دورية أكاديمية
Directed inhibition of nuclear import in cellular hypertrophy.
| العنوان: | Directed inhibition of nuclear import in cellular hypertrophy. |
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| المؤلفون: | Perez-Terzic C; Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Mayo Foundation, Rochester, Minnesota 55905, USA. terzic.andre@mayo.edu, Gacy AM, Bortolon R, Dzeja PP, Puceat M, Jaconi M, Prendergast FG, Terzic A |
| المصدر: | The Journal of biological chemistry [J Biol Chem] 2001 Jun 08; Vol. 276 (23), pp. 20566-71. Date of Electronic Publication: 2001 Mar 30. |
| نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
| اللغة: | English |
| بيانات الدورية: | Publisher: Elsevier Inc. on behalf of American Society for Biochemistry and Molecular Biology Country of Publication: United States NLM ID: 2985121R Publication Model: Print-Electronic Cited Medium: Print ISSN: 0021-9258 (Print) Linking ISSN: 00219258 NLM ISO Abbreviation: J Biol Chem Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: 2021- : [New York, NY] : Elsevier Inc. on behalf of American Society for Biochemistry and Molecular Biology Original Publication: Baltimore, MD : American Society for Biochemistry and Molecular Biology |
| مواضيع طبية MeSH: | Cell Size*, Cell Nucleus/*metabolism , Nucleotides/*metabolism, Animals ; Biological Transport ; Down-Regulation ; Phenotype ; Rats |
| مستخلص: | Each nuclear pore is responsible for both nuclear import and export with a finite capacity for bidirectional transport across the nuclear envelope. It remains poorly understood how the nuclear transport pathway responds to increased demands for nucleocytoplasmic communication. A case in point is cellular hypertrophy in which increased amounts of genetic material need to be transported from the nucleus to the cytosol. Here, we report an adaptive down-regulation of nuclear import supporting such an increased demand for nuclear export. The induction of cardiac cell hypertrophy by phenylephrine or angiotensin II inhibited the nuclear translocation of H1 histones. The removal of hypertrophic stimuli reversed the hypertrophic phenotype and restored nuclear import. Moreover, the inhibition of nuclear export by leptomycin B rescued import. Hypertrophic reprogramming increased the intracellular GTP/GDP ratio and promoted the nuclear redistribution of the GTP-binding transport factor Ran, favoring export over import. Further, in hypertrophy, the reduced creatine kinase and adenylate kinase activities limited energy delivery to the nuclear pore. The reduction of activities was associated with the closure of the cytoplasmic phase of the nuclear pore preventing import at the translocation step. Thus, to overcome the limited capacity for nucleocytoplasmic transport, cells requiring increased nuclear export regulate the nuclear transport pathway by undergoing a metabolic and structural restriction of nuclear import. |
| معلومات مُعتمدة: | HL07111 United States HL NHLBI NIH HHS; HL64822 United States HL NHLBI NIH HHS |
| المشرفين على المادة: | 0 (Nucleotides) |
| تواريخ الأحداث: | Date Created: 20010403 Date Completed: 20010712 Latest Revision: 20210209 |
| رمز التحديث: | 20240627 |
| DOI: | 10.1074/jbc.M101950200 |
| PMID: | 11283025 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 0021-9258 |
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| DOI: | 10.1074/jbc.M101950200 |