دورية أكاديمية
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Nischarin Deletion Reduces Oxidative Metabolism and Overall ATP: A Study Using a Novel NISCH Δ5-6 Knockout Mouse Model.

التفاصيل البيبلوغرافية
العنوان: Nischarin Deletion Reduces Oxidative Metabolism and Overall ATP: A Study Using a Novel NISCH Δ5-6 Knockout Mouse Model.
المؤلفون: Nguyen TH; Department of Biochemistry and Molecular Biology, Louisiana State University Health Science Center, New Orleans, LA 70112, USA., Yousefi H; Department of Biochemistry and Molecular Biology, Louisiana State University Health Science Center, New Orleans, LA 70112, USA., Okpechi SC; Department of Biochemistry and Molecular Biology, Louisiana State University Health Science Center, New Orleans, LA 70112, USA., Lauterboeck L; Cardiovascular Center of Excellence, School of Medicine, Louisiana State University Health Science Center, New Orleans, LA 70112, USA.; Department of Pharmacology, Louisiana State University Health Science Center, New Orleans, LA 70112, USA., Dong S; Department of Biochemistry and Molecular Biology, Louisiana State University Health Science Center, New Orleans, LA 70112, USA., Yang Q; Cardiovascular Center of Excellence, School of Medicine, Louisiana State University Health Science Center, New Orleans, LA 70112, USA.; Department of Pharmacology, Louisiana State University Health Science Center, New Orleans, LA 70112, USA., Alahari SK; Department of Biochemistry and Molecular Biology, Louisiana State University Health Science Center, New Orleans, LA 70112, USA.
المصدر: International journal of molecular sciences [Int J Mol Sci] 2022 Jan 25; Vol. 23 (3). Date of Electronic Publication: 2022 Jan 25.
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: Adenosine Triphosphate/*metabolism , Imidazoline Receptors/*metabolism , Oxygen Consumption/*genetics, Adenosine Triphosphate/genetics ; Animals ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Cell Respiration ; Fibroblasts ; Gene Expression/genetics ; Imidazoline Receptors/genetics ; Intracellular Signaling Peptides and Proteins ; Lipid Metabolism/genetics ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Oxidative Stress ; Oxygen Consumption/physiology
مستخلص: Nischarin (Nisch) is a cytosolic scaffolding protein that harbors tumor-suppressor-like characteristics. Previous studies have shown that Nisch functions as a scaffolding protein and regulates multiple biological activities. In the current study, we prepared a complete Nisch knockout model, for the first time, by deletion of exons 5 and 6. This knockout model was confirmed by Qrt-PCR and Western blotting with products from mouse embryonic fibroblast (MEF) cells. Embryos and adult mice of knockouts are significantly smaller than their wild-type counterparts. Deletion of Nisch enhanced cell migration, as demonstrated by wound type and transwell migration assays. Since the animals were small in size, we investigated Nisch's effect on metabolism by conducting several assays using the Seahorse analyzer system. These data indicate that Nisch null cells have lower oxygen consumption rates, lower ATP production, and lower levels of proton leak. We examined the expression of 15 genes involved in lipid and fat metabolism, as well as cell growth, and noted a significant increase in expression for many genes in Nischarin null animals. In summary, our results show that Nischarin plays an important physiological role in metabolic homeostasis.
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معلومات مُعتمدة: R01 HL135336 United States HL NHLBI NIH HHS
فهرسة مساهمة: Keywords: Nischarin; knockout mouse model; metabolism; migration
المشرفين على المادة: 0 (Imidazoline Receptors)
0 (Intracellular Signaling Peptides and Proteins)
0 (Nisch protein, mouse)
8L70Q75FXE (Adenosine Triphosphate)
تواريخ الأحداث: Date Created: 20220215 Date Completed: 20220304 Latest Revision: 20220716
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC8835720
DOI: 10.3390/ijms23031374
PMID: 35163298
قاعدة البيانات: MEDLINE
الوصف
تدمد:1422-0067
DOI:10.3390/ijms23031374