دورية أكاديمية
أعرض في EDS

Evidence for a Conserved Function of Eukaryotic Pantothenate Kinases in the Regulation of Mitochondrial Homeostasis and Oxidative Stress.

التفاصيل البيبلوغرافية
العنوان: Evidence for a Conserved Function of Eukaryotic Pantothenate Kinases in the Regulation of Mitochondrial Homeostasis and Oxidative Stress.
المؤلفون: Ceccatelli Berti C; Department of Chemistry, Life Sciences and Environmental Sustainability, University of Parma, 43124 Parma, Italy., Gihaz S; Department of Internal Medicine, Section of Infectious Diseases, Yale School of Medicine, New Haven, CT 06520, USA., Figuccia S; Department of Chemistry, Life Sciences and Environmental Sustainability, University of Parma, 43124 Parma, Italy.; Department of Internal Medicine, Section of Infectious Diseases, Yale School of Medicine, New Haven, CT 06520, USA., Choi JY; Department of Internal Medicine, Section of Infectious Diseases, Yale School of Medicine, New Haven, CT 06520, USA., Pal AC; Department of Internal Medicine, Section of Infectious Diseases, Yale School of Medicine, New Haven, CT 06520, USA., Goffrini P; Department of Chemistry, Life Sciences and Environmental Sustainability, University of Parma, 43124 Parma, Italy., Ben Mamoun C; Department of Internal Medicine, Section of Infectious Diseases, Yale School of Medicine, New Haven, CT 06520, USA.
المصدر: International journal of molecular sciences [Int J Mol Sci] 2022 Dec 27; Vol. 24 (1). Date of Electronic Publication: 2022 Dec 27.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: MDPI Country of Publication: Switzerland NLM ID: 101092791 Publication Model: Electronic Cited Medium: Internet ISSN: 1422-0067 (Electronic) Linking ISSN: 14220067 NLM ISO Abbreviation: Int J Mol Sci Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Basel, Switzerland : MDPI, [2000-
مواضيع طبية MeSH: Oxidative Stress*/genetics , Pantothenate Kinase-Associated Neurodegeneration*/metabolism , Saccharomyces cerevisiae*/genetics , Saccharomyces cerevisiae*/metabolism, Humans ; Homeostasis ; Iron/metabolism ; Mitochondria/genetics ; Mitochondria/metabolism ; Pantothenic Acid ; Phosphotransferases (Alcohol Group Acceptor)/metabolism
مستخلص: Human PANK1 , PANK2 , and PANK3 genes encode several pantothenate kinase isoforms that catalyze the phosphorylation of vitamin B5 (pantothenic acid) to phosphopantothenate, a critical step in the biosynthesis of the major cellular cofactor, Coenzyme A (CoA). Mutations in the PANK2 gene, which encodes the mitochondrial pantothenate kinase (PanK) isoform, have been linked to pantothenate-kinase associated neurodegeneration (PKAN), a debilitating and often fatal progressive neurodegeneration of children and young adults. While the biochemical properties of these enzymes have been well-characterized in vitro, their expression in a model organism such as yeast in order to probe their function under cellular conditions have never been achieved. Here we used three yeast mutants carrying missense mutations in the yeast PanK gene, CAB1 , which are associated with defective growth at high temperature and iron, mitochondrial dysfunction, increased iron content, and oxidative stress, to assess the cellular function of human PANK genes and functional conservation of the CoA-controlled processes between humans and yeast. Overexpression of human PANK1 and PANK3 in these mutants restored normal cellular activity whereas complementation with PANK2 was partial and could only be achieved with an isoform, PanK2 mtmΔ , lacking the mitochondrial transit peptide. These data, which demonstrate functional conservation of PanK activity between humans and yeast, set the stage for the use of yeast as a model system to investigate the impact of PKAN-associated mutations on the metabolic pathways altered in this disease.
