دورية أكاديمية
أعرض في EDS

Akt-mTORC1 signaling regulates Acly to integrate metabolic input to control of macrophage activation.

التفاصيل البيبلوغرافية
العنوان: Akt-mTORC1 signaling regulates Acly to integrate metabolic input to control of macrophage activation.
المؤلفون: Covarrubias AJ; Department of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, United States., Aksoylar HI; Department of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, United States., Yu J; Department of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, United States., Snyder NW; Center of Excellence in Environmental Toxicology, University of Pennsylvania, Philadelphia, United States.; A.J. Drexel Autism Institute, Drexel University, Philadelphia, United States., Worth AJ; Center of Excellence in Environmental Toxicology, University of Pennsylvania, Philadelphia, United States., Iyer SS; Department of Medicine, Brigham and Women's Hospital, Boston, United States., Wang J; Institute for Plant Physiology and Ecology, Shanghai Institute for Biological Sciences, Chinese Academy of Sciences, Shanghai, China., Ben-Sahra I; Department of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, United States., Byles V; Department of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, United States., Polynne-Stapornkul T; Department of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, United States., Espinosa EC; Department of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, United States., Lamming D; Department of Medicine, University of Wisconsin-Madison, Madison, United States., Manning BD; Department of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, United States., Zhang Y; Institute for Plant Physiology and Ecology, Shanghai Institute for Biological Sciences, Chinese Academy of Sciences, Shanghai, China., Blair IA; Center of Excellence in Environmental Toxicology, University of Pennsylvania, Philadelphia, United States., Horng T; Department of Genetics and Complex Diseases, Harvard T.H. Chan School of Public Health, Boston, United States.
المصدر: ELife [Elife] 2016 Feb 19; Vol. 5. Date of Electronic Publication: 2016 Feb 19.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural
اللغة: English
بيانات الدورية: Publisher: eLife Sciences Publications, Ltd Country of Publication: England NLM ID: 101579614 Publication Model: Electronic Cited Medium: Internet ISSN: 2050-084X (Electronic) Linking ISSN: 2050084X NLM ISO Abbreviation: Elife Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Cambridge, UK : eLife Sciences Publications, Ltd., 2012-
مواضيع طبية MeSH: Macrophage Activation* , Signal Transduction*, ATP Citrate (pro-S)-Lyase/*metabolism , Macrophages/*metabolism , Multiprotein Complexes/*metabolism , Proto-Oncogene Proteins c-akt/*metabolism , TOR Serine-Threonine Kinases/*metabolism, Acetylation ; Animals ; Cell Proliferation ; Chemokines/metabolism ; Gene Expression Regulation ; Histones/metabolism ; Interleukin-4/metabolism ; Macrophages/physiology ; Mechanistic Target of Rapamycin Complex 1 ; Mice, Inbred C57BL ; Protein Processing, Post-Translational
مستخلص: Macrophage activation/polarization to distinct functional states is critically supported by metabolic shifts. How polarizing signals coordinate metabolic and functional reprogramming, and the potential implications for control of macrophage activation, remains poorly understood. Here we show that IL-4 signaling co-opts the Akt-mTORC1 pathway to regulate Acly, a key enzyme in Ac-CoA synthesis, leading to increased histone acetylation and M2 gene induction. Only a subset of M2 genes is controlled in this way, including those regulating cellular proliferation and chemokine production. Moreover, metabolic signals impinge on the Akt-mTORC1 axis for such control of M2 activation. We propose that Akt-mTORC1 signaling calibrates metabolic state to energetically demanding aspects of M2 activation, which may define a new role for metabolism in supporting macrophage activation.
التعليقات: Comment in: Elife. 2016 Feb 19;5:null. (PMID: 26894957)
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معلومات مُعتمدة: R00 AG041765 United States AG NIA NIH HHS; R35CA197459 United States CA NCI NIH HHS; T32 DK007260 United States DK NIDDK NIH HHS; R21 AI119763 United States AI NIAID NIH HHS; P30 ES013508 United States ES NIEHS NIH HHS; R01 AI102964 United States AI NIAID NIH HHS; T32 ES019851 United States ES NIEHS NIH HHS; R35 CA197459 United States CA NCI NIH HHS; K99 AG041765 United States AG NIA NIH HHS; R01AI102964 United States AI NIAID NIH HHS
فهرسة مساهمة: Keywords: acly; akt; cell biology; immunology; immunometabolism; mTORC1; macrophage activation; macrophage metabolism; mouse
المشرفين على المادة: 0 (Chemokines)
0 (Histones)
0 (IL4 protein, human)
0 (Multiprotein Complexes)
207137-56-2 (Interleukin-4)
EC 2.3.3.8 (ATP Citrate (pro-S)-Lyase)
EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1)
EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
EC 2.7.11.1 (TOR Serine-Threonine Kinases)
تواريخ الأحداث: Date Created: 20160220 Date Completed: 20170110 Latest Revision: 20211203
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC4769166
DOI: 10.7554/eLife.11612
PMID: 26894960
قاعدة البيانات: MEDLINE
الوصف
تدمد:2050-084X
DOI:10.7554/eLife.11612