PMID- 16357103
OWN - NLM
STAT- MEDLINE
DCOM- 20060623
LR  - 20220331
IS  - 0888-8809 (Print)
IS  - 0888-8809 (Linking)
VI  - 20
IP  - 4
DP  - 2006 Apr
TI  - An essential role of the CAAT/enhancer binding protein-alpha in the vitamin 
      D-induced expression of the human steroid/bile acid-sulfotransferase (SULT2A1).
PG  - 795-808
AB  - The vitamin D receptor (VDR) regulates steroid and drug metabolism by inducing 
      the genes encoding phase I and phase II enzymes. SULT2A1 is a liver- and 
      intestine-expressed sulfo-conjugating enzyme that converts the alcohol-OH of 
      neutral steroids, bile acids, and drugs to water-soluble sulfated metabolites. 
      1alpha,25-Dihydroxyvitamin D3 [1,25-(OH)2D3] induces SULT2A1 gene transcription 
      after the recruitment of VDR to the vitamin D-responsive chromatin region of 
      SULT2A1. A composite element in human SULT2A1 directs the 1,25-(OH)2D3-mediated 
      induction of natural and heterologous promoters. This element combines a 
      VDR/retinoid X receptor-alpha-binding site [vitamin D response element (VDRE)], 
      which is an imperfect inverted repeat 2 of AGCTCA, and a CAAT/enhancer binding 
      protein (C/EBP)-binding site located 9 bp downstream to VDRE. The binding sites 
      were identified by EMSA, antibody supershift, and deoxyribonuclease I 
      footprinting. C/EBP-alpha at the composite element plays an essential role in the 
      VDR regulation of SULT2A1, because 1) induction was lost for promoters with 
      inactivating mutations at the VDRE or C/EBP element; 2) SULT2A1 induction by 
      1,25-(OH)2D3 in C/EBP-alpha-deficient cells required the expression of 
      cotransfected C/EBP-alpha; and 3) C/EBP-beta did not substitute for C/EBP-alpha 
      in this regulation. VDR and C/EBP-alpha were recruited concurrently to the 
      composite element along with the coactivators p300, steroid receptor coactivator 
      1 (SRC-1), and SRC-2, but not SRC-3. VDR and C/EBP-alpha associated endogenously 
      as a DNA-dependent, coimmunoprecipitable complex, which was detected at a 
      markedly higher level in 1,25-(OH)2D3-treated cells. These results provide the 
      first example of the essential role of the interaction in cis between C/EBP-alpha 
      and VDR in directing 1,25-(OH)2D3-induced expression of a VDR target gene.
FAU - Song, Chung S
AU  - Song CS
AD  - Department of Molecular Medicine/Institute of Biotechnology, The University of 
      Texas Health Science Center, San Antonio, Texas 78245, USA.
FAU - Echchgadda, Ibtissam
AU  - Echchgadda I
FAU - Seo, Young-Kyo
AU  - Seo YK
FAU - Oh, Taesung
AU  - Oh T
FAU - Kim, Soyoung
AU  - Kim S
FAU - Kim, Sung-A
AU  - Kim SA
FAU - Cho, Sunghwan
AU  - Cho S
FAU - Shi, Liheng
AU  - Shi L
FAU - Chatterjee, Bandana
AU  - Chatterjee B
LA  - eng
GR  - AG-10486/AG/NIA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
DEP - 20051215
PL  - United States
TA  - Mol Endocrinol
JT  - Molecular endocrinology (Baltimore, Md.)
JID - 8801431
RN  - 0 (CCAAT-Enhancer-Binding Protein-alpha)
RN  - 0 (RARA protein, human)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Calcitriol)
RN  - 0 (Receptors, Retinoic Acid)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Retinoic Acid Receptor alpha)
RN  - 9007-49-2 (DNA)
RN  - EC 2.8.2.- (Sulfotransferases)
RN  - EC 2.8.2.2 (alcohol sulfotransferase)
RN  - FXC9231JVH (Calcitriol)
SB  - IM
EIN - Mol Endocrinol. 2006 Jun;20(6):1286
MH  - Base Sequence
MH  - Binding Sites/genetics
MH  - CCAAT-Enhancer-Binding Protein-alpha/genetics/*metabolism
MH  - Calcitriol/*pharmacology
MH  - Cell Line
MH  - DNA/genetics/metabolism
MH  - Gene Expression/drug effects
MH  - Humans
MH  - In Vitro Techniques
MH  - Mutagenesis, Site-Directed
MH  - Promoter Regions, Genetic
MH  - RNA, Messenger/genetics/metabolism
MH  - Receptors, Calcitriol/metabolism
MH  - Receptors, Retinoic Acid/metabolism
MH  - Recombinant Proteins/genetics/metabolism
MH  - Retinoic Acid Receptor alpha
MH  - Sulfotransferases/*genetics
MH  - Transfection
MH  - Vitamin D Response Element
EDAT- 2005/12/17 09:00
MHDA- 2006/06/24 09:00
CRDT- 2005/12/17 09:00
PHST- 2005/12/17 09:00 [pubmed]
PHST- 2006/06/24 09:00 [medline]
PHST- 2005/12/17 09:00 [entrez]
AID - me.2005-0428 [pii]
AID - 10.1210/me.2005-0428 [doi]
PST - ppublish
SO  - Mol Endocrinol. 2006 Apr;20(4):795-808. doi: 10.1210/me.2005-0428. Epub 2005 Dec 
      15.