What areas of the brain do you think are affected when there is a decreased expression of ERα mRNA and how may this lead to behavioral changes in the brain

Mutant tyrosine kinase signaling proteins are implicated in many types of human cancer. Hundreds of millions of dollars are required for the basic research and development of a new drug. Tyrosine kinase inhibitor drugs have been approved for cancer treatments by the U.S. Food and Drug Administration. What do you think would be some of the difficulties of finding these drugs given that similar kinases are active in normal cells? Do you think new medications of this type should be developed through government-sponsored research? Why or why not? If not, what alternatives do you propose?

When glucose is low and CAMP is present, CAMP's role is to O Activate catabolite activator protein (CAP) Activate RNA Polymerase Activate the repressor Deactivate the repressor

Many organisms have a class of genes called ' heat shock proteins.' These genes are expressed at high levels when cells are exposed to high temperatures. once they are transcribed and translated, they help stabilize other proteins in the cell to protect them form the high temperature. What kind of response to the enviornment is the elevated expression of heat-shock proteins? - mutational response - direct response - gene-mediated response

What type of experiment can be performed to confirm that the C-terminal KDEL tetrapeptide is both necessary and sufficient in ER localization?  (Necessary meaning that without KDEL, ER retrieval would not occur, and sufficient meaning that with KDEL, we would definitely see its effect (ER retrieval would occur))

Please asap

How would a human cell normally change its expression of the gene for tyrosine aminotransferase? adipose cells will turn on this gene in the presence of glucocorticoids liver cells will turn on this gene in the presence of glucocorticoids liver cells will turn on this gene in the absence of glucocorticoids liver cells will turn off this gene in the presence of glucocorticoids  adipose cells will turn off this gene in the absence of glucocorticoids

The G-protein Ras is involved in proliferative signaling, and is mutated is a large fraction of human cancers. Almost all mutations in Ras mutate the glycine at codon 12. These mutations lock Ras in an active conformation. How will the GTPase activity of a Ras protein with a G12 mutation compare to a normal Ras protein without the mutation? (10 words maximum)

Which of the following types of mutations would be most likely to cause cells to undergo apoptosis (programmed cell death)?     One that increases the affinity of p21 for Cdks     One that decreases the affinity of Rb for the transcription factor E2F     One that decreases the ability of p53 to bind to DNA     One that causes p53 to be constitutively phosphorylated

You have developed an activator of a non-receptor tyrosine kinase. In three different cell types that all contain this receptor your drug has different effects. In cell type A you see activation of gene X and gene Y; in cell type B you note activation of Gene X, but no change in the mRNA levels for Gene Y. In cell type C your drug has no effect on either Gene X or Y. Describe how could each choice (A-D) be a possibility to suit the scenario? a. Genes X & Y are controlled by two separate STATs (STAT X & STAT Y). Cell type A contains both STATs; cell type B contains STAT X only; cell type C has neither STAT. b. Genes X & Y are controlled by two separate STATs (STAT X & STAT Y) and two separate JAKs (JAK X & JAK Y). Cell type A contains both STATs and JAKs; cell type B contains both STATs but JAK X only; cell type C has both STATs but neither JAK. c. Genes X & Y are controlled by two separate STATs (STAT X & STAT Y), two separate JAKs (JAK X & JAK Y) and…