Please use this identifier to cite or link to this item: https://apo.ansto.gov.au/dspace/handle/10238/9158
Title: Lost in translocation: the functions of the 18-kD translocator protein
Authors: Gut, P
Zweckstetter, M
Banati, RB
Keywords: Mitochondria
Cell constituents
Membranes
Proteins
Membrane proteins
Receptors
Heme
Metabolism
Gene repressors
Transcriptional factors
Mitochondria
Cholesterol
Issue Date: 1-Jul-2015
Publisher: Elsevier B.V.
Citation: Gut, P., Zweckstetter, M., & Banati, R. B. (2015). Lost in translocation: the functions of the 18-kD translocator protein. Trends in Endocrinology & Metabolism, 26(7), 349-356. doi:10.1016/j.tem.2015.04.001
Abstract: Research spanning nearly four decades has assigned to the translocator protein (18 kDa) (TSPO) a critical role, among others, in the mitochondrial import of cholesterol, the subsequent steps of (neuro)steroid production, and systemic endocrine regulation, with implications for the pathophysiology of immune, inflammatory, neurodegenerative, and psychiatric as well as neoplastic diseases. Recent knockout studies in mice unexpectedly report normal or latent phenotypes, raising doubts about the protein's role in steroidogenesis and other previously postulated functions and challenging the validity of earlier data on the selectivity of TSPO-binding drugs. Here we provide a synthesis of the current debate from a structural and molecular biology perspective, discuss the limits of inference in loss-of-function (gene knockout) studies, and suggest new functions of TSPO. © 2015 Elsevier Inc.
Gov't Doc #: 8764
URI: https://doi.org/10.1016/j.tem.2015.04.001
http://apo.ansto.gov.au/dspace/handle/10238/9158
ISSN: 1043-2760
Appears in Collections:Journal Articles

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