References: Hum Mol Genet. 2003 Feb 1;12(3):321-7. (PMID: 12554685)
Nat Genet. 2001 Aug;28(4):345-9. (PMID: 11479594)
Biochem Soc Trans. 2014 Aug;42(4):1033-6. (PMID: 25109998)
Semin Pediatr Neurol. 2006 Sep;13(3):182-5. (PMID: 17101457)
Mov Disord. 2021 Sep;36(9):2005-2016. (PMID: 34002881)
J Neurosci. 2005 Jan 19;25(3):689-98. (PMID: 15659606)
Int J Mol Sci. 2020 Dec 30;22(1):. (PMID: 33396642)
Nat Chem Biol. 2016 Aug;12(8):621-7. (PMID: 27322068)
Nature. 2003 Oct 16;425(6959):686-91. (PMID: 14562095)
Front Pharmacol. 2014 Mar 10;5:38. (PMID: 24653700)
Front Pharmacol. 2014 May 07;5:99. (PMID: 24847269)
Biochim Biophys Acta Mol Basis Dis. 2020 May 1;1866(5):165663. (PMID: 31918006)
Protein Sci. 2019 Jun;28(6):1031-1047. (PMID: 30927326)
PLoS One. 2017 Sep 1;12(9):e0184104. (PMID: 28863176)
PLoS One. 2014 Oct 30;9(10):e111585. (PMID: 25356756)
Sci Rep. 2017 Oct 27;7(1):14234. (PMID: 29079738)
EMBO Mol Med. 2016 Oct 4;8(10):1197-1211. (PMID: 27516453)
J Biol Chem. 2022 Mar;298(3):101577. (PMID: 35041826)
FASEB J. 2019 Aug;33(8):9551-9564. (PMID: 31145863)
Nat Commun. 2018 Oct 23;9(1):4399. (PMID: 30352999)
Structure. 2022 Nov 3;30(11):1494-1507.e6. (PMID: 36167065)
EMBO Mol Med. 2019 Dec;11(12):e10488. (PMID: 31701655)
Nat Chem Biol. 2015 Oct;11(10):784-92. (PMID: 26322826)
Ann N Y Acad Sci. 2004 Mar;1012:282-98. (PMID: 15105273)
Curr Genet. 2009 Apr;55(2):163-73. (PMID: 19266201)
Int J Mol Sci. 2021 Apr 24;22(9):. (PMID: 33923309)
FEBS Lett. 2018 Mar;592(5):692-702. (PMID: 29292494)
Vitam Horm. 2001;61:157-71. (PMID: 11153265)
FEBS Lett. 1997 Jul 14;411(2-3):373-7. (PMID: 9271239)
Biochem Soc Trans. 2018 Jun 19;46(3):721-728. (PMID: 29802218)
Nature. 2022 Aug;608(7921):192-198. (PMID: 35896750)
Biochim Biophys Acta Mol Cell Res. 2019 Dec;1866(12):118540. (PMID: 31473256)
J Biol Chem. 2019 Oct 4;294(40):14757-14767. (PMID: 31409644)
Antioxidants (Basel). 2020 Oct 20;9(10):. (PMID: 33092153)
Methods Mol Biol. 2014;1205:1-12. (PMID: 25213235)
PLoS One. 2012;7(11):e49509. (PMID: 23152917)
Folia Neuropathol. 2005;43(4):286-96. (PMID: 16416393)
Hum Mol Genet. 2009 May 15;18(10):1860-8. (PMID: 19261679)
Proc Natl Acad Sci U S A. 2010 Apr 13;107(15):6988-93. (PMID: 20351285)
Hum Mol Genet. 2009 Oct 1;18(19):3659-72. (PMID: 19602483)
EMBO Mol Med. 2019 Dec;11(12):e10489. (PMID: 31660701)
معلومات مُعتمدة: R01 AI153100 United States AI NIAID NIH HHS; UL1 TR001863 United States TR NCATS NIH HHS
فهرسة مساهمة: Keywords: PKAN; Saccharomyces cerevisiae; genetic complementation; model; pantothenate kinase; pantothenic acid; vitamin B5
المشرفين على المادة: E1UOL152H7 (Iron)
EC 2.7.1.33 (pantothenate kinase)
19F5HK2737 (Pantothenic Acid)
EC 2.7.1.- (Phosphotransferases (Alcohol Group Acceptor))
1SCE5NG3E8 (phosphopantothenic acid)
تواريخ الأحداث: Date Created: 20230108 Date Completed: 20230505 Latest Revision: 20230505
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC9820505
DOI: 10.3390/ijms24010435
PMID: 36613877
قاعدة البيانات: MEDLINE
الوصف
تدمد:1422-0067
DOI:10.3390/ijms24010435