دورية أكاديمية
أعرض في EDS

Exposure to BMAA mirrors molecular processes linked to neurodegenerative disease.

التفاصيل البيبلوغرافية
العنوان: Exposure to BMAA mirrors molecular processes linked to neurodegenerative disease.
المؤلفون: Beri J; Department of Chemistry, North Carolina State University, Raleigh, NC, USA., Nash T; Center for Human Health and the Environment, North Carolina State University, Raleigh, NC, USA., Martin RM; Department of Biological Sciences, North Carolina State University, Raleigh, NC, USA., Bereman MS; Department of Chemistry, North Carolina State University, Raleigh, NC, USA.; Center for Human Health and the Environment, North Carolina State University, Raleigh, NC, USA.; Department of Biological Sciences, North Carolina State University, Raleigh, NC, USA.
المصدر: Proteomics [Proteomics] 2017 Sep; Vol. 17 (17-18). Date of Electronic Publication: 2017 Aug 24.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Wiley-VCH Country of Publication: Germany NLM ID: 101092707 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1615-9861 (Electronic) Linking ISSN: 16159853 NLM ISO Abbreviation: Proteomics Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Weinheim, Germany : Wiley-VCH,
مواضيع طبية MeSH: Amino Acids, Diamino/*toxicity , Amyotrophic Lateral Sclerosis/*chemically induced , Excitatory Amino Acid Agonists/*toxicity , Gene Expression Regulation/*drug effects , Motor Neurons/*metabolism , Neuroblastoma/*metabolism, Amyotrophic Lateral Sclerosis/metabolism ; Amyotrophic Lateral Sclerosis/pathology ; Animals ; Cell Line ; Cyanobacteria Toxins ; Diet/adverse effects ; Mice ; Motor Neurons/pathology ; Neuroblastoma/pathology
مستخلص: The goal of this study is to investigate the molecular pathways perturbed by in vitro exposure of beta-methylamino-L-alanine (BMAA) to NSC-34 cells via contemporary proteomics. Our analysis of differentially regulated proteins reveals significant enrichment (p < 0.01) of pathways related to ER stress, protein ubiquitination, the unfolded protein response, and mitochondrial dysfunction. Upstream regulator analysis indicates that exposure to BMAA induces activation of transcription factors (X-box binding protein 1; nuclear factor 2 erythroid like 2; promyelocytic leukemia) involved in regulation of the UPR, oxidative stress, and cellular senescence. Furthermore, the authors examine the hypothesis that BMAA causes protein damage via misincorporation in place of L-Serine. The authors are unable to detect misincorporation of BMAA into protein via analysis of cellular protein, secreted protein, targeted detection of BMAA after protein hydrolysis, or through the use of in vitro protein translation kits.
(© 2017 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)
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معلومات مُعتمدة: P30 ES025128 United States ES NIEHS NIH HHS; T32 ES007046 United States ES NIEHS NIH HHS
فهرسة مساهمة: Keywords: Amyotrophic lateral sclerosis; BMAA; Exposures; LC-MS/MS; Neurodegeneration
المشرفين على المادة: 0 (Amino Acids, Diamino)
0 (Cyanobacteria Toxins)
0 (Excitatory Amino Acid Agonists)
108SA6URTV (beta-N-methylamino-L-alanine)
تواريخ الأحداث: Date Created: 20170825 Date Completed: 20171226 Latest Revision: 20211204
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC5828681
DOI: 10.1002/pmic.201700161
PMID: 28837265
قاعدة البيانات: MEDLINE
الوصف
تدمد:1615-9861
DOI:10.1002/pmic.201700161