The end-point result of the signaling depicted here is 2 CYTOSOL 3 NUCLEUS Change in gene expression Phosphortylation of an enzyme Release of the protein Binding of the ligand Alternative splicing of exons

The end-point result of the signaling depicted here is 2 CYTOSOL 3 NUCLEUS Change in gene expression Phosphortylation of an enzyme Release of the protein Binding of the ligand Alternative splicing of exons

Human Anatomy & Physiology (11th Edition)

11th Edition

ISBN:9780134580999

Author:Elaine N. Marieb, Katja N. Hoehn

Publisher:Elaine N. Marieb, Katja N. Hoehn

Chapter1: The Human Body: An Orientation

Section: Chapter Questions

Problem 1RQ: The correct sequence of levels forming the structural hierarchy is A. (a) organ, organ system,...

See similar textbooks

Similar questions

You have discovered two new inhibitors that inhibit enzymes involved in the apoptotic pathway shown below. Both inhibitors are newly identified proteins. You know that one of these proteins is a noncompetitive inhibitor of the kinase, Akt. Another protein is a competitive inhibitor of the phosphatase (i.e. a regulatory enzyme) that removes phosphates from Akt. survival signal inactive Bad active Akt Bad PHOSPHORYLATION OF Bad PROMOTION OF CELL RELEASES ACTIVE Bcl2 SURVIVAL BY INHIBITION inactive Bcl2 OF APOPTOSIS active Bcl2 Describe how each inhibitor would affect the apoptotic pathway shown above. Be specific about how the normal cascade works and how the inhibitor would change the signaling cascade or final outcome of the pathway. Which inhibitor will cause an artificial amplification of the cascade shown above and why? Which of the inhibitors would you prescribe to a cancer patient and why?
Many common medications function by interrupting the normal operation of certain signal transduction pathways. Which of the following describes a possible mechanism by which a certain medication may interrupt a signal transduction pathway? A A medication enters the target cell and triggers apoptosis by causing the release of di- gestive enzymes from cell lysosomes. B A medication interacts with the phospholipid bi-layer of the cell membrane and in- creases its permeability. с D A medication binds to membrane-bound glucose proteins and acts as an allosteric in- hibitor that prevents the intake of glucose by the cell. A medication diffuses through the membrane of a target cell and inhibits an enzyme that normally synthesizes a second messenger.
According to the “Hawaiian Punch” principle, different compartments of the secretory and endocytic pathways are topologically equivalent to each other and to the extracellular space. Explain how vesicular transport generates this topological equivalence. These compartments are topologically equivalent because molecules can move between them without having to move out of the cell. Transport vesicles cause this “topological equivalence” because they are responsible for the actual movement of the molecules mentioned above. They break off from one compartment, carrying the necessary molecules, and then fuse to its targeted compartment; thus, making the compartments topologically equivalent. During mitosis in mammalian cells, the nuclear envelope breaks down into vesicles. Are the topological properties of the cell altered by this event? Justify your answer.
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?
Many different cellular processes are regulated by GTP binding proteins - a kind of molecular switch. Their activity is regulated by their GTP/GDP binding status. Select the correct function and activity of Rab-GTP. O A. Rab in its GTP bound state is active and able to participate in vesicle transport B. Rab in its GTP bound state is inactive and prevents vesicle transport O C. Rab in its GTP bound state is active and prevents vesicle transport O D. Rab in its GTP bound state is inactive and able participate in vesicle transport
Which of the following is true of nuclear regulatory effects, as compared to cytosolic regulatory effects? they begin faster, they have a longer duration of effect they have a shorter duration of effect they are the same. it's not known
Animal cells need both oxygen and nutrients to survive is it more likely that a Cell would have a plasma membrane receptor for O2 or for sugar? Explain
In the normal cycle of Ras activity, when Ras is bound to y activity that removes a phosphate to convert GTP back to GDP and this it is inactive. Activation of Ras involves exchanging GDP for The Ras protein has intrinsic Ras. inactivates activates ATP GTP «< Questic A Moving to another question will save this response. ADP GDP GTPase Clo nuclease
What would happen to nuclear transport if you removed all of the Ran-GAP? For a while nuclear import receptors will still deliver cargo to the inside of the nucleus Nuclear import receptors will be loaded with RanGTP and will gradually stop binding to the proteins with NLS signals Nuclear export receptors will no longer deliver their cargo to the outside of the membrane and will probably shuttle in and out of the nucleus full of cargo Ran-GDP will no longer be made All of the above
What would most likely occur to nuclear-cytoplasmic shuttling if the intrinsic GTPase activity of RAN was slowed down by 50%? Group of answer choices RAN would not bind exportin and proteins would accumulate in the nucleus All of the answers are likely None of the answers are likely Importin beta would not release from RAN in the cytoplasm and nuclear import would slow down RAN would not bind to importin beta and protein cargo in the nucleus would not release
The seed of the castor bean (Ricinus communis) contains large amounts of ricin, a deadly poison for animals, including humans. One of the two subunits of this toxin is a lectin that binds terminal N-acetylgalactosamine residues on glycoproteins on the surface of eukaryotic cells, allowing the other subunit to enter the cell and kill it by preventing proteins from being made. Select the possible antidotes that could prevent or reverse ricin-mediated entry of the toxin. a high concentration of N-acetylgalactosamine an oligosaccharide with the same structure as that recognized by ricin a compound that prevents synthesis of extracellular glycoproteins a compound that activates enzymes that break down glycogen into glucose an enzyme that degrades lipopolysaccharides
Please help me with this