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The glucocorticoid receptor and the CREB protein are two examples of transcriptional activators. These proteins bind to response elements and activate transcription. (Note: The answers to this question are not directly described in this chapter. You have to rely on your understanding of the functioning of other proteins that are modulated by the binding of effector molecules, such as lac repressor.) A. How could the function of the glucocorticoid receptor be shut off? B. What type of enzyme would be needed to shut off the activation of transcription by the CREB protein?

Short Answer

Expert verified
The function of the glucocorticoid receptor can be shut off by blocking the binding to its hormone ligand, degradation, or modification such that it cannot bind to the DNA. A protein phosphatase enzyme would be required to shut off the activation of transcription by the CREB protein by stopping its phosphorylation.

Step by step solution

01

Understanding the Glucocorticoid Receptor

The glucocorticoid receptor is a type of transcriptional activator that binds to response elements and activates transcription. When it binds with its hormone ligand, glucocorticoid, it is activated to bind to the DNA and initiate transcription. The function of the receptor can be shut off by preventing this binding. This can occur in several ways: by absence or blocking of the hormone ligand, degradation of the receptor, or modification of the receptor such that it cannot bind to the DNA.
02

Understanding the CREB Protein

The CREB protein is another transcriptional activator. It binds to DNA upon phosphorylation. Therefore, to turn off its function, its activation must be stopped. The activation occurs via phosphorylation, which is driven by protein kinases. To stop this phosphorylation and thus block CREB's function, a protein phosphatase would be needed.
03

Final Understanding

To turn off the activation of transcription by the glucocorticoid receptor or the CREB protein, one would need to prevent the specific activation events that allow these proteins to bind to DNA and stimulate transcription. This includes blocking the binding of the receptor to its hormone ligand or utilizing a protein phosphatase to stop CREB's phosphorylation.

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Most popular questions from this chapter

Let's suppose a mutation in the glucocorticoid receptor does not prevent the binding of the glucocorticoid hormone to the protein but prevents the ability of the receptor to activate transcription. Make a list of all the possible defects that may explain why transcription cannot be activated.

What is meant by the term histone code? With regard to gene regulation, what is the proposed role of the histone code?

The DNA-binding domain of each CREB protein subunit recognizes the sequence \(5^{\prime}\)-TGACGTCA-3'. Due to random chance, how often would you expect this sequence to occur in the human genome, which contains approximately 3 billion base pairs? Actually, only a few dozen genes are activated by the CREB protein. Does the value of a few dozen agree with the number of random occurrences expected in the human genome? If the number of random occurrences of the sequence in the human genome is much higher than a few dozen, provide at least one explanation why the CREB protein is not activating more than a few dozen genes.

An enhancer, located upstream from a gene, has the following sequence: $$ \begin{aligned} &5^{\prime}-\mathrm{GTAG}-3^{\prime} \\ &3^{\prime}-\mathrm{CATC}-5^{\prime} \end{aligned} $$ This enhancer is orientation-independent. Which of the following sequences also works as an enhancer? A. 5'-CTAC-3' \(3^{\prime}-\mathrm{GATG}-5^{\prime}\) B. \(5^{\prime}-\mathrm{GATG}-3^{\prime}\) \(3^{\prime}-\mathrm{CTAC}-5^{\prime}\) C. \(5^{\prime}-\mathrm{CATC}-3^{\prime}\) \(3^{\prime}-\mathrm{GTAG}-5^{\prime}\)

Describe the steps that need to occur for the glucocorticoid receptor to bind to a GRE.

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