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J. Biol. Chem., Vol. 277, Issue 10, 8648-8657, March 8, 2002
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From the Division of Endocrinology and Metabolism, the Center for
Osteoporosis and Metabolic Bone Diseases, and the Central Arkansas
Veterans Healthcare System, University of Arkansas for Medical
Sciences, Little Rock, Arkansas 72205
Bisphosphonates, drugs used widely in the
treatment of bone diseases, prevent osteoblast and osteocyte
apoptosis by a mechanism involving extracellular signal-regulated
kinase (ERK) activation. We report herein that hexameric connexin
(Cx)-43 hemichannels, but not gap junctions, are the essential
transducers of the ERK-activating/anti-apoptotic effects of
bisphosphonates. Transfection of Cx-43, but not other Cxs, into Cx-43
naïve cells confers de novo responsiveness to the
drugs. The signal-transducing property of Cx-43 requires the pore
forming as well as the C-terminal domains of the protein, the
activation of both Src and ERK kinases, and the SH2 and SH3 domains of
Src. This evidence adds Cx-43 to the list of transmembrane proteins
capable of transducing survival signals in response to extracellular
cues and raises the possibility that it may serve in this capacity for
endogenously produced molecules or even other drugs.
Transduction of Cell Survival Signals by Connexin-43
Hemichannels*
*
This work was supported by National Institutes of Health
Grants R29-AR43453, KO2-AR02127, and P01-AG13918 and by the Department of Veterans Affairs.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Division of
Endocrinology and Metabolism, University of Arkansas for Medical
Sciences, 4301 West Markham, Mail Slot 587, Little Rock, AR
72205. Tel.: 501-686-8971; Fax: 501-686-8148; E-mail:
bellidoteresitam@uams.edu.
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