scholarly journals Prostaglandin E2-Mediated Activation of HIV-1 Long Terminal Repeat Transcription in Human T Cells Necessitates CCAAT/Enhancer Binding Protein (C/EBP) Binding Sites in Addition to Cooperative Interactions Between C/EBPβ and Cyclic Adenosine 5′-Monophosphate Response Element Binding Protein

2002 ◽  
Vol 168 (1) ◽  
pp. 274-282 ◽  
Author(s):  
Nancy Dumais ◽  
Salim Bounou ◽  
Martin Olivier ◽  
Michel J. Tremblay
Keyword(s):  
T Cells ◽  
Long Terminal Repeat ◽  
Binding Sites ◽  
Protein C ◽  
Binding Protein ◽  
Cooperative Interactions ◽  
Human T Cells ◽  
Enhancer Binding Protein ◽  
Element Binding Protein ◽  
Hiv 1

scholarly journals Interaction between CCAAT/Enhancer Binding Protein and Cyclic AMP Response Element Binding Protein 1 Regulates Human Immunodeficiency Virus Type 1 Transcription in Cells of the Monocyte/Macrophage Lineage

2001 ◽  
Vol 75 (4) ◽  
pp. 1842-1856 ◽  
Author(s):  
Heather L. Ross ◽  
Michael R. Nonnemacher ◽  
Tricia H. Hogan ◽  
Shane J. Quiterio ◽  
Andrew Henderson ◽  
...  
Keyword(s):  
Binding Site ◽  
Binding Sites ◽  
Sequence Variation ◽  
Binding Protein ◽  
Enhancer Binding Protein ◽  
Immunodeficiency Virus ◽  
Element Binding Protein ◽  
Cyclic Amp Response Element ◽  
Creb Binding Site ◽  
Hiv 1

ABSTRACT Recent observations have shown two CCAAT/enhancer binding protein (C/EBP) binding sites to be critically important for efficient human immunodeficiency virus type 1 (HIV-1) replication within cells of the monocyte/macrophage lineage, a cell type likely involved in transport of the virus to the brain. Additionally, sequence variation at C/EBP site I, which lies immediately upstream of the distal nuclear factor kappa B site and immediately downstream of a binding site for activating transcription factor (ATF)/cyclic AMP response element binding protein (CREB), has been shown to affect HIV-1 long terminal repeat (LTR) activity. Given that C/EBP proteins have been shown to interact with many other transcription factors including members of the ATF/CREB family, we proceeded to determine whether an adjacent ATF/CREB binding site could affect C/EBP protein binding to C/EBP site I. Electrophoretic mobility shift analyses indicated that selected ATF/CREB site variants assisted in the recruitment of C/EBP proteins to an adjacent, naturally occurring, low-affinity C/EBP site. This biophysical interaction appears to occur via at least two mechanisms. First, low amounts of CREB-1 and C/EBP appear to heterodimerize and bind to a site consisting of a half site from both the ATF/CREB and C/EBP binding sites. In addition, CREB-1 homodimers bind to the ATF/CREB site and recruit C/EBP dimers to their cognate weak binding sites. This interaction is reciprocal, since C/EBP dimer binding to a strong C/EBP site leads to enhanced CREB-1 recruitment to ATF/CREB sites that are weakly bound by CREB. Sequence variation at both C/EBP and ATF/CREB sites affects the molecular interactions involved in mediating both of these mechanisms. Most importantly, sequence variation at the ATF/CREB binding site affected basal LTR activity as well as LTR function following interleukin-6 stimulation, a treatment that leads to increases in C/EBP activation. Thus, HIV-1 LTR ATF/CREB binding site sequence variation may modulate cellular signaling at the viral promoter through the C/EBP pathway.

scholarly journals FoxP3 Enhances HIV-1 Gene Expression by Modulating NFκB Occupancy at the Long Terminal Repeat in Human T Cells

2007 ◽  
Vol 282 (22) ◽  
pp. 15973-15980 ◽  
Author(s):  
Derek Holmes ◽  
Geoffry Knudsen ◽  
Stephanie Mackey-Cushman ◽  
Lishan Su
Keyword(s):  
Gene Expression ◽  
T Cells ◽  
Long Terminal Repeat ◽  
Terminal Repeat ◽  
Human T Cells ◽  
Hiv 1

scholarly journals Complexes containing activating transcription factor (ATF)/cAMP-responsive-element-binding protein (CREB) interact with the CCAAT/enhancer-binding protein (C/EBP)–ATF composite site to regulate Gadd153 expression during the stress response

