Transcription factor Ets-1 in cytokine and chemokine gene regulation

Russell, Lisa; Garrett‐Sinha, Lee Ann

doi:10.1016/j.cyto.2010.03.006

Cited by 88 publications

(72 citation statements)

References 141 publications

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“…Ets-1 is a transcription factor known to induce the expression of growth factors and has been reported to directly activate the promoter of VEGFR1 (35,40,45,48). Therefore, we next examined the ability of Ets-1 to activate the promoter of VEGFR3.…”

Section: Figmentioning

confidence: 99%

“…Ets-1 is found in a variety of cell and tissue types, including lymphocytes, fibroblasts, mesenchymal cells, and endothelial cells of the developing vasculature (30)(31)(32)(33)(34). Ets-1 induces angiogenic and invasive phenotypes in endothelial cells, including wound healing, cell proliferation, and cell survival during embryonic angiogenesis (35)(36)(37)(38). Ets-1 belongs to the ETS family of transcription factors due to the presence of the ETS DNA binding domain.…”

mentioning

confidence: 99%

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Ets-1 Is Required for the Activation of VEGFR3 during Latent Kaposi's Sarcoma-Associated Herpesvirus Infection of Endothelial Cells

Gutierrez

Morris

et al. 2013

J Virol

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Section: Figmentioning

confidence: 99%

mentioning

confidence: 99%

Ets-1 Is Required for the Activation of VEGFR3 during Latent Kaposi's Sarcoma-Associated Herpesvirus Infection of Endothelial Cells

Gutierrez

Morris

et al. 2013

J Virol

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“…Ets-1 is a transcription factor and has a dual function, acting as both a transcriptional activator and repressor (16,42,43). In most cases, Ets-1 positively regulates the expression of its target genes (23). However, Ets-1 can also suppress its target gene through interacting with repressive factors like EAP1/Daxx (44).…”

Section: Discussionmentioning

confidence: 99%

“…Ets-1 is a negative regulator of Th17 differentiation, and Th17 cells deficient of Ets-1 express increased IL-17 and IL-17-related cytokines (22). On the contrary, Ets-1 positively regulates several cytokine genes such as Il2, Il5, and Gmcsf (23). These studies suggest that Ets-1 may modulate the effector function of Th cells by acting as a positive or negative regulator in a context-dependent manner (24)(25)(26).…”

Section: Naive Cd4mentioning

confidence: 99%

Interaction of Ets-1 with HDAC1 Represses IL-10 Expression in Th1 Cells

Lee

Kwon

Sahoo

et al. 2012

The Journal of Immunology

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IL-10 is a multifunctional cytokine that plays a crucial role in immunity and tolerance. IL-10 is produced by diverse immune cell types, including B cells and subsets of T cells. Although Th1 produce IL-10, their expression levels are much lower than Th2 cells under conventional stimulation conditions. The potential role of E26 transformation-specific 1 (Ets-1) transcription factor as a negative regulator for Il10 gene expression in CD4+ T cells has been implicated previously. In this study, we investigated the underlying mechanism of Ets-1–mediated Il10 gene repression in Th1 cells. Compared with wild type Th1 cells, Ets-1 knockout Th1 cells expressed a significantly higher level of IL-10, which is comparable with that of wild type Th2 cells. Upregulation of IL-10 expression in Ets-1 knockout Th1 cells was accompanied by enhanced chromatin accessibility and increased recruitment of histone H3 acetylation at the Il10 regulatory regions. Reciprocally, Ets-1 deficiency significantly decreased histone deacetylase 1 (HDAC1) enrichment at the Il10 regulatory regions. Treatment with trichostatin A, an inhibitor of HDAC family, significantly increased Il10 gene expression by increasing histone H3 acetylation recruitment. We further demonstrated a physical interaction between Ets-1 and HDAC1. Coexpression of Ets-1 with HDAC1 synergistically repressed IL-10 transcription activity. In summary, our data suggest that an interaction of Ets-1 with HDAC1 represses the Il10 gene expression in Th1 cells.

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“…ETS1, erythroblastosis virus E26 oncogene homolog 1, regulates numerous genes and is involved in stem cell development, cell senescence and death, and tumorigenesis (Russell and Garrett-Sinha, 2010). ETS1 is up-regulated in leukemia cells after combination treatment with 5-azacytidine and scriptaid.…”

Section: Discussionmentioning

confidence: 99%

Recovery of Genes Epigenetically Altered by the Histone Deacetylase Inhibitor Scriptaid and Demethylating Agent 5-Azacytidine in Human Leukemia Cells

Park¹,

Jeon²,

Kim³

et al. 2010

Genomics & Informatics

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Histone deacetylation and demethylation are epigenetic mechanisms implicated in cancer. Studies regarding the role of modulation of gene expression utilizing the histone deacetylase inhibitor scriptaid and the demethylating agent 5-azacytidine in HL-60 leukemia cells have been limited. We studied the possibility of recovering epigenetically silenced genes by scriptaid and 5-azacytidine in human leukemia cells by DNA microarray analysis. The first group was leukemia cells that were cultured with 5-azacytidine. The second group was cultured with scriptaid. The other group was cultured with both agents. Two hundred seventy newly developed genes were expressed after the combination of 5-azacytidine and scriptaid. Twenty-nine genes were unchanged after the combination treatment of 5-azacytidine and scriptaid. Among the 270 genes, 13 genes were differed significantly from the control. HPGD, CPA3, CEACAM6, LOC653907, ETS1, RAB37, PMP22, FST, FOXC1, and CCL2 were up-regulated, and IGLL3, IGLL1, and ASS1were down-regulated. Eleven genes associated with oncogenesis were found among the differentially expressed genes: ETS1, ASCL2, BTG2, BTG1, SLAMF6, CDKN2D, RRAS, RET, GIPC1, MAGEB, and RGL4. We report the results of our leukemia cell microarray profiles after epigenetic combination therapy with the hope that they are the starting point of selectively targeted epigenetic therapy.

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Transcription factor Ets-1 in cytokine and chemokine gene regulation

Cited by 88 publications

References 141 publications

Ets-1 Is Required for the Activation of VEGFR3 during Latent Kaposi's Sarcoma-Associated Herpesvirus Infection of Endothelial Cells

Ets-1 Is Required for the Activation of VEGFR3 during Latent Kaposi's Sarcoma-Associated Herpesvirus Infection of Endothelial Cells

Interaction of Ets-1 with HDAC1 Represses IL-10 Expression in Th1 Cells

Recovery of Genes Epigenetically Altered by the Histone Deacetylase Inhibitor Scriptaid and Demethylating Agent 5-Azacytidine in Human Leukemia Cells

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