Identification of a Novel Sonic Hedgehog Response Element in the Chicken Ovalbumin Upstream Promoter-Transcription Factor II Promoter

1997 ◽  
Vol 11 (10) ◽  
pp. 1458-1466 ◽  
Author(s):  
Venkatesh Krishnan ◽  
Gerard Elberg ◽  
Ming-Jer Tsai ◽  
Sophia Y. Tsai
Keyword(s):  
Transcription Factor ◽  
Motor Neuron ◽  
Sonic Hedgehog ◽  
Point Mutations ◽  
Protein S ◽  
Response Element ◽  
Enhancer Element ◽  
Factor Ii ◽  
Upstream Promoter ◽  
Chicken Ovalbumin

Abstract Sonic hedgehog (Shh) is a secreted morphogen that regulates dorso-ventral patterning within the neural tube during embryonic development. It is well established that Shh can induce motor-neuron differentiation that coincides with the appearance of specific motor-neuron markers including chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII) and Isl1. However, the mechanism of Shh-induced signaling pathway in vertebrates is not clearly defined. In this report we have identified COUP-TFII as a target gene for Shh. In addition we have used a 1.6-kb region of the COUP-TFII promoter to identify a target element that mediates the Shh-induced activity. Extensive deletions introduced within this region have further enabled us to identify a novel sonic hedgehog response element (ShhRE) in the COUP-TFII promoter. Point mutations introduced within the ShhRE reveal some key nucleotides that are essential for protein(s)-binding activity. Finally, the ShhRE is capable of functioning as a true enhancer element and can mediate Shh-induced transactivation of reporter gene via a heterologous promoter.

scholarly journals Recent progress on the role and molecular mechanism of chicken ovalbumin upstream promoter-transcription factor II in cancer

2020 ◽  
Vol 48 (4) ◽  
pp. 030006052091923
Author(s):  
Seong-Hoon Yun ◽  
Joo-In Park
Keyword(s):  
Transcription Factor ◽  
Recent Progress ◽  
Molecular Mechanisms ◽  
Orphan Receptor ◽  
Expression Of Genes ◽  
Factor Ii ◽  
Upstream Promoter ◽  
Cancer Types ◽  
Breast And Prostate Cancer ◽  
Chicken Ovalbumin

Chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII) is an orphan receptor that regulates the expression of genes involved in development and homeostasis. COUP-TFII is also dysregulated in cancer, where it plays important roles in oncogenesis and malignant progression. Recent studies have also investigated altered microRNA-mediated regulation of COUP-TFII in cancer. Although many investigators have studied the expression and clinical significance of COUP-TFII in several cancer types, there remain many controversies regarding its role in these diseases. In this review, we will describe the functions and underlying molecular mechanisms of COUP-TFII in several cancers, especially colorectal, gastric, breast, and prostate cancer; additionally, we will briefly summarize what is known about microRNA-mediated regulation of COUP-TFII.

scholarly journals Decreased Chicken Ovalbumin Upstream Promoter Transcription Factor II Expression in Tamoxifen-Resistant Breast Cancer Cells

2006 ◽  
Vol 66 (20) ◽  
pp. 10188-10198 ◽  
Author(s):  
Krista A. Riggs ◽  
Nalinie S. Wickramasinghe ◽  
Renate K. Cochrum ◽  
Mary Beth Watts ◽  
Carolyn M. Klinge
Keyword(s):  
Breast Cancer ◽  
Transcription Factor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Factor Ii ◽  
Upstream Promoter ◽  
Tamoxifen Resistant ◽  
Chicken Ovalbumin

Chicken ovalbumin upstream promoter-transcription factor II regulates nuclear receptor, myogenic, and metabolic gene expression in skeletal muscle cells

2011 ◽  
Vol 43 (4) ◽  
pp. 213-227 ◽  
Author(s):  
Lisa M. Crowther ◽  
Shu-Ching Mary Wang ◽  
Natalie A. Eriksson ◽  
Stephen A. Myers ◽  
Lauren A. Murray ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Transcription Factor ◽  
Muscle Cells ◽  
Internal Controls ◽  
C2c12 Cells ◽  
Low Density ◽  
Factor Ii ◽  
Upstream Promoter ◽  
Chicken Ovalbumin

We demonstrate that chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII) mRNA is more abundantly expressed (than COUP-TFI mRNA) in skeletal muscle C2C12 cells and in (type I and II) skeletal muscle tissue from C57BL/10 mice. Consequently, we have utilized the ABI TaqMan Low Density Array (TLDA) platform to analyze gene expression changes specifically attributable to ectopic COUP-TFII (relative to vector only) expression in muscle cells. Utilizing a TLDA-based platform and 5 internal controls, we analyze the entire NR superfamily, 96 critical metabolic genes, and 48 important myogenic regulatory genes on the TLDA platform utilizing 5 internal controls. The low density arrays were analyzed by rigorous statistical analysis (with Genorm normalization, Bioconductor R, and the Empirical Bayes statistic) using the (integromics) statminer software. In addition, we validated the differentially expressed patho-physiologically relevant gene (identified on the TLDA platform) glucose transporter type 4 (Glut4). We demonstrated that COUP-TFII expression increased the steady state levels of Glut4 mRNA and protein, while ectopic expression of truncated COUP-TFII lacking helix 12 (COUP-TFΔH12) reduced Glut4 mRNA expression in C2C12 cells. Moreover, COUP-TFII expression trans-activated the Glut4 promoter (−997/+3), and ChIP analysis identified selective recruitment of COUP-TFII to a region encompassing a highly conserved SP1 binding site (in mouse, rat, and human) at nt positions −131/−118. Mutation of the SpI site ablated COUP-TFII mediated trans-activation of the Glut4 promoter. In conclusion, this study demonstrates that in skeletal muscle cells, COUP-TFII regulates several nuclear hormone receptors, and critical metabolic and muscle specific genes.

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