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

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 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.

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

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 Bacterial recognition by PGRP-SA and downstream signalling by Toll/DIF sustain commensal gut bacteria in Drosophila

PLoS Genetics ◽  
2022 ◽  
Vol 18 (1) ◽  
pp. e1009992
Author(s):  
Shivohum Bahuguna ◽  
Magda Atilano ◽  
Marcus Glittenberg ◽  
Dohun Lee ◽  
Srishti Arora ◽  
...  
Keyword(s):  
Translational Regulation ◽  
Feedback Loop ◽  
Gut Bacteria ◽  
Commensal Bacteria ◽  
Bacterial Density ◽  
Metabolic Parameters ◽  
Indigenous Bacteria ◽  
Immune Sensing ◽  
Reduced Density ◽  
Transcriptional Target

The gut sets the immune and metabolic parameters for the survival of commensal bacteria. We report that in Drosophila, deficiency in bacterial recognition upstream of Toll/NF-κB signalling resulted in reduced density and diversity of gut bacteria. Translational regulation factor 4E-BP, a transcriptional target of Toll/NF-κB, mediated this host-bacteriome interaction. In healthy flies, Toll activated 4E-BP, which enabled fat catabolism, which resulted in sustaining of the bacteriome. The presence of gut bacteria kept Toll signalling activity thus ensuring the feedback loop of their own preservation. When Toll activity was absent, TOR-mediated suppression of 4E-BP made fat resources inaccessible and this correlated with loss of intestinal bacterial density. This could be overcome by genetic or pharmacological inhibition of TOR, which restored bacterial density. Our results give insights into how an animal integrates immune sensing and metabolism to maintain indigenous bacteria in a healthy gut.

scholarly journals Isoform resolved measurements of absolute translational efficiency define interplay of HIF and mTOR dysregulation in kidney cancer

2021 ◽  
Author(s):  
Yoichiro Sugimoto ◽  
Peter J. Ratcliffe
Keyword(s):  
Kidney Cancer ◽  
Target Gene ◽  
Mammalian Target Of Rapamycin ◽  
Hypoxia Inducible Factor ◽  
Mtor Inhibitors ◽  
Translational Efficiency ◽  
Transcription Start ◽  
Transcription Start Sites ◽  
Combined Use ◽  
Transcriptional Target

Hypoxia inducible factor (HIF) and mammalian target of rapamycin (mTOR) pathways orchestrate responses to oxygen and nutrient availability. These pathways are frequently dysregulated in cancer, but their interplay is poorly understood, in part because of difficulties in simultaneous measurement of global and mRNA-specific translation. Here we describe a workflow for measurement of absolute translational efficiency of mRNAs resolved by their transcription start sites (TSSs). Its application to kidney cancer cells revealed a remarkable extent of translational reprogramming by mTOR, strongly affecting many metabolic enzymes and pathways. By contrast, global effects of HIF on translation were limited, and we did not observe reported translational activation by HIF2A. In contrast HIF-dependent alterations in TSS usage were associated with robust changes in translational efficiency in a subset of genes. Analyses of the interplay of HIF and mTOR revealed that specific classes of HIF1A and HIF2A transcriptional target gene manifest markedly different sensitivity to mTOR, in a manner that supports combined use of HIF2A and mTOR inhibitors in treatment of kidney cancer.

VIP is a transcriptional target of Nurr1 in dopaminergic cells

2007 ◽  
Vol 203 (1) ◽  
pp. 221-232 ◽  
Author(s):  
Yu Luo ◽  
Leigh A. Henricksen ◽  
Rita E. Giuliano ◽  
Llanda Prifti ◽  
Linda M. Callahan ◽  
...  
Keyword(s):  
Dopaminergic Cells ◽  
Transcriptional Target
Sign in / Sign up

Export Citation Format

Share Document