1999 ◽  
Vol 339 (1) ◽  
pp. 135-141 ◽  
Author(s):  
Timothy W. FAWCETT ◽  
Jennifer L. MARTINDALE ◽  
Kathryn Z. GUYTON ◽  
Tsonwin HAI ◽  
Nikki J. HOLBROOK
Keyword(s):  
Transcription Factor ◽  
Pc12 Cells ◽  
Protein C ◽  
Binding Protein ◽  
Enhancer Binding Protein ◽  
Element Binding Protein ◽  
Activating Transcription Factor ◽  
Responsive Element ◽  
Camp Responsive Element Binding ◽  
Gadd153 Expression

Gadd153, also known as chop, encodes a member of the CCAAT/enhancer-binding protein (C/EBP) transcription factor family and is transcriptionally activated by cellular stress signals. We recently demonstrated that arsenite treatment of rat pheochromocytoma PC12 cells results in the biphasic induction of Gadd153 mRNA expression, controlled in part through binding of C/EBPβ and two uncharacterized protein complexes to the C/EBP–ATF (activating transcription factor) composite site in the Gadd153 promoter. In this report, we identified components of these additional complexes as two ATF/CREB (cAMP-responsive-element-binding protein) transcription factors having differential binding activities dependent upon the time of arsenite exposure. During arsenite treatment of PC12 cells, we observed enhanced binding of ATF4 to the C/EBP–ATF site at 2 h as Gadd153 mRNA levels increased, and enhanced binding of ATF3 complexes at 6 h as Gadd153 expression declined. We further demonstrated that ATF4 activates, while ATF3 represses, Gadd153 promoter activity through the C/EBP–ATF site. ATF3 also repressed ATF4-mediated transactivation and arsenite-induced activation of the Gadd153 promoter. Our results suggest that numerous members of the ATF/CREB family are involved in the cellular stress response, and that regulation of stress-induced biphasic Gadd153 expression in PC12 cells involves the ordered, sequential binding of multiple transcription factor complexes to the C/EBP–ATF composite site.

scholarly journals Type I Interferon Induces Inhibitory 16-kD CCAAT/ Enhancer Binding Protein (C/EBP)β, Repressing the HIV-1 Long Terminal Repeat in Macrophages: Pulmonary Tuberculosis Alters C/EBP Expression, Enhancing HIV-1 Replication

1998 ◽  
Vol 188 (7) ◽  
pp. 1255-1265 ◽  
Author(s):  
Yoshihiro Honda ◽  
Linda Rogers ◽  
Koh Nakata ◽  
Ben-Yang Zhao ◽  
Richard Pine ◽  
...  
Keyword(s):  
Pulmonary Tuberculosis ◽  
Alveolar Macrophages ◽  
Protein C ◽  
Type I Interferon ◽  
Binding Protein ◽  
Type I ◽  
Enhancer Binding Protein ◽  
Hiv 1

We have previously observed that HIV-1 replication is suppressed in uninflamed lung and increased during tuberculosis. In vitro THP-1 cell–derived macrophages inhibited HIV-1 replication after infection with Mycobacterium tuberculosis. Suppression of HIV-1 replication was associated with inhibition of the HIV-1 long terminal repeat (LTR) and induction of ISGF-3, a type I interferon (IFN)–specific transcription factor. Repression of the HIV-1 LTR required intact CCAAT/enhancer binding protein (C/EBP) sites. THP-1 cell–derived macrophages infected with M. tuberculosis, lipopolysaccharide, or IFN-β induced the 16-kD inhibitory C/EBPβ isoform and coincidentally repressed HIV-1 LTR transcription. C/EBPβ was the predominant C/EBP family member produced in THP-1 macrophages during HIV-1 LTR repression. In vivo, alveolar macrophages from uninflamed lung strongly expressed inhibitory 16-kD C/EBPβ, but pulmonary tuberculosis abolished inhibitory C/EBPβ expression and induced a novel C/EBP DNA binding protein. Therefore, in vitro, proinflammatory stimulation produces an IFN response inhibiting viral replication by induction of a C/EBPβ transcriptional repressor. THP-1 cell–derived macrophages stimulated with type I IFN are similar to alveolar macrophages in the uninflamed lung in vivo. In contrast, the cellular immune response in active pulmonary tuberculosis disrupts this innate immunity, switching C/EBP expression and allowing high level viral replication.

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