Activation of p53 during cellular stress will generally Select one: o a. Increase transcription of cyclin-dependent kinase inhibitors and decrease the likelihood of apoptosis. o b. Decrease transcription of cyclin-dependent kinase inhibitors and decrease the likelihood of apoptosis. o c. Increase transcription of cyclin-dependent kinase inhibitors and increase the likelihood of apoptosis. o d. Decrease transcription of cyclin-dependent kinase inhibitors and increase the likelihood of apoptosis.

Activation of p53 during cellular stress will generally Select one: o a. Increase transcription of cyclin-dependent kinase inhibitors and decrease the likelihood of apoptosis. o b. Decrease transcription of cyclin-dependent kinase inhibitors and decrease the likelihood of apoptosis. o c. Increase transcription of cyclin-dependent kinase inhibitors and increase the likelihood of apoptosis. o d. Decrease transcription of cyclin-dependent kinase inhibitors and increase the likelihood of apoptosis.

Biology 2e

2nd Edition

ISBN:9781947172517

Author:Matthew Douglas, Jung Choi, Mary Ann Clark

Publisher:Matthew Douglas, Jung Choi, Mary Ann Clark

Chapter9: Cell Communication

Section: Chapter Questions

Problem 1VCQ: Figure 9.8 HER2 is a receptor tyrosine kinase. In 30 percent of human breast cancers, HER2 is...

See similar textbooks

Similar questions

Cell specializations are usually a modification or elaboration of one of the basic cell functions. (True or fa1se?)
Figure 9.10 In certain cancers, the GTPase activity of the RAS G-protein is inhibited. This means that the RAS protein can no longer hydrolyze GTP into GDP What effect would this have on downstream cellular events?
List the regulatory mechanisms that might be lost in a cell producing faulty p53.
Suppose that in the formation of phenylalanine hydroxylase mRNA, the exons of the pre-mRNA fail to splice together properly and the resulting enzyme is nonfunctional. This produces an accumulation of high levels of phenylalanine and other compounds, which causes neurological damage. What phenotype would be produced in the affected individual?
Which of the following mutations will result in cancer? a. homozygous recessive mutation in a tumor-suppressor gene coding for a nonfunctional protein b. dominant mutation in a tumor-suppressor gene in which the normal protein product is overexpressed c. homozygous recessive mutation in which there is a deletion in the coding region of a proto-oncogene, leaving it nonfunctional d. dominant mutation in a proto-oncogene in which the normal protein product is overexpressed
A gene that codes for a positive cell cycle regulator is called a(n) _______. a. kinase inhibitor b. tumor suppressor gene c. proto-oncogene d. oncogene
If a cell developed a mutation in its MAP2K1 gene (encodes the MEK protein) that prevented MIEK from being recognized by phosphatases, how would the EGFR signaling cascade and the cell’s behavior change?
Another model, the random model, proposes that any cell in a malignant tumor has the potential to form a new tumor. Does the cancer stem cell hypothesis contradict this idea?
Some cancer cells are insensitive to typical chemotherapy. Research into the mechanisms underlying this insensitivity uncovered an ability by these cells to pump the treatment drug out of the cell against its concentration gradient. Additional drugs have been developed that inhibit the pump, thus trapping the chemotherapeutic agent inside to promote cancer cell destruction. The Figure shows what happens when two types of cells are treated with a 3H-labeled anti-cancer drug, paclitaxel. Which set of cells (A or B) would be described as resistant to the cancer treatment? Explain your answer. What type of transport are the resistant cells using?
Control of gene expression in eukaryotic cells occurs at which level(s)? a. only the transcriptional level b. epigenetic and transcriptional levels c. epigenetic, transcriptional, and translational levels d. epigenetic, transcriptional, post-transcriptional, translational, and post-translational levels
Targeted therapies are used in patients with a set gene expression pattern. A targeted therapy that prevents the activation of the estrogen receptor in breast cancer would be beneficial to which type of patient? patients who express the EGFR receptor in normal cells patients with a mutation that inactivates the estrogen receptor patients with lots of the estrogen receptor expressed in their tumor patients that have no estrogen receptor expressed in their tumor
How does PKC’s signaling role change in response to growth factor signaling versus an immune response? PKC interacts directly with signaling molecules in both cascades, but only exhibits kinase activity during growth factor signaling. PKC interacts directly with signaling molecules in growth factor cascades, but interacts with signaling inhibitors during immune signaling. PKC amplifies growth factor cascades, but turns off immune cascades. PKC is activated during growth factor cascades, but is inactivated during immune response cascades.