CREB regulates MHC class II expression in a CIITA-dependent manner

Carlos S. Moreno; Guy W. Beresford; Pascale Louis-Plence; Ann C. Morris; Jeremy M. Boss

doi:10.1016/S1074-7613(00)80015-1

CREB regulates MHC class II expression in a CIITA-dependent manner

Carlos S. Moreno, Guy W. Beresford, Pascale Louis-Plence, Ann C. Morris, Jeremy M. Boss

Research output: Contribution to journal › Article › peer-review

164 Scopus citations

Abstract

The X2 box of MHC class II promoters is homologous to TRE/CRE elements and is required for expression of MHC class II genes. The X2 box-specific DNA binding activity, X2BP, was purified to homogeneity, sequenced, and identified as CREB. Transient transactivation experiments showed that CREB can cooperate with CIITA to enhance activation of transcription from MHC class II promoters in a dose-dependent manner. Binding of CREB to the class II promoter in vivo was demonstrated by a chromatin immunoprecipitation assay. Additionally, ICER, a dominant inhibitor of CREB function, was found to repress class II expression. These results demonstrate that CREB binds to the X2 box in vivo and cooperates with CIITA to direct MHC class II expression.

Original language	English
Pages (from-to)	143-151
Number of pages	9
Journal	Immunity
Volume	10
Issue number	2
DOIs	https://doi.org/10.1016/S1074-7613(00)80015-1
State	Published - Feb 1999

Bibliographical note

Funding Information:
We are indebted to R. Goodman for providing the RSV-CREBWT mammalian expression construct, M. Green for providing the ATF-1 and ATF-2 constructs, and P. Quinn for providing the pSG-ICER construct. We also thank C. Molina for providing ICER antisera, the laboratory of P. Farnham for the ChIP protocol, and M. Montminy for the PET-CREB bacterial expression construct. Peptide digests and internal amino acid microsequencing were performed under the direction of J. Pohl at the Emory Microchemical Facility, Winship Cancer Center, Emory University School of Medicine. Mass spectrometry analysis was performed under the direction of K. Stone at the W. M. Keck Foundation Biotechnology Resource Laboratory, Yale University. We thank C. Moran, G. Churchward, D. Pallas, P. Doetsch, and D. Reines for a critical reading of the manuscript. This work was supported by National Institutes of Health Grant GM43710 (J. M. B.). C. S. M. was supported by National Institutes of Health predoctoral fellowship AI09106.

ASJC Scopus subject areas

Immunology and Allergy
Immunology
Infectious Diseases

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1016/S1074-7613(00)80015-1

Cite this

@article{4194c0ef875b4eabbbf6f5f419fa5d8c,

title = "CREB regulates MHC class II expression in a CIITA-dependent manner",

abstract = "The X2 box of MHC class II promoters is homologous to TRE/CRE elements and is required for expression of MHC class II genes. The X2 box-specific DNA binding activity, X2BP, was purified to homogeneity, sequenced, and identified as CREB. Transient transactivation experiments showed that CREB can cooperate with CIITA to enhance activation of transcription from MHC class II promoters in a dose-dependent manner. Binding of CREB to the class II promoter in vivo was demonstrated by a chromatin immunoprecipitation assay. Additionally, ICER, a dominant inhibitor of CREB function, was found to repress class II expression. These results demonstrate that CREB binds to the X2 box in vivo and cooperates with CIITA to direct MHC class II expression.",

author = "Moreno, {Carlos S.} and Beresford, {Guy W.} and Pascale Louis-Plence and Morris, {Ann C.} and Boss, {Jeremy M.}",

