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NFβA, a factor required for maximal interleukin-1β gene expression is identical to the ets family member PU.1. Evidence for structural alteration following LPS activation

Identifieur interne : 000E86 ( Main/Exploration ); précédent : 000E85; suivant : 000E87

NFβA, a factor required for maximal interleukin-1β gene expression is identical to the ets family member PU.1. Evidence for structural alteration following LPS activation

Auteurs : Jon A. Buras [États-Unis] ; Wende R. Reenstra [États-Unis] ; Matthew J. Fenton [États-Unis]

Source :

RBID : ISTEX:2CCB0B6119BF3A9E06923A52E844ADF76C416B67

Abstract

We have previously identified and characterized the macrophage-, neutrophil- and B cell-specific nuclear factor βA (NFβA), which is involved in transcriptional regulation of the interleukin-1β (IL-1β) gene. NFβA binds to a highly conserved sequence element located 6 bp upstream of the TATA motif within the IL-1β promoter and is required for maximal expression of the IL-1β gene. Here we show that NFβA is identical to the previously identified ets gene family member PU.1. The NFβA binding element shares 100% sequence identity with a novel PU.1 binding element recently found in the immunoglobulin J-chain promoter. Methylation interference DNA footprinting data demonstrated that NFβA and PU.1 make identical protein/DNA contacts. In vitro synthesized PU.1 possesses a mobility and binding specificity identical to NFβA as determined by electrophoretic mobility shift analysis (EMSA). Antisera directed against amino acids 39–55 of PU.1 recognizes NFβA in a manner indistinguishable from PU.1 in EMSA ‘supershift’ studies. NFβA and PU.1 also possess similiar protein structure as determined by proteolytic clipping bandshift analysis. Furthermore, we show that PU.1 is able to transactivate an NFβA-dependent promoter when co-transfected into HeLa cells which lack PU.1 NFβA. EMSA studies using recombinant TATA binding protein (TBP) and PU.1 suggest that PU.1 may induce assembly of a distinct TBP-dependent complex on the IL-1β promoter. Finally, immunohistochemical confocal laser scanning microscopy studies suggest that LPS stimulation of RAW macrophages induces a structural change in the N-terminal transcriptional activation domain of PU.1.


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DOI: 10.1016/0161-5890(95)00018-A


Affiliations:


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<div type="abstract" xml:lang="en">We have previously identified and characterized the macrophage-, neutrophil- and B cell-specific nuclear factor βA (NFβA), which is involved in transcriptional regulation of the interleukin-1β (IL-1β) gene. NFβA binds to a highly conserved sequence element located 6 bp upstream of the TATA motif within the IL-1β promoter and is required for maximal expression of the IL-1β gene. Here we show that NFβA is identical to the previously identified ets gene family member PU.1. The NFβA binding element shares 100% sequence identity with a novel PU.1 binding element recently found in the immunoglobulin J-chain promoter. Methylation interference DNA footprinting data demonstrated that NFβA and PU.1 make identical protein/DNA contacts. In vitro synthesized PU.1 possesses a mobility and binding specificity identical to NFβA as determined by electrophoretic mobility shift analysis (EMSA). Antisera directed against amino acids 39–55 of PU.1 recognizes NFβA in a manner indistinguishable from PU.1 in EMSA ‘supershift’ studies. NFβA and PU.1 also possess similiar protein structure as determined by proteolytic clipping bandshift analysis. Furthermore, we show that PU.1 is able to transactivate an NFβA-dependent promoter when co-transfected into HeLa cells which lack PU.1 NFβA. EMSA studies using recombinant TATA binding protein (TBP) and PU.1 suggest that PU.1 may induce assembly of a distinct TBP-dependent complex on the IL-1β promoter. Finally, immunohistochemical confocal laser scanning microscopy studies suggest that LPS stimulation of RAW macrophages induces a structural change in the N-terminal transcriptional activation domain of PU.1.</div>
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