دورية أكاديمية
أعرض في EDS

Diverse cytopathologies in mitochondrial disease are caused by AMP-activated protein kinase signaling.

التفاصيل البيبلوغرافية
العنوان: Diverse cytopathologies in mitochondrial disease are caused by AMP-activated protein kinase signaling.
المؤلفون: Bokko PB; Department of Microbiology, La Trobe University, Melbourne, Victoria 3086, Australia., Francione L, Bandala-Sanchez E, Ahmed AU, Annesley SJ, Huang X, Khurana T, Kimmel AR, Fisher PR
المصدر: Molecular biology of the cell [Mol Biol Cell] 2007 May; Vol. 18 (5), pp. 1874-86. Date of Electronic Publication: 2007 Mar 01.
نوع المنشور: Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: American Society for Cell Biology Country of Publication: United States NLM ID: 9201390 Publication Model: Print-Electronic Cited Medium: Print ISSN: 1059-1524 (Print) Linking ISSN: 10591524 NLM ISO Abbreviation: Mol Biol Cell Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Bethesda, MD : American Society for Cell Biology, c1992-
مواضيع طبية MeSH: Mitochondrial Diseases/*enzymology , Mitochondrial Diseases/*pathology , Multienzyme Complexes/*metabolism , Protein Serine-Threonine Kinases/*metabolism, AMP-Activated Protein Kinases ; Adenosine Triphosphate/biosynthesis ; Amino Acid Sequence ; Animals ; Base Sequence ; DNA, Protozoan/genetics ; Dictyostelium/enzymology ; Dictyostelium/genetics ; Dictyostelium/growth & development ; Gene Dosage ; Genes, Protozoan ; Humans ; Mitochondrial Diseases/genetics ; Models, Biological ; Molecular Sequence Data ; Multienzyme Complexes/antagonists & inhibitors ; Multienzyme Complexes/chemistry ; Multienzyme Complexes/genetics ; Phagocytosis ; Photobiology ; Pinocytosis ; Protein Serine-Threonine Kinases/antagonists & inhibitors ; Protein Serine-Threonine Kinases/chemistry ; Protein Serine-Threonine Kinases/genetics ; Protein Structure, Tertiary ; Recombinant Proteins/chemistry ; Recombinant Proteins/genetics ; Recombinant Proteins/metabolism ; Signal Transduction
مستخلص: The complex cytopathology of mitochondrial diseases is usually attributed to insufficient ATP. AMP-activated protein kinase (AMPK) is a highly sensitive cellular energy sensor that is stimulated by ATP-depleting stresses. By antisense-inhibiting chaperonin 60 expression, we produced mitochondrially diseased strains with gene dose-dependent defects in phototaxis, growth, and multicellular morphogenesis. Mitochondrial disease was phenocopied in a gene dose-dependent manner by overexpressing a constitutively active AMPK alpha subunit (AMPKalphaT). The aberrant phenotypes in mitochondrially diseased strains were suppressed completely by antisense-inhibiting AMPKalpha expression. Phagocytosis and macropinocytosis, although energy consuming, were unaffected by mitochondrial disease and AMPKalpha expression levels. Consistent with the role of AMPK in energy homeostasis, mitochondrial "mass" and ATP levels were reduced by AMPKalpha antisense inhibition and increased by AMPKalphaT overexpression, but they were near normal in mitochondrially diseased cells. We also found that 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside, a pharmacological AMPK activator in mammalian cells, mimics mitochondrial disease in impairing Dictyostelium phototaxis and that AMPKalpha antisense-inhibited cells were resistant to this effect. The results show that diverse cytopathologies in Dictyostelium mitochondrial disease are caused by chronic AMPK signaling not by insufficient ATP.
