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Deficiency of MIP/MTMR14 phosphatase induces a muscle disorder by disrupting Ca(2+) homeostasis.

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  • معلومة اضافية
    • المصدر:
      Publisher: Macmillan Magazines Ltd Country of Publication: England NLM ID: 100890575 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1476-4679 (Electronic) Linking ISSN: 14657392 NLM ISO Abbreviation: Nat Cell Biol Subsets: MEDLINE
    • بيانات النشر:
      Original Publication: London : Macmillan Magazines Ltd., [1999-
    • الموضوع:
      Homeostasis*; Calcium/*metabolism ; Muscular Diseases/*enzymology ; Phosphoric Monoester Hydrolases/*deficiency; Amino Acid Sequence ; Animals ; Calcium Signaling/physiology ; Electrophysiology ; Female ; Heart/anatomy & histology ; Humans ; Mice ; Mice, Knockout ; Molecular Sequence Data ; Muscle, Skeletal/cytology ; Muscle, Skeletal/physiology ; Myocardial Contraction/physiology ; Myocardium/metabolism ; Phosphatidylinositol Phosphates/chemistry ; Phosphatidylinositol Phosphates/metabolism ; Phosphoric Monoester Hydrolases/genetics ; Rabbits ; Ryanodine Receptor Calcium Release Channel/metabolism ; Sarcoplasmic Reticulum Calcium-Transporting ATPases/antagonists & inhibitors ; Sarcoplasmic Reticulum Calcium-Transporting ATPases/metabolism ; Sequence Alignment ; Sequence Homology, Amino Acid ; Tissue Distribution
    • نبذة مختصرة :
      The intracellular Ca(2+) concentration ([Ca(2+)](i)) in skeletal muscles must be rapidly regulated during the excitation-contraction-relaxation process. However, the signalling components involved in such rapid Ca(2+) movement are not fully understood. Here we report that mice deficient in the newly identified PtdInsP (phosphatidylinositol phosphate) phosphatase MIP/MTMR14 (muscle-specific inositol phosphatase) show muscle weakness and fatigue. Muscles isolated from MIP/MTMR14(-/-) mice produced less contractile force, had markedly prolonged relaxation and showed exacerbated fatigue relative to normal muscles. Further analyses revealed that MIP/MTMR14 deficiency resulted in spontaneous Ca(2+) leakage from the internal store - the sarcoplasmic reticulum. This was attributed to decreased metabolism (dephosphorylation) and the subsequent accumulation of MIP/MTMR14 substrates, especially PtdIns(3,5)P(2) and PtdIns (3,4)P(2). Furthermore, we found that PtdIns(3,5)P(2) and PtdIns(3,4)P(2) bound to, and directly activated, the Ca(2+) release channel (ryanodine receptor 1, RyR1) of the sarcoplasmic reticulum. These studies provide the first evidence that finely controlled PtdInsP levels in muscle cells are essential for maintaining Ca(2+) homeostasis and muscle performance.
    • References:
      Proc Natl Acad Sci U S A. 1990 Apr;87(7):2466-70. (PMID: 2138778)
      Biophys J. 1997 Aug;73(2):920-8. (PMID: 9251808)
      Physiol Genomics. 2000 Nov 09;4(1):25-33. (PMID: 11074010)
      Sci STKE. 2001 Dec 04;2001(111):re19. (PMID: 11734659)
      Cell Calcium. 2004 Feb;35(2):165-77. (PMID: 14706290)
      Nature. 2006 Oct 12;443(7112):651-7. (PMID: 17035995)
      Nature. 2007 Mar 15;446(7133):284-7. (PMID: 17361175)
      Curr Opin Pharmacol. 2008 Jun;8(3):319-26. (PMID: 18313359)
      Nature. 1988 Jan 28;331(6154):315-9. (PMID: 2448641)
      Nature. 1994 Jun 16;369(6481):556-9. (PMID: 7515481)
      Proc Natl Acad Sci U S A. 1994 Jun 21;91(13):6103-7. (PMID: 8016122)
      Biochem Biophys Res Commun. 2004 Oct 1;322(4):1280-5. (PMID: 15336975)
      Eur J Biochem. 2000 Sep;267(17):5291-7. (PMID: 10951187)
      Am J Physiol. 1998 Nov;275(5):H1652-62. (PMID: 9815073)
      Hum Mol Genet. 2006 Nov 1;15(21):3098-106. (PMID: 17008356)
      Genes Dev. 2006 Feb 15;20(4):486-500. (PMID: 16481476)
      J Biol Chem. 2006 Apr 7;281(14):9547-51. (PMID: 16452481)
      Cell. 2004 Jun 11;117(6):699-711. (PMID: 15186772)
      Physiol Genomics. 2005 Sep 21;23(1):72-8. (PMID: 15998745)
      Cardiovasc Drug Rev. 2003 Winter;21(4):255-76. (PMID: 14647531)
      Trends Cell Biol. 2002 Dec;12(12):579-85. (PMID: 12495846)
      Physiol Genomics. 2000 Nov 09;4(1):43-9. (PMID: 11074012)
      Biochem J. 1990 Oct 15;271(2):515-22. (PMID: 2173565)
      Nat Cell Biol. 2002 May;4(5):379-83. (PMID: 11988740)
      J Biol Chem. 2004 Jun 18;279(25):26588-96. (PMID: 15067003)
      Nat Chem Biol. 2007 Jan;3(1):55-9. (PMID: 17115034)
      Nat Cell Biol. 2002 Jan;4(1):83-8. (PMID: 11744924)
      Exp Physiol. 2002 Jan;87(1):77-82. (PMID: 11805861)
      Trends Biochem Sci. 2006 Jan;31(1):52-63. (PMID: 16364647)
      Ann N Y Acad Sci. 1998 Sep 16;853:260-3. (PMID: 10603954)
      J Biol Chem. 2003 Jan 31;278(5):3286-92. (PMID: 12419813)
      J Histochem Cytochem. 2003 Mar;51(3):275-83. (PMID: 12588955)
    • Grant Information:
      HL55438 United States HL NHLBI NIH HHS; R01 HL068212-06 United States HL NHLBI NIH HHS; R01 HL068212 United States HL NHLBI NIH HHS; R21 HL082670-02 United States HL NHLBI NIH HHS; HL082670 United States HL NHLBI NIH HHS; HL068212 United States HL NHLBI NIH HHS; R01 HL055438 United States HL NHLBI NIH HHS; R21 HL082670 United States HL NHLBI NIH HHS
    • الرقم المعرف:
      0 (Phosphatidylinositol Phosphates)
      0 (Ryanodine Receptor Calcium Release Channel)
      EC 3.1.3.- (MTMR14 protein, mouse)
      EC 3.1.3.2 (Phosphoric Monoester Hydrolases)
      EC 3.1.3.25 (myo-inositol-1 (or 4)-monophosphatase)
      EC 3.6.3.8 (Sarcoplasmic Reticulum Calcium-Transporting ATPases)
      SY7Q814VUP (Calcium)
    • الموضوع:
      Date Created: 20090526 Date Completed: 20090707 Latest Revision: 20211020
    • الموضوع:
      20231215
    • الرقم المعرف:
      PMC2693472
    • الرقم المعرف:
      10.1038/ncb1884
    • الرقم المعرف:
      19465920