자료유형 | 학위논문 |
---|---|
서명/저자사항 | The Tmem135 Overexpression Mouse: A New Model of Cardiomyopathy. |
개인저자 | Lewis, Sarah A. |
단체저자명 | The University of Wisconsin - Madison. Genetics. |
발행사항 | [S.l.]: The University of Wisconsin - Madison., 2018. |
발행사항 | Ann Arbor: ProQuest Dissertations & Theses, 2018. |
형태사항 | 114 p. |
기본자료 저록 | Dissertation Abstracts International 80-01B(E). Dissertation Abstract International |
ISBN | 9780438360600 |
학위논문주기 | Thesis (Ph.D.)--The University of Wisconsin - Madison, 2018. |
일반주기 |
Source: Dissertation Abstracts International, Volume: 80-01(E), Section: B.
Adviser: Akihiro Ikeda. |
요약 | The process of aging is the decline of an organism's lifespan and is defined by changes at distinct levels of organizational structures: molecular, cellular, tissue level, and systemic. Aging increases the susceptibility for disease states that |
요약 | The basis of my thesis is the study of transmembrane protein 135 ( Tmem135), whose anomalous expression leads to aging and age-related disease phenotypes. TMEM135 is a highly conserved protein that localizes to the outer membrane of mitochondria |
요약 | In Chapter 1, we examined the effect of Tmem135 overexpression in the adult mouse heart. The heart, like the retina, has high energy demands met largely by mitochondria. Perturbations in mitochondrial dynamics and functions have detrimental effe |
요약 | In Chapter 2, we sought to identify factors that interact with Tmem135 to help further elucidate TMEM135 functions in the heart. We found that overexpression of Tmem135 on the mixed genetic background (FVB and C57BL6/J) leads to sudden death in |
요약 | Our study indicates that mitochondrial dynamics are important for the maintenance of normal heart function and may have significant roles in the aging of the heart. We also identified molecular pathways that are affected by overexpression of Tme |
일반주제명 | Genetics. |
언어 | 영어 |
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