scholarly journals p21WAF1/CIP1Is a Common Transcriptional Target of Retinoid Receptors

2007 ◽  
Vol 282 (41) ◽  
pp. 29987-29997 ◽  
Author(s):  
Takemi Tanaka ◽  
Kwang S. Suh ◽  
Angela M. Lo ◽  
Luigi M. De Luca
Keyword(s):  
Retinoid Receptors ◽  
Transcriptional Target

scholarly journals The HIF target MAFF promotes tumor invasion and metastasis through IL11 and STAT3 signaling

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Eui Jung Moon ◽  
Stephano S. Mello ◽  
Caiyun G. Li ◽  
Jen-Tsan Chi ◽  
Kaushik Thakkar ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Invasion ◽  
Critical Role ◽  
Metastatic Breast ◽  
Breast Cancer Patients ◽  
Invasion And Metastasis ◽  
Stat3 Signaling ◽  
Inducible Genes ◽  
Transcriptional Target

AbstractHypoxia plays a critical role in tumor progression including invasion and metastasis. To determine critical genes regulated by hypoxia that promote invasion and metastasis, we screen fifty hypoxia inducible genes for their effects on invasion. In this study, we identify v-maf musculoaponeurotic fibrosarcoma oncogene homolog F (MAFF) as a potent regulator of tumor invasion without affecting cell viability. MAFF expression is elevated in metastatic breast cancer patients and is specifically correlated with hypoxic tumors. Combined ChIP- and RNA-sequencing identifies IL11 as a direct transcriptional target of the heterodimer between MAFF and BACH1, which leads to activation of STAT3 signaling. Inhibition of IL11 results in similar levels of metastatic suppression as inhibition of MAFF. This study demonstrates the oncogenic role of MAFF as an activator of the IL11/STAT3 pathways in breast cancer.

scholarly journals Furin, a transcriptional target of NKX2-5, has an essential role in heart development and function

PLoS ONE ◽  
2019 ◽  
Vol 14 (3) ◽  
pp. e0212992 ◽  
Author(s):  
Laurent Dupays ◽  
Norma Towers ◽  
Sophie Wood ◽  
Anna David ◽  
Daniel J. Stuckey ◽  
...  
Keyword(s):  
Heart Development ◽  
Essential Role ◽  
And Function ◽  
Transcriptional Target

scholarly journals Functional retinoid receptors in budding ascidians

2000 ◽  
Vol 42 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Mika Kamimura ◽  
Shigeki Fujiwara ◽  
Kazuo Kawamura ◽  
Toshitsugu Yubisui
Keyword(s):  
Retinoid Receptors

scholarly journals Targeted disruption of retinoic acid receptor alpha (RAR alpha) and RAR gamma results in receptor-specific alterations in retinoic acid-mediated differentiation and retinoic acid metabolism.

1995 ◽  
Vol 15 (2) ◽  
pp. 843-851 ◽  
Author(s):  
J F Boylan ◽  
T Lufkin ◽  
C C Achkar ◽  
R Taneja ◽  
P Chambon ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Retinoic Acid Receptor ◽  
Specific Gene ◽  
Cell Type ◽  
Targeted Disruption ◽  
F9 Cells ◽  
Retinoid Receptors ◽  
Alpha Gene ◽  
Polar Derivatives ◽  
Crabp Ii

F9 embryonic teratocarcinoma stem cells differentiate into an epithelial cell type called extraembryonic endoderm when treated with retinoic acid (RA), a derivative of retinol (vitamin A). This differentiation is presumably mediated through the actions of retinoid receptors, the RARs and RXRs. To delineate the functions of each of the different retinoid receptors in this model system, we have generated F9 cell lines in which both copies of either the RAR alpha gene or the RAR gamma gene are disrupted by homologous recombination. The absence of RAR alpha is associated with a reduction in the RA-induced expression of both the CRABP-II and Hoxb-1 (formerly 2.9) genes. The absence of RAR gamma is associated with a loss of the RA-inducible expression of the Hoxa-1 (formerly Hox-1.6), Hoxa-3 (formerly Hox-1.5), laminin B1, collagen IV (alpha 1), GATA-4, and BMP-2 genes. Furthermore, the loss of RAR gamma is associated with a reduction in the metabolism of all-trans-RA to more polar derivatives, while the loss of RAR alpha is associated with an increase in metabolism of RA relative to wild-type F9 cells. Thus, each of these RARs exhibits some specificity with respect to the regulation of differentiation-specific gene expression. These results provide an explanation for the expression of multiple RAR types within one cell type and suggest that each RAR has specific functions.

scholarly journals RUNX1/core binding factor A2 regulates platelet 12-lipoxygenase gene (ALOX12): studies in human RUNX1 haplodeficiency

Blood ◽  
2010 ◽  
Vol 115 (15) ◽  
pp. 3128-3135 ◽  
Author(s):  
Gurpreet Kaur ◽  
Gauthami Jalagadugula ◽  
Guangfen Mao ◽  
A. Koneti Rao
Keyword(s):  
Expression Profiling ◽  
Region Of Interest ◽  
Luciferase Reporter ◽  
Direct Transcriptional Target ◽  
Erythroleukemia Cells ◽  
12 Lipoxygenase ◽  
Sirna Knockdown ◽  
Induced Aggregation ◽  
Transcriptional Target

