skeletal radiology

    2021  Volume 50, Issue 4, Page(s) 843

    Language English
    Publishing date 2021-01-22
    Publishing country Germany
    Document type Published Erratum
    ZDB-ID 527592-1
    ISSN 1432-2161 ; 0364-2348
    ISSN (online) 1432-2161
    ISSN 0364-2348
    DOI 10.1007/s00256-021-03717-8
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1304: Show issues Location:
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  7. Article ; Online: PIEZO1 Channel Is a Potential Regulator of Synovial Sarcoma Cell-Viability.

    Suzuki, Takahisa / Muraki, Yukiko / Hatano, Noriyuki / Suzuki, Hiroka / Muraki, Katsuhiko

    International journal of molecular sciences

    2018  Volume 19, Issue 5

    Abstract: Detection of mechanical stress is essential for diverse biological functions including touch, audition, and maintenance of vascular myogenic tone. PIEZO1, a mechano-sensing cation channel, is widely expressed in neuronal and non-neuronal cells and is ... ...

    Abstract Detection of mechanical stress is essential for diverse biological functions including touch, audition, and maintenance of vascular myogenic tone. PIEZO1, a mechano-sensing cation channel, is widely expressed in neuronal and non-neuronal cells and is expected to be involved in important biological functions. Here, we examined the possibility that PIEZO1 is involved in the regulation of synovial sarcoma cell-viability. Application of a PIEZO1 agonist Yoda1 effectively induced Ca
    MeSH term(s) Action Potentials/drug effects ; Cell Line, Tumor ; Cell Survival/genetics ; Gene Knockdown Techniques ; Humans ; Ion Channel Gating/drug effects ; Ion Channels/genetics ; Ion Channels/metabolism ; Mechanotransduction, Cellular ; Sarcoma, Synovial/genetics ; Sarcoma, Synovial/metabolism ; Stress, Mechanical
    Chemical Substances Ion Channels ; PIEZO1 protein, human
    Language English
    Publishing date 2018-05-14
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms19051452
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  8. Article ; Online: Impaired TRPM3-dependent calcium influx and restoration using Naltrexone in natural killer cells of myalgic encephalomyelitis/chronic fatigue syndrome patients.

    Eaton-Fitch, Natalie / Du Preez, Stanley / Cabanas, Hélène / Muraki, Katsuhiko / Staines, Donald / Marshall-Gradisnik, Sonya

    Journal of translational medicine

    2022  Volume 20, Issue 1, Page(s) 94

    Abstract: Background: Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a serious disorder of unknown aetiology. While the pathomechanism of ME/CFS remains elusive, reduced natural killer (NK) cell cytotoxic function is a consistent immunological ... ...

    Abstract Background: Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a serious disorder of unknown aetiology. While the pathomechanism of ME/CFS remains elusive, reduced natural killer (NK) cell cytotoxic function is a consistent immunological feature. NK cell effector functions rely on long-term sustained calcium (Ca
    Methods: Live cell immunofluorescent imaging was used to measure TRPM3-dependent Ca
    Results: The amplitude (p < 0.0001) and half-time of Ca
    Conclusion: TRPM3-dependent Ca
    MeSH term(s) Calcium/metabolism ; Fatigue Syndrome, Chronic ; Humans ; Killer Cells, Natural ; Naltrexone/pharmacology ; Naltrexone/therapeutic use ; TRPM Cation Channels/metabolism
    Chemical Substances TRPM Cation Channels ; TRPM3 protein, human ; Naltrexone (5S6W795CQM) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2022-02-16
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2118570-0
    ISSN 1479-5876 ; 1479-5876
    ISSN (online) 1479-5876
    ISSN 1479-5876
    DOI 10.1186/s12967-022-03297-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Potential Therapeutic Benefit of Low Dose Naltrexone in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Role of Transient Receptor Potential Melastatin 3 Ion Channels in Pathophysiology and Treatment.

    Cabanas, Helene / Muraki, Katsuhiko / Eaton-Fitch, Natalie / Staines, Donald Ross / Marshall-Gradisnik, Sonya

    Frontiers in immunology

    2021  Volume 12, Page(s) 687806

    Abstract: Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a debilitating multi-systemic chronic condition of unknown aetiology classified as an immune dysfunction syndrome and neurological disorder. The discovery of the widely expressed Transient ... ...

