True or false If cells were treated with a weak base such as ammonia or chloroquine, which raises the pH of organelles toward neutrality, M6P receptors would be expected to accumulate in the Golgi because they could not bind to the lysosomal enzymes. Loss-of-function mutations are usually recessive.
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True or false
If cells were treated with a weak base such as ammonia or chloroquine, which raises the pH of organelles toward neutrality, M6P receptors would be expected to accumulate in the Golgi because they could not bind to the lysosomal enzymes.
Loss-of-function mutations are usually recessive.
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- The retinoblastoma tumor suppressor gene Rb (RB1) codes forthe retinoblastoma protein (pRB). pRB prevents the progression of the cell cycle through G1 if DNA has been damaged. Itdoes so in part because it binds a transcription-activatingdimer referred to as E2F-DP. The pRB-E2F/DP complex recruits a histone deacetylase to chromatin. Explain.In tumor cells obtained from patients with Burkittlymphoma, a cancer of the immune system’s B cells,the myc gene often appears close to one of the breakpoints of a reciprocal translocation between chromosomes 8 and 14. In this translocated position, myc is expressed at a higher-than-normal level. Scientists hypothesize that Myc protein overexpression in B cellscontributes to lymphoma formation.a. Explain how transgenic mice produced using pronuclear injection could be used to test this hypothesis. (Assume that you previously cloned a generegulatory region that is active specifically in Bcells throughout the life of the mouse.)b. Suppose you wanted to overexpress Myc only inthe immune cells of mice, starting at one week ofage. To restrict Myc transcription spatially, youwill use same promoter described in part (a). Torestrict Myc transcription temporally, you will usea cre transgene whose expression is controlled byheat shock (hs-cre). Describe the mouse you wouldcreate to accomplish…A current focus of molecular medicine is to trigger or promote apoptosis of specific cells. several components of the apoptotic pathways are being targeted using this approach. for each of the following, state specifically how the treatment would be expected to stimulate or inhbit apoptosis. b. exposing cells to recombinant TRAIL protein, a ligand for thr tumor necrosis factor family of receptors
- You are looking at the results of a western blot from the lysates of cells harvested from a suspected breast cancer tumor and you see that there is an increased expression of INK4-p16, you suspect that this will______________? Group of answer choices Increase S to G2 phase transition Initiate a cell cycle arrest in G1 Block M to G1 phase transition Promote tumorigenesisThe expression patterns as well as activation of different types of CDKs happen at different stages of the cell cycle. Explain why.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
- Not all genes encoded in the DNA are transcribed into RNA or translated into protein. Explain how this mechanism protects the integrity of the cell.Which of the following statements is true? Question 9 options: a) Executioner caspases are activated by cleavage. b) Initiator caspases are activated by cleavage. c) Executioner caspases are activated by dimerization. d) Executioner caspases trigger apoptosis but initiator caspases does not.Tumor cells from a person with leukemia have been analyzed to determine which oncogene is involved in the transformation. After partial sequencing of the gene, the predicted gene product is identified as a tyrosine kinase. Which of the following proteins would most likely be encoded by an oncogene and exhibit tyrosine kinase activity? A. Nuclear transcriptional activator B. Epidermal growth factor C. Membrane-associated G protein D. Platelet-derived growth factor E. Growth factor receptor
- Which of the following defects in RAS would be tumorigenic? multiple answers A. Deletion of nucleotide binding domain B. Inactivation of Guanine Exchange Factor (GEF) C. Mutation at amino acid 61 that prevents hydrolysis of bound GTP D. Inactivation of GTPase Protein (GAPS) E. Mutation that prevents binding of GTPThe tumor suppressor pRB also binds to and suppresses theactivity of retinoblastoma binding protein 2 (RBP2), ahistone demethylase that removes methyl groups from diand trimethylated lysines in histone 3. What is the possibleconsequence of an inactivating mutation in RB1 that causesan inability of pRB to bind RBP2?The destruction of the various cyclins is commonly used to inactivate the Cdk/cyclin complexes. Why is it advantageous to inactivate these complexes via protein destruction instead of some other method that does not require the re-synthesis of a cyclin protein the next time the cell divides?