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Biomolecules 2012, 2(1), 143-164; doi:10.3390/biom2010143
Review

Mortalin, Apoptosis, and Neurodegeneration

1
, 2
, 3
 and 4,*
Received: 31 January 2012; in revised form: 22 February 2012 / Accepted: 23 February 2012 / Published: 1 March 2012
(This article belongs to the Special Issue Feature Papers)
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Abstract: Mortalin is a highly conserved heat-shock chaperone usually found in multiple subcellular locations. It has several binding partners and has been implicated in various functions ranging from stress response, control of cell proliferation, and inhibition/prevention of apoptosis. The activity of this protein involves different structural and functional mechanisms, and minor alterations in its expression level may lead to serious biological consequences, including neurodegeneration. In this article we review the most current data associated with mortalin’s binding partners and how these protein-protein interactions may be implicated in apoptosis and neurodegeneration. A complete understanding of the molecular pathways in which mortalin is involved is important for the development of therapeutic strategies for cancer and neurodegenerative diseases.
Keywords: Alzheimer’s disease; apoptosis; GRP75; mortalin; mtHsp70; neurodegeneration; oxidative stress; Quantitative Intact Proteomics; p53 Alzheimer’s disease; apoptosis; GRP75; mortalin; mtHsp70; neurodegeneration; oxidative stress; Quantitative Intact Proteomics; p53
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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MDPI and ACS Style

Londono, C.; Osorio, C.; Gama, V.; Alzate, O. Mortalin, Apoptosis, and Neurodegeneration. Biomolecules 2012, 2, 143-164.

AMA Style

Londono C, Osorio C, Gama V, Alzate O. Mortalin, Apoptosis, and Neurodegeneration. Biomolecules. 2012; 2(1):143-164.

Chicago/Turabian Style

Londono, Carolina; Osorio, Cristina; Gama, Vivian; Alzate, Oscar. 2012. "Mortalin, Apoptosis, and Neurodegeneration." Biomolecules 2, no. 1: 143-164.


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