References: Mol Cell Biol. 2000 Sep;20(18):6704-11. (PMID: 10958668)
Eur J Cell Biol. 2006 Sep;85(9-10):1099-106. (PMID: 16735078)
J Biol Chem. 2001 Jun 1;276(22):19102-10. (PMID: 11262401)
Am J Physiol Endocrinol Metab. 2001 Dec;281(6):E1340-6. (PMID: 11701451)
Bioessays. 2001 Dec;23(12):1112-9. (PMID: 11746230)
Dev Biol. 2002 Jan 1;241(1):183-94. (PMID: 11784104)
Microbiology. 2002 Feb;148(Pt 2):413-20. (PMID: 11832505)
J Cell Sci. 2002 May 1;115(Pt 9):1907-18. (PMID: 11956322)
J Biomed Sci. 2002;9(6 Pt 1):475-87. (PMID: 12372986)
Proc Natl Acad Sci U S A. 2002 Dec 10;99(25):15983-7. (PMID: 12444247)
Traffic. 2003 Jan;4(1):1-5. (PMID: 12535269)
Hum Mol Genet. 2003 Feb 15;12(4):399-413. (PMID: 12566387)
Biochem J. 2003 Mar 15;370(Pt 3):751-62. (PMID: 12467494)
J Mol Endocrinol. 2003 Apr;30(2):151-61. (PMID: 12683939)
Diabetes. 2004 Feb;53 Suppl 1:S103-9. (PMID: 14749274)
Plasmid. 1998;39(2):141-53. (PMID: 9514707)
Nucleic Acids Res. 1998 Jul 1;26(13):3317-8. (PMID: 9628938)
J Biol Chem. 1998 Dec 25;273(52):35347-54. (PMID: 9857077)
Diabetes. 1999 Aug;48(8):1667-71. (PMID: 10426389)
Am J Physiol. 1999 Aug;277(2 Pt 2):H643-9. (PMID: 10444490)
Muscle Nerve. 1999 Sep;22(9):1228-33. (PMID: 10454718)
Blood. 2003 May 1;101(9):3674-80. (PMID: 12522004)
FEBS Lett. 2003 Jul 3;546(1):113-20. (PMID: 12829246)
Proc Natl Acad Sci U S A. 2003 Jul 22;100(15):8839-43. (PMID: 12847291)
J Muscle Res Cell Motil. 2002;23(7-8):839-52. (PMID: 12952082)
Eukaryot Cell. 2003 Dec;2(6):1315-26. (PMID: 14665465)
J Clin Invest. 2004 Jan;113(2):274-84. (PMID: 14722619)
Circ Res. 2004 Mar 5;94(4):e27-31. (PMID: 14752031)
Proc Natl Acad Sci U S A. 2004 Mar 9;101(10):3329-35. (PMID: 14985505)
Neurochem Res. 2004 Mar;29(3):589-600. (PMID: 15038606)
Am J Hum Genet. 2004 Jun;74(6):1276-81. (PMID: 15114530)
J Cell Sci. 2004 Jul 1;117(Pt 15):3141-52. (PMID: 15226392)
J Biol. 2003;2(4):28. (PMID: 14511394)
Circulation. 2004 Jul 27;110(4):444-51. (PMID: 15262850)
Cytometry A. 2004 Oct;61(2):162-9. (PMID: 15382028)
J Cell Sci. 2004 Nov 1;117(Pt 23):5479-87. (PMID: 15509864)
Cell. 1981 Mar;23(3):799-807. (PMID: 7226230)
Biochem Biophys Res Commun. 1986 Aug 14;138(3):1146-52. (PMID: 2428360)
J Biol Chem. 1992 Feb 15;267(5):2864-7. (PMID: 1346611)
Eur J Biochem. 1994 Feb 1;219(3):751-7. (PMID: 8112325)
Eur J Biochem. 1995 Apr 15;229(2):558-65. (PMID: 7744080)
FEBS Lett. 1997 Feb 24;403(3):254-8. (PMID: 9091312)
Biochem Biophys Res Commun. 1997 May 8;234(1):39-43. (PMID: 9168956)
Bioessays. 1997 May;19(5):397-407. (PMID: 9174405)
Nat Genet. 1997 Jul;16(3):226-34. (PMID: 9207786)
Biochem Biophys Res Commun. 1997 Sep 18;238(2):323-5. (PMID: 9299504)
Nat Genet. 1998 Jan;18(1):38-43. (PMID: 9425897)
Nature. 1998 Jan 8;391(6663):184-7. (PMID: 9428765)
Plant J. 1999 Aug;19(4):433-9. (PMID: 10504565)
Biochem Biophys Res Commun. 2005 Mar 11;328(2):449-54. (PMID: 15694368)
Microbiol Mol Biol Rev. 2005 Mar;69(1):79-100. (PMID: 15755954)
J Biol Chem. 2005 Apr 8;280(14):13395-400. (PMID: 15695819)
Nature. 2005 May 5;435(7038):43-57. (PMID: 15875012)
Proc Natl Acad Sci U S A. 2005 Jun 7;102(23):8204-9. (PMID: 15928081)
Cell Metab. 2005 Jan;1(1):15-25. (PMID: 16054041)
Dev Biol. 2005 Aug 1;284(1):25-36. (PMID: 15964562)
Circ Res. 2005 Oct 14;97(8):837-44. (PMID: 16151020)
Dev Cell. 2005 Dec;9(6):843-54. (PMID: 16326395)
Nucleic Acids Res. 2006 Jan 1;34(Database issue):D423-7. (PMID: 16381903)
Immunol Cell Biol. 2006 Feb;84(1):6-12. (PMID: 16405649)
Physiology (Bethesda). 2006 Feb;21:48-60. (PMID: 16443822)
EMBO Rep. 2006 Jul;7(7):694-8. (PMID: 16819464)
Methods Mol Biol. 2006;346:137-70. (PMID: 16957289)
Traffic. 2001 May;2(5):311-20. (PMID: 11350627)
معلومات مُعتمدة: United States Intramural NIH HHS
المشرفين على المادة: 0 (DNA, Protozoan)
0 (Multienzyme Complexes)
0 (Recombinant Proteins)
8L70Q75FXE (Adenosine Triphosphate)
EC 2.7.11.1 (Protein Serine-Threonine Kinases)
EC 2.7.11.31 (AMP-Activated Protein Kinases)
تواريخ الأحداث: Date Created: 20070303 Date Completed: 20070711 Latest Revision: 20211203
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC1855013
DOI: 10.1091/mbc.e06-09-0881
PMID: 17332500
قاعدة البيانات: MEDLINE
الوصف
تدمد:1059-1524
DOI:10.1091/mbc.e06-09-0881