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Transcriptional regulation of RACK1 and modulation of its expression: Role of steroid hormones and significance in health and aging.
- Source :
-
Cellular signalling [Cell Signal] 2017 Jul; Vol. 35, pp. 264-271. Date of Electronic Publication: 2017 Feb 09. - Publication Year :
- 2017
-
Abstract
- The Receptor for Activated C Kinase 1 (RACK1) is a scaffold protein for different kinases and membrane receptors. RACK1 can shuttle proteins to their sites of action, facilitate cross-talk among distinct signaling pathways or recruit other signaling proteins into the complexes. Therefore, it is a key mediator of various pathways and is involved in various biological events including development, immune response, brain activity and cancer. Because of its importance, it is of extreme significance to understand the transcriptional mechanisms governing its expression. The identification of regulatory elements in the promoter of RACK1 shed some light on its transcriptional modulation in physiological and pathological context. Literature data support the existence of a complex hormonal balance, between glucocorticoids and androgens, in the control of RACK1 expression due to specific and complex interactions on the RACK1 promoter. These and other informations suggest that a better understanding of RACK1 transcriptional regulation is essential to unravel its role. Furthermore, the modulation of its expression in physiological or pathological conditions may be of interest in different context, such as aging and cancer.<br /> (Copyright © 2017. Published by Elsevier Inc.)
- Subjects :
- Aging pathology
Gene Expression Regulation
Humans
Neoplasms pathology
Promoter Regions, Genetic
Receptors, Cell Surface
Regulatory Sequences, Nucleic Acid genetics
Signal Transduction
Aging genetics
Neoplasm Proteins genetics
Neoplasms genetics
Receptors for Activated C Kinase genetics
Transcription, Genetic
Subjects
Details
- Language :
- English
- ISSN :
- 1873-3913
- Volume :
- 35
- Database :
- MEDLINE
- Journal :
- Cellular signalling
- Publication Type :
- Academic Journal
- Accession number :
- 28192162
- Full Text :
- https://doi.org/10.1016/j.cellsig.2017.02.010