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Consequences of Altered Mortalin Expression in Control of Cell Proliferation and Brain Function

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Abstract

Mortalin, a member of Hsp70 family, was first cloned as a mortality factor in mouse fibroblasts in 1993. It was subsequently determined as a key player of mitochondrial biogenesis, ATP production, stress responses, chaperoning, intracellular trafficking and continued proliferation of cancer cells. Besides its role in cancer, mortalin is also an important protein for the brain that utilizes high energy and depends heavily on mitochondrial functions. In a proteomic screening, mortalin was detected as a downregulated protein in Parkinson’s disease and oxidized in Alzheimer’s disease depicting that the “functional lack of mortalin” is related to these diseases. Knockdown of mortalin homologue in worms (C. elegans) caused abnormalities in mitochondria, premature senescence and progeria like phenotype. These studies have demonstrated that mortalin-mediated mitochondrial functions are not only the key factors in maintaining the continued proliferation of cancer cells but also the normal neuronal physiology. Lack of a functional mortalin leads to cancer cell death and neurodegenerative phenotype.

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Wadhwa, R., Kaul, S.C. (2012). Consequences of Altered Mortalin Expression in Control of Cell Proliferation and Brain Function. In: Thakur, M., Rattan, S. (eds) Brain Aging and Therapeutic Interventions. Springer, Dordrecht. https://doi.org/10.1007/978-94-007-5237-5_7

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