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J. Biol. Chem., Vol. 275, Issue 52, 40749-40756, December 29, 2000
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From the The vitamin D receptor (VDR) is a member of the
steroid/retinoid receptor superfamily of nuclear receptors that has
potential tumor-suppressive functions. We show here that VDR interacts
with and is regulated by BAG1L, a nuclear protein that binds heat shock 70-kDa (Hsp70) family molecular chaperones. Endogenous BAG1L can be
co-immunoprecipitated with VDR from prostate cancer cells (ALVA31; LNCaP) in a ligand-dependent manner. BAG1L, but not shorter
non-nuclear isoforms of this protein (BAG1; BAG1M/Rap46), markedly
enhanced, in a ligand-dependent manner, the ability of VDR
to trans-activate reporter gene plasmids containing a vitamin D
response element in transient transfection assays. Mutant BAG1L lacking
the C-terminal Hsc70-binding domain suppressed (in a
concentration-dependent fashion) VDR-mediated trans-activation
of vitamin D response element-containing reporter gene plasmids,
without altering levels of VDR or endogenous BAG1L protein, suggesting
that it operates as a trans-dominant inhibitor of BAG1L. Gene
transfer-mediated elevations in BAG1L protein levels in a prostate
cancer cell line (PC3), which is moderately responsive to VDR
ligands, increased the ability of natural
(1
BAG1L Enhances Trans-activation Function of the Vitamin D
Receptor*
§¶,, and
Burnham Institute, La Jolla, California
92037 and § RIGEB, MAM-TÜBITAK,
P. K. 21 Gebze 41 470, Kocaeli, Turkey
,25(OH)2 vitamin D3) and synthetic
(1,25-dihydroxy-19-nor-22(E)-vitamin D3) VDR
ligands to induce expression of the VDR target gene,
p21Waf1, and suppress DNA synthesis. Thus, BAG1L is a
direct regulator of VDR, which enhances its trans-activation function
and improves tumor cell responses to growth-suppressive VDR ligands.
*
This work was supported in part by Department of Defense
Prostate Research Program Grant DAMD17-98-1-8584.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: Burnham Inst.,
10901 N. Torrey Pines Rd., La Jolla, CA 92037. Tel.: 858-646-3140; Fax:
858-646-3194; E-mail: jreed@burnham-inst.org.
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