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Autophagy is a major intracellular degradation system by which cytoplasmic components are enclosed by autophagosomes and delivered to lysosomes. Formation of the autophagosome requires a set of autophagy-related (Atg) proteins. Among these proteins, the ULK1 complex, which is composed of ULK1 (or ULK2), FIP200, Atg13, and Atg101, acts at an initial step. Previous studies showed that ULK1 and FIP200 also function in pathways other than autophagy. However, whether Atg13 and Atg101 act similarly to ULK1 and FIP200 remains unknown. In the present study, we generated Atg13 knockout mice. Like FIP200-deficient mice, Atg13-deficient mice die in utero, which is distinct from most other types of Atg-deficient mice. Atg13-deficient embryos show growth retardation and myocardial growth defects. In cultured fibroblasts, Atg13 deficiency blocks autophagosome formation at an upstream step. In addition, sensitivity to tumor necrosis factor alpha (TNF-α)-induced apoptosis is enhanced by deletion of Atg13 or FIP200, but not by other Atg proteins, as well as by simultaneous deletion of ULK1 and ULK2. These results suggest that Atg13 has both autophagic and nonautophagic functions and that the latter are essential for cardiac development and likely shared with FIP200 but not with ULK1/2.

Titel:	Atg13 Is Essential for Autophagy and Cardiac Development in Mice.
Autor/in / Beteiligte Person:	Kaizuka, T ; Mizushima, N
Zeitschrift:	Molecular and cellular biology, Jg. 36 (2015-12-07), Heft 4, S. 585-95
Veröffentlichung:	2023- : [Philadelphia] : Taylor & Francis ; <i>Original Publication</i>: [Washington, D.C.] : American Society for Microbiology, [c1981-, 2015
Medientyp:	academicJournal
ISSN:	1098-5549 (electronic)
DOI:	10.1128/MCB.01005-15
Schlagwort:	Animals Apoptosis Regulatory Proteins metabolism Base Sequence Cell Line Gene Deletion Heart Defects, Congenital metabolism Mice genetics Mice metabolism Mice, Inbred C57BL Mice, Knockout Molecular Sequence Data Tumor Necrosis Factor-alpha metabolism Apoptosis Regulatory Proteins genetics Autophagy Heart embryology Heart Defects, Congenital genetics Mice embryology
Sonstiges:	Nachgewiesen in: MEDLINE Sprachen: English Publication Type: Journal Article; Research Support, Non-U.S. Gov't Language: English [Mol Cell Biol] 2015 Dec 07; Vol. 36 (4), pp. 585-95. <i>Date of Electronic Publication: </i>2015 Dec 07 (<i>Print Publication: </i>2016). MeSH Terms: Autophagy* ; Apoptosis Regulatory Proteins / genetics ; Heart / embryology ; Heart Defects, Congenital / genetics ; Mice / embryology ; Animals ; Apoptosis Regulatory Proteins / metabolism ; Base Sequence ; Cell Line ; Gene Deletion ; Heart Defects, Congenital / metabolism ; Mice / genetics ; Mice / metabolism ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular Sequence Data ; Tumor Necrosis Factor-alpha / metabolism References: Nature. 2004 Dec 23;432(7020):1032-6. (PMID: 15525940) ; Cell. 2008 Jan 11;132(1):27-42. (PMID: 18191218) ; Mol Biol Cell. 2008 Feb;19(2):668-81. (PMID: 18077553) ; Cell Signal. 2008 May;20(5):787-94. (PMID: 18036779) ; Mol Biol Cell. 2008 May;19(5):2039-50. (PMID: 18287526) ; Genes Dev. 2008 Dec 1;22(23):3292-307. (PMID: 19056884) ; Mol Cell Biol. 2009 Jan;29(1):157-71. (PMID: 18936157) ; Mol Biol Cell. 2009 Apr;20(7):1981-91. (PMID: 19211835) ; Mol Biol Cell. 2009 Apr;20(7):1992-2003. (PMID: 19225151) ; J Cell Biol. 2005 May 9;169(3):425-34. (PMID: 15866887) ; Physiology (Bethesda). 2005 Jun;20:180-93. (PMID: 15888575) ; Proc Natl Acad Sci U S A. 2005 Sep 20;102(38):13484-9. (PMID: 16157885) ; Development. 