Nuclear integration of JAK/STAT and Ras/AP-1 signaling by CBP and p300

Horvai, Andrew E.; Xu, Lan; Korzus, Edward; Brard, Gyan; Kalafus, Daniel; Mullen, Tina-Marie; Rose, David W.; Rosenfeld, Michael G.; Glass, Christopher K.

doi:10.1073/pnas.94.4.1074

Cited by 399 publications

(286 citation statements)

References 42 publications

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“…MSR1 transcription is positively regulated by AP-1/ets -two transcription factors which can be inhibited by IFNγ treatment [51,52]. This inhibition is dependent on STAT1 binding to CBP and can be relieved by overexpressing CBP [51]. Our results are consistent with this model of transcriptional regulation although further studies would be required to confirm the functionality of this pathway in primary human MDMs.…”

Section: Discussionsupporting

confidence: 80%

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Macrophage heterogeneity and cholesterol homeostasis: Classically-activated macrophages are associated with reduced cholesterol accumulation following treatment with oxidized LDL

Chu¹,

Tai²,

Beer³

et al. 2013

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

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Macrophages are centrally involved during atherosclerosis development and are the predominant cell type that accumulates cholesterol in the plaque. Macrophages however, are heterogeneous in nature reflecting a variety of microenvironments and different phenotypes may be more prone to contribute towards atherosclerosis progression. Using primary human monocyte-derived macrophages, we sought to evaluate one aspect of atherogenic potential of different macrophage phenotypes by determining their propensity to associate with and accumulate oxidized low density lipoprotein (oxLDL). Classically-activated macrophages treated simultaneously with interferon γ (IFNγ) and tumour necrosis factor α (TNFα) associated with less oxLDL and accumulated less cholesterol compared to untreated controls. The combined treatment of IFNγ and TNFα reduced the mRNA expression of CD36 and the expression of both cell surface CD36 and macrophage scavenger receptor 1 (MSR1) protein. Under oxLDL loaded conditions, IFNγ and TNFα did not reduce macrophage protein expression of the transcription factor peroxisome proliferator-actived receptor γ (PPARγ) which is known to positively regulate CD36 expression. However, macrophages treated with IFNγ did prevent the PPARγ-specific agonist rosiglitazone from upregulating cell surface CD36 protein expression. Our results demonstrate that the observed reduction of cholesterol accumulation in macrophages treated with IFNγ and TNFα following oxLDL treatment was due at least in part to reduced cell surface CD36 and MSR1 protein expression.

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Section: Discussionsupporting

confidence: 80%

“…MSR1 protein expression may be being regulated in a similar manner. MSR1 transcription is positively regulated by AP-1/ets -two transcription factors which can be inhibited by IFNγ treatment [51,52]. This inhibition is dependent on STAT1 binding to CBP and can be relieved by overexpressing CBP [51].…”

Section: Discussionmentioning

confidence: 99%

Macrophage heterogeneity and cholesterol homeostasis: Classically-activated macrophages are associated with reduced cholesterol accumulation following treatment with oxidized LDL

Chu¹,

Tai²,

Beer³

et al. 2013

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

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“…From this analysis, we conclude that the C-terminal activation domain of STAT1 is required for maximal synergy but that the N-terminal region is essential for functional interaction with GATA-4. The finding that the activation domains of both GATA-4 and STAT1 are needed for maximal synergy, given that both proteins interact with the CBP/p300 coactivators (6,31), led us to investigate whether GATA-4/STAT1 cooperativity involves corecruitment of CBP. As shown in Fig.…”

Section: Resultsmentioning

confidence: 99%

“…In addition to STATinteracting kinases and phosphatases, several transcription factors and coactivators/corepressors were shown to associate with and modulate STAT activity. They include CBP/p300 (31) and histone deacetylases (82), as well as inducible regulators such as c-Jun (85) and members of the nuclear receptor family (22,67,71). Finally, a role for tissue-specific transcription factors in STAT transcriptional regulation is emerging.…”

mentioning

confidence: 99%

Convergence of Protein Kinase C and JAK-STAT Signaling on Transcription Factor GATA-4