note = "Funding Information: We are indebted to R. Goodman for providing the RSV-CREBWT mammalian expression construct, M. Green for providing the ATF-1 and ATF-2 constructs, and P. Quinn for providing the pSG-ICER construct. We also thank C. Molina for providing ICER antisera, the laboratory of P. Farnham for the ChIP protocol, and M. Montminy for the PET-CREB bacterial expression construct. Peptide digests and internal amino acid microsequencing were performed under the direction of J. Pohl at the Emory Microchemical Facility, Winship Cancer Center, Emory University School of Medicine. Mass spectrometry analysis was performed under the direction of K. Stone at the W. M. Keck Foundation Biotechnology Resource Laboratory, Yale University. We thank C. Moran, G. Churchward, D. Pallas, P. Doetsch, and D. Reines for a critical reading of the manuscript. This work was supported by National Institutes of Health Grant GM43710 (J. M. B.). C. S. M. was supported by National Institutes of Health predoctoral fellowship AI09106.",

year = "1999",

month = feb,

doi = "10.1016/S1074-7613(00)80015-1",

language = "English",

volume = "10",

pages = "143--151",

number = "2",

}

TY - JOUR

T1 - CREB regulates MHC class II expression in a CIITA-dependent manner

AU - Moreno, Carlos S.

AU - Beresford, Guy W.

AU - Louis-Plence, Pascale

AU - Morris, Ann C.

AU - Boss, Jeremy M.

N1 - Funding Information: We are indebted to R. Goodman for providing the RSV-CREBWT mammalian expression construct, M. Green for providing the ATF-1 and ATF-2 constructs, and P. Quinn for providing the pSG-ICER construct. We also thank C. Molina for providing ICER antisera, the laboratory of P. Farnham for the ChIP protocol, and M. Montminy for the PET-CREB bacterial expression construct. Peptide digests and internal amino acid microsequencing were performed under the direction of J. Pohl at the Emory Microchemical Facility, Winship Cancer Center, Emory University School of Medicine. Mass spectrometry analysis was performed under the direction of K. Stone at the W. M. Keck Foundation Biotechnology Resource Laboratory, Yale University. We thank C. Moran, G. Churchward, D. Pallas, P. Doetsch, and D. Reines for a critical reading of the manuscript. This work was supported by National Institutes of Health Grant GM43710 (J. M. B.). C. S. M. was supported by National Institutes of Health predoctoral fellowship AI09106.

PY - 1999/2

Y1 - 1999/2

N2 - The X2 box of MHC class II promoters is homologous to TRE/CRE elements and is required for expression of MHC class II genes. The X2 box-specific DNA binding activity, X2BP, was purified to homogeneity, sequenced, and identified as CREB. Transient transactivation experiments showed that CREB can cooperate with CIITA to enhance activation of transcription from MHC class II promoters in a dose-dependent manner. Binding of CREB to the class II promoter in vivo was demonstrated by a chromatin immunoprecipitation assay. Additionally, ICER, a dominant inhibitor of CREB function, was found to repress class II expression. These results demonstrate that CREB binds to the X2 box in vivo and cooperates with CIITA to direct MHC class II expression.

AB - The X2 box of MHC class II promoters is homologous to TRE/CRE elements and is required for expression of MHC class II genes. The X2 box-specific DNA binding activity, X2BP, was purified to homogeneity, sequenced, and identified as CREB. Transient transactivation experiments showed that CREB can cooperate with CIITA to enhance activation of transcription from MHC class II promoters in a dose-dependent manner. Binding of CREB to the class II promoter in vivo was demonstrated by a chromatin immunoprecipitation assay. Additionally, ICER, a dominant inhibitor of CREB function, was found to repress class II expression. These results demonstrate that CREB binds to the X2 box in vivo and cooperates with CIITA to direct MHC class II expression.

UR - http://www.scopus.com/inward/record.url?scp=0033083701&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0033083701&partnerID=8YFLogxK

U2 - 10.1016/S1074-7613(00)80015-1

DO - 10.1016/S1074-7613(00)80015-1

M3 - Article

C2 - 10072067

AN - SCOPUS:0033083701

SN - 1074-7613

VL - 10

SP - 143

EP - 151

JO - Immunity

JF - Immunity

IS - 2

ER -

CREB regulates MHC class II expression in a CIITA-dependent manner

Abstract

Bibliographical note

ASJC Scopus subject areas

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this