Abstract Haploinsufficiency of RUNX1 (also known as CBFA2/AML1) is associated with familial thrombocytopenia, platelet dysfunction, and predisposition to acute leukemia. We have reported on a patient with thrombocytopenia and impaired agonist-induced aggregation, secretion, and protein phosphorylation associated with a RUNX1 mutation. Expression profiling of platelets revealed approximately 5-fold decreased expression of 12-lipoxygenase (12-LO, gene ALOX12), which catalyzes 12-hydroxyeicosatetraenoic acid production from arachidonic acid. We hypothesized that ALOX12 is a direct transcriptional target gene of RUNX1. In present studies, agonist-induced platelet 12-HETE production was decreased in the patient. Four RUNX1 consensus sites were identified in the 2-kb promoter region of ALOX12 (at −1498, −1491, −708, −526 from ATG). In luciferase reporter studies in human erythroleukemia cells, mutation of each site decreased activity; overexpression of RUNX1 up-regulated promoter activity, which was abolished by mutation of RUNX1 sites. Gel shift studies, including with recombinant protein, revealed RUNX1 binding to each site. Chromatin immunoprecipitation revealed in vivo RUNX1 binding in the region of interest. siRNA knockdown of RUNX1 decreased RUNX1 and 12-LO proteins. ALOX12 is a direct transcriptional target of RUNX1. Our studies provide further proof of principle that platelet expression profiling can elucidate novel alterations in platelets with inherited dysfunction.

scholarly journals Effect of Retinoid Status on the Messenger Ribonucleic Acid Expression of Nuclear Retinoid Receptors α, β, and γ, and Retinoid X Receptors α, β, and γ in the Mouse Testis1

Endocrinology ◽  
1997 ◽  
Vol 138 (4) ◽  
pp. 1544-1551 ◽  
Author(s):  
Ingrid C. Gaemers ◽  
Ans M. M. van Pelt ◽  
Paul T. van der Saag ◽  
Jos W. Hoogerbrugge ◽  
Axel P. N. Themmen ◽  
...  
Keyword(s):  
Ribonucleic Acid ◽  
Retinoid X Receptors ◽  
Messenger Ribonucleic Acid ◽  
Retinoid Receptors ◽  
X Receptors

Apaf-1 is a transcriptional target for E2F and p53

2001 ◽  
Vol 3 (6) ◽  
pp. 552-558 ◽  
Author(s):  
M. Cristina Moroni ◽  
Emma S. Hickman ◽  
Eros Lazzerini Denchi ◽  
Greta Caprara ◽  
Elena Colli ◽  
...  
Keyword(s):  
Transcriptional Target

The Mediator captures CDK7, an attractive transcriptional target in cancer

Cancer Cell ◽  
2021 ◽  
Vol 39 (9) ◽  
pp. 1184-1186
Author(s):  
Yubao Wang ◽  
Cherubin Manokaran ◽  
Su Wu ◽  
Thomas M. Roberts
Keyword(s):  
Transcriptional Target

Expression of SMRTβ promotes ligand-induced activation of mutated and wild-type retinoid receptors

Blood ◽  
2004 ◽  
Vol 104 (13) ◽  
pp. 4226-4235 ◽  
Author(s):  
Sylvie Côté ◽  
Suzan McNamara ◽  
Daria Brambilla ◽  
Andrea Bianchini ◽  
Giovanni Rizzo ◽  
...  
Keyword(s):  
Ligand Binding ◽  
Nuclear Receptors ◽  
Transcriptional Activation ◽  
Leukemic Cell ◽  
Wild Type ◽  
Specific Expression ◽  
Retinoid Receptors ◽  
Leukemic Cell Lines ◽  
All Trans Retinoic Acid ◽  
New Evidence

Abstract Nuclear receptors are ligand-modulated transcription factors regulated by interactions with corepressors and coactivators, whose functions are not fully understood. Acute promyelocytic leukemia (APL) is characterized by a translocation, t(15;17), that produces a PML/RARα fusion oncoprotein, whose abnormal transcriptional function is successfully targeted by pharmacologic levels of all-trans-retinoic acid (ATRA). Mutations in the ligand-binding domain of PML/RARα that confer resistance to ATRA have been studied by expression in nonhematopoietic cells, such as Cos-1. Here, we show that ATRA binding and transcriptional activation by the same PML/RARα mutant differ markedly between nonhematopoietic and leukemic cell lines. Differential expression of the corepressor isoform silencing mediator for retinoid and thyroid receptors β (SMRTβ) correlates with increased ligand binding and transcription by the mutant PML/RARα. Transient and stable overexpression of SMRTβ in hematopoietic cells that only express SMRTα increased ATRA binding, ligand-induced transcription, and ATRA-induced cell differentiation. This effect may not be limited to abnormal nuclear receptors, because overexpression of SMRTβ increased ATRA-induced binding and transcriptional activation of wild-type receptors PML/RARα and RARα. Our results suggest a novel role for the SMRTβ isoform whereby its cell-specific expression may influence the binding and transcriptional capacities of nuclear receptors, thus providing new evidence of distinct functions of corepressor isoforms and adding complexity to transcriptional regulation.

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