    Abstract Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a debilitating multi-systemic chronic condition of unknown aetiology classified as an immune dysfunction syndrome and neurological disorder. The discovery of the widely expressed Transient Receptor Potential Melastatin 3 (TRPM3) as a nociceptor channel substantially targeted by certain opioid receptors, and its implication in calcium (Ca
    MeSH term(s) Adult ; Calcium Signaling/drug effects ; Case-Control Studies ; Drug Repositioning ; Fatigue Syndrome, Chronic/drug therapy ; Fatigue Syndrome, Chronic/immunology ; Fatigue Syndrome, Chronic/metabolism ; Fatigue Syndrome, Chronic/physiopathology ; Female ; Humans ; Killer Cells, Natural/drug effects ; Killer Cells, Natural/immunology ; Killer Cells, Natural/metabolism ; Lymphocyte Activation/drug effects ; Male ; Membrane Potentials/drug effects ; Middle Aged ; Naltrexone/administration & dosage ; Naltrexone/adverse effects ; Narcotic Antagonists/administration & dosage ; Narcotic Antagonists/adverse effects ; Receptors, Opioid, mu/antagonists & inhibitors ; Receptors, Opioid, mu/metabolism ; TRPM Cation Channels/drug effects ; TRPM Cation Channels/metabolism ; Treatment Outcome
    Chemical Substances Narcotic Antagonists ; Receptors, Opioid, mu ; TRPM Cation Channels ; TRPM3 protein, human ; Naltrexone (5S6W795CQM)
    Language English
    Publishing date 2021-07-13
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2021.687806
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  10. Article ; Online: Transient receptor potential melastatin 3 dysfunction in post COVID-19 condition and myalgic encephalomyelitis/chronic fatigue syndrome patients.

    Sasso, Etianne Martini / Muraki, Katsuhiko / Eaton-Fitch, Natalie / Smith, Peter / Lesslar, Olivia Ly / Deed, Gary / Marshall-Gradisnik, Sonya

    Molecular medicine (Cambridge, Mass.)

    2022  Volume 28, Issue 1, Page(s) 98

    Abstract: Background: Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a severe multisystemic condition associated with post-infectious onset, impaired natural killer (NK) cell cytotoxicity and impaired ion channel function, namely Transient ... ...

    Abstract Background: Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a severe multisystemic condition associated with post-infectious onset, impaired natural killer (NK) cell cytotoxicity and impaired ion channel function, namely Transient Receptor Potential Melastatin 3 (TRPM3). Long-term effects of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus has resulted in neurocognitive, immunological, gastrointestinal, and cardiovascular manifestations recently recognised as post coronavirus disease 2019 (COVID-19) condition. The symptomatology of ME/CFS overlaps significantly with post COVID-19; therefore, this research aimed to investigate TRPM3 ion channel function in post COVID-19 condition patients.
    Methods: Whole-cell patch-clamp technique was used to measure TRPM3 ion channel activity in isolated NK cells of N = 5 ME/CFS patients, N = 5 post COVID-19 patients, and N = 5 healthy controls (HC). The TRPM3 agonist, pregnenolone sulfate (PregS) was used to activate TRPM3 function, while ononetin was used as a TRPM3 antagonist.
    Results: As reported in previous research, PregS-induced TRPM3 currents were significantly reduced in ME/CFS patients compared with HC (p = 0.0048). PregS-induced TRPM3 amplitude was significantly reduced in post COVID-19 condition compared with HC (p = 0.0039). Importantly, no significant difference was reported in ME/CFS patients compared with post COVID-19 condition as PregS-induced TRPM3 currents of post COVID-19 condition patients were similar of ME/CFS patients currents (p > 0.9999). Isolated NK cells from post COVID-19 condition and ME/CFS patients were resistant to ononetin and differed significantly with HC (p < 0.0001).
    Conclusion: The results of this investigation suggest that post COVID-19 condition patients may have impaired TRPM3 ion channel function and provide further evidence regarding the similarities between post COVID-19 condition and ME/CFS. Impaired TRPM3 channel activity in post COVID-19 condition patients suggest impaired ion mobilisation which may consequently impede cell function resulting in chronic post-infectious symptoms. Further investigation into TRPM3 function may elucidate the pathomechanism, provide a diagnostic and therapeutic target for post COVID-19 condition patients and commonalities with ME/CFS patients.
    MeSH term(s) COVID-19/complications ; Fatigue Syndrome, Chronic ; Humans ; Killer Cells, Natural ; Patch-Clamp Techniques ; SARS-CoV-2
    Language English
    Publishing date 2022-08-19
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1283676-x
    ISSN 1528-3658 ; 1076-1551
    ISSN (online) 1528-3658
    ISSN 1076-1551
    DOI 10.1186/s10020-022-00528-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4456: Show issues Location:
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