Wang

Paradis

Aries

et al. 2005

Molecular and Cellular Biology

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Angiotensin II (AII), a potent vasoactive hormone, acts on numerous organs via G-protein-coupled receptors and elicits cell-specific responses. At the level of the heart, AII stimulation alters gene transcription and leads to cardiomyocyte hypertrophy. Numerous intracellular signaling pathways are activated in this process; however, which of these directly link receptor activation to transcriptional regulation remains undefined. We used the atrial natriuretic factor (ANF) gene (NPPA) as a marker to elucidate the signaling cascades involved in AII transcriptional responses. We show that ANF transcription is activated directly by the AII type 1 receptor and precedes the development of myocyte hypertrophy. This response maps to STAT and GATA binding sites, and the two elements transcriptionally cooperate to mediate signaling through the JAK-STAT and protein kinase C (PKC)-GATA-4 pathways. PKC phosphorylation enhances GATA-4 DNA binding activity, and STAT-1 functionally and physically interacts with GATA-4 to synergistically activate AII and other growth factor-inducible promoters. Moreover, GATA factors are able to recruit STAT proteins to target promoters via GATA binding sites, which are sufficient to support synergy. Thus, STAT proteins can act as growth factor-inducible coactivators of tissue-specific transcription factors. Interactions between STAT and GATA proteins may provide a general paradigm for understanding cell specificity of cytokine and growth factor signaling.

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“…In addition, p300/CBP possesses histone acetylase activity either intrinsic or via associated proteins such as P/ CAF and the recently identi®ed ACTR (Bannister and Kouzarides, 1996;Ogryzko et al, 1996;Yang et al, 1996;Chen et al, 1997). Finally, p300/CBP could play a pivotal role in the control of cell growth and di erentiation by integrating transcriptional responses from diverse signal transduction pathways (Lee et al, 1996;Horvai et al, 1997;Avantaggiati et al, 1997;Kurokawa et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Cooperation of Sp1 and p300 in the induction of the CDK inhibitor p21WAF1/CIP1 during NGF-mediated neuronal differentiation

et al. 1999

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Addition of nerve growth factor (NGF) to PC12 cells promotes neuronal di erentiation while inhibiting cell proliferation. In order to understand how NGF exerts its antimitogenic e ect during di erentiation, we have studied the mechanism by which this factor activates the promoter of the CDK inhibitor p21 WAF1/CIP1 . The minimal region of the p21 promoter required for the NGF-induction was mapped to a contiguous stretch of 10 bp located 83 bases upstream of the transcription initiation site. This GC-rich region was shown to interact speci®cally with the transcription factor Sp1 and the related protein Sp3, in either exponentiallygrowing or NGF-treated PC12 cells. The addition of NGF resulted in an accumulation of the transcriptional co-activator p300 in complexes associated with the NGF-responsive region. Transcriptional activity of Sp1, Sp3 and p300 was speci®cally induced by NGF in a Gal4-fusion assay, indicating that induction of p21 during neuronal di erentiation may involve regulation of the activity of these factors by NGF. Furthermore, p300 was able to act as a co-activator for Sp1-mediated transcriptional activation in PC12 cells, suggesting that p300 and Sp1 may cooperate in activating p21 transcription during the withdrawal of neuronal precursors from the cell cycle. This hypothesis is supported by experiments showing that p300 and Sp1 form complexes in PC12 cells.

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Nuclear integration of JAK/STAT and Ras/AP-1 signaling by CBP and p300

Cited by 399 publications

References 42 publications

Macrophage heterogeneity and cholesterol homeostasis: Classically-activated macrophages are associated with reduced cholesterol accumulation following treatment with oxidized LDL

Macrophage heterogeneity and cholesterol homeostasis: Classically-activated macrophages are associated with reduced cholesterol accumulation following treatment with oxidized LDL

Convergence of Protein Kinase C and JAK-STAT Signaling on Transcription Factor GATA-4

Cooperation of Sp1 and p300 in the induction of the CDK inhibitor p21WAF1/CIP1 during NGF-mediated neuronal differentiation

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