Mitogen Activated Protein kinase signal transduction pathways in the prostate
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BioMed Central
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Mitogen Activated Protein kinase signal transduction pathways in the prostate Paul D Maroni1,2, Sweaty Koul1,2, Randall B Meacham2 and Hari K Koul*1,2 Address: 1Signal Transduction and Molecular Biology Laboratory, Division of Urology, Department of Surgery, University of Colorado School of Medicine, 4200 East Ninth Avenue, C-319, Denver, CO 80262, USA and 2Division of Urology, Department of Surgery, University of Colorado School of Medicine, 4200 East Ninth Avenue, C-319, Denver, CO 80262, USA Email: Paul D Maroni - [email protected]; Sweaty Koul - [email protected]; Randall B Meacham - [email protected]; Hari K Koul* - [email protected] * Corresponding author
Published: 25 June 2004 Cell Communication and Signaling 2004, 2:5
doi:10.1186/1478-811X-2-5
Received: 23 January 2004 Accepted: 25 June 2004
This article is available from: http://www.biosignaling.com/content/2/1/5 © 2004 Maroni et al; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.
MAP kinasesprostate cancerandrogenmitogen
Abstract The biochemistry of the mitogen activated protein kinases ERK, JNK, and p38 have been studied in prostate physiology in an attempt to elucidate novel mechanisms and pathways for the treatment of prostatic disease. We reviewed articles examining mitogen-activated protein kinases using prostate tissue or cell lines. As with other tissue types, these signaling modules are links/ transmitters for important pathways in prostate cells that can result in cellular survival or apoptosis. While the activation of the ERK pathway appears to primarily result in survival, the roles of JNK and p38 are less clear. Manipulation of these pathways could have important implications for the treatment of prostate cancer and benign prostatic hypertrophy.
Background Signal transduction via mitogen activated protein (MAP) kinases plays a key role in a variety of cellular responses, including proliferation, differentiation, and cell death. MAP kinases have provided a focal point for remarkably rapid advances in our understanding of the control of cellular events by growth factors and stresses. Since their initial discovery in yeast, over a dozen MAP kinase families have been identified of these highly genetically conserved proteins. MAP kinase signal transduction pathways have not been studied in great detail in the prostate; however over one hundred publications describing the effects of various manipulations, including growth factors, chemical modifiers and androgens on prostatic cells have been described in the literature. Despite these studies, the struc-
ture and function of the MAP kinase pathways in prostate are far from clearly understood. Diseases of the prostate are a tremendous source of morbidity and mortality in aging males. Benign enlargement of the prostate gland is a significant source of discomfor
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