2006 Sep;133(17):3441-50. (PMID: 16887826) ; J Cell Biol. 2006 Oct 9;175(1):121-33. (PMID: 17015619) ; Mol Biol Cell. 2006 Nov;17(11):4675-85. (PMID: 16914516) ; Proc Natl Acad Sci U S A. 2007 Apr 3;104(14):5842-7. (PMID: 17389358) ; Mol Biol Cell. 2008 Dec;19(12):5360-72. (PMID: 18843052) ; J Cell Biol. 2008 May 5;181(3):497-510. (PMID: 18443221) ; Dev Cell. 2008 Sep;15(3):344-57. (PMID: 18804433) ; Mol Biol Cell. 2008 Nov;19(11):4762-75. (PMID: 18768753) ; Nature. 2008 Nov 13;456(7219):264-8. (PMID: 18849965) ; J Biol Chem. 2009 May 1;284(18):12297-305. (PMID: 19258318) ; Cell. 2009 May 15;137(4):721-35. (PMID: 19427028) ; Mol Biol Rep. 2009 Jul;36(6):1311-21. (PMID: 18636236) ; Nat Rev Mol Cell Biol. 2009 Jul;10(7):458-67. (PMID: 19491929) ; Autophagy. 2009 Jul;5(5):649-62. (PMID: 19287211) ; Autophagy. 2009 Jul;5(5):608-15. (PMID: 19377305) ; Autophagy. 2009 Oct;5(7):973-9. (PMID: 19597335) ; Cell. 2010 Feb 5;140(3):313-26. (PMID: 20144757) ; FEBS Lett. 2010 Apr 2;584(7):1359-66. (PMID: 20146925) ; Curr Opin Cell Biol. 2010 Apr;22(2):132-9. (PMID: 20056399) ; Development. 2010 May;137(10):1657-67. (PMID: 20392746) ; Proc Natl Acad Sci U S A. 2009 Dec 8;106(49):20842-6. (PMID: 19926846) ; Autophagy. 2010 Aug;6(6):764-76. (PMID: 20639694) ; Nat Cell Biol. 2010 Sep;12(9):831-5. (PMID: 20811355) ; J Cell Biol. 2011 Jan 10;192(1):17-27. (PMID: 21220506) ; Nature. 2011 Jan 20;469(7330):323-35. (PMID: 21248839) ; Proc Natl Acad Sci U S A. 2011 Mar 22;108(12):4788-93. (PMID: 21383122) ; PLoS One. 2011;6(5):e19632. (PMID: 21589871) ; Proc Natl Acad Sci U S A. 2011 Jul 5;108(27):11121-6. (PMID: 21690395) ; J Biol Chem. 2011 Sep 16;286(37):32502-12. (PMID: 21795712) ; Annu Rev Cell Dev Biol. 2011;27:107-32. (PMID: 21801009) ; Nat Rev Mol Cell Biol. 2011 Nov;12(11):757-63. (PMID: 22016059) ; Cell. 2011 Nov 11;147(4):728-41. (PMID: 22078875) ; Vet Pathol. 2012 Jan;49(1):64-70. (PMID: 21233329) ; Autophagy. 2011 Dec;7(12):1423-33. (PMID: 22024743) ; J Cell Sci. 2012 Mar 15;125(Pt 6):1488-99. (PMID: 22275429) ; Cell Rep. 2012 May 31;1(5):401-7. (PMID: 22675671) ; Autophagy. 2012 Oct;8(10):1426-33. (PMID: 22885670) ; J Biol Chem. 2013 Jan 11;288(2):1125-34. (PMID: 23209294) ; Autophagy. 2013 Feb 1;9(2):124-37. (PMID: 23295650) ; Autophagy. 2013 Mar;9(3):361-73. (PMID: 23291478) ; EMBO Rep. 2013 Mar 1;14(3):284-91. (PMID: 23392225) ; Oncogene. 2013 May 9;32(19):2421-32. (PMID: 22751121) ; Genes Cells. 2013 Jun;18(6):450-8. (PMID: 23573916) ; Nat Cell Biol. 2013 Jul;15(7):741-50. (PMID: 23685627) ; Autophagy. 2013 Aug;9(8):1201-13. (PMID: 23819996) ; PLoS One. 2013;8(9):e75313. (PMID: 24066173) ; Autophagy. 2014 Jan;10(1):45-56. (PMID: 24275123) ; Nat Biotechnol. 2014 Apr;32(4):347-55. (PMID: 24584096) ; Autophagy. 2014 Apr;10(4):572-87. (PMID: 24441423) ; Autophagy. 2015;11(1):145-54. (PMID: 25585051) ; Reprod Biol. 2015 Sep;15(3):131-8. (PMID: 26370455) ; Autophagy. 2015;11(9):1471-83. (PMID: 26213203) ; Neuron. 1999 Dec;24(4):833-46. (PMID: 10624947) ; Immunity. 2000 Jun;12(6):633-42. (PMID: 10894163) ; Mol Cell Biol. 2001 Jun;21(12):3964-73. (PMID: 11359904) ; J Cell Sci. 2003 May 1;116(Pt 9):1679-88. (PMID: 12665549) ; Cell. 2004 Feb 20;116(4):491-7. (PMID: 14980217) ; Genes Dev. 2004 Mar 1;18(5):541-58. (PMID: 15014045) ; Genes Dev. 1994 Oct 15;8(20):2389-400. (PMID: 7958904) ; Genes Dev. 1997 Jul 15;11(14):1801-11. (PMID: 9242488) ; Development. 2004 Dec;131(23):5991-6000. (PMID: 15539493) Substance Nomenclature: 0 (ATG13 protein, mouse) ; 0 (Apoptosis Regulatory Proteins) ; 0 (Tumor Necrosis Factor-alpha) Entry Date(s): Date Created: 20151209 Date Completed: 20160621 Latest Revision: 20181113 Update Code: 20231215 PubMed Central ID: PMC4751695

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Atg13 Is Essential for Autophagy and Cardiac Development in Mice.