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The Tmem135 Overexpression Mouse: A New Model of Cardiomyopathy

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서명/저자사항The Tmem135 Overexpression Mouse: A New Model of Cardiomyopathy.
개인저자Lewis, Sarah A.
단체저자명The University of Wisconsin - Madison. Genetics.
발행사항[S.l.]: The University of Wisconsin - Madison., 2018.
발행사항Ann Arbor: ProQuest Dissertations & Theses, 2018.
형태사항114 p.
기본자료 저록Dissertation Abstracts International 80-01B(E).
Dissertation Abstract International
ISBN9780438360600
학위논문주기Thesis (Ph.D.)--The University of Wisconsin - Madison, 2018.
일반주기 Source: Dissertation Abstracts International, Volume: 80-01(E), Section: B.
Adviser: Akihiro Ikeda.
요약The 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
요약The 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
요약In 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
요약In 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
요약Our 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
일반주제명Genetics.
언어영어
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