25 Jun What localization and/or topogenic sequence(s) does
Question
The following amino acid sequence was derived from the DNA sequence of a gene encoding a hypothetical type I integral plasma membrane protein. (The • merely indicate every 10 amino acids beginning with M1 & ending with V140). Use this information as necessary to answer questions 1-2.
MGIIVLLLLW•VIALILAVAV•EKCPLLYINC•TRLSPQRTNY•SQRPLLFFWM•VILIVLALIF• LVIIVMPKKP• KDSHYRILVT•KHEDQNITEH•KRPDGEECTS•KRIANPTYCP•RKDELQLHDV•KRIANPLWCP• RKDELQLHDV
What localization and/or topogenic sequence(s) does this hypothetical protein contain?
A. Internal signal anchor.
B. N-terminal signal sequence + internal signal anchor.
C. N-terminal signal sequence + stop transfer anchor.
D. N-terminal signal sequence + stop transfer anchor + ER retrieval sequence.
E. Internal signal anchor + ER retrieval sequence.
Question 2 of 5
Which amino acids could undergo Man8 glycosylation in the ER?
A. N29 & N39
B. N86 & N105
C. S34 & S41
D. S73 & S100
E. None of the above. Man8 glycosylation occurs in the cis-golgi
Question 3 of 5
Time for a chimeric protein.
As you’ll recall, Hac1 protein (HAC1P) is involved in the unfolded protein response. Using recombinant DNA techniques, you generate a chimeric HAC1P to which you have added the the first 21 amino acids encoded by the LDL receptor gene at its N-terminus, recognition sites for NAGPT, a binding site for AP2, and finally, changed the last 4 amino acids to leu-asn-gly-lys. Where is this chimeric HAC1P going to be directed as its final destination?
A. Chimeric HAC1P will remain in the cytosol.
B. Chimeric HAC1P will be targeted to the nucleus.
C. Chimeric HAC1P will become a resident ER protein.
D. Chimeric HAC1P will be targeted to the lysosome.
E. Chimeric HAC1P will be targeted to the plasma membrane.
Question 4 of 5
Which of the following would you observe for a GFP fusion protein containing an N-terminal signal sequence & whose last 4 amino acids are Asn-Pro-Val-Tyr?
A. It’s a type I integral plasma membrane protein with NANA glycosylation.
B. It’s a protein that is targeted to the lysosome with Man8 glycosylation.
C. It’s a resident ER protein with Man5 glycosylation.
D. It’s endocytosed from the plasma membrane, dissociates in the late endosome and recycled back to the plasma membrane.
E. It’s secreted with NANA glycosylation.
Question 5 of 5
Using recombinant DNA techniques, you generate a chimeric glutathione reductase (GR) that now has the first 21 amino acids encoded by the LDL receptor gene at its N-terminus and the last 4 amino acids also from the LDL receptor at its C-terminus. What are you likely to observe if you expressed this chimeric GR gene in an otherwise normal cell?
A. Chimeric GR protein would undergo Mannose-6P modification in the cis-golgi and accumulate in the lysosome bound to intracellular cholesterol.
B. Chimeric GR protein would be a type I integral membrane protein capable of endocytosing LDL particles.
C. Chimeric GR protein would accumulate in the ER; increase the ratio of GSSG:GSH thereby promoting disulfide bond formation & enhancing protein folding.
D. Chimeric GR protein would accumulate in the ER; increase the ratio of GSH:GSSG thereby inhibiting disulfide bond formation & enhancing protein misfolding.
E. Chimeric GR protein would be secreted with no physiological effects.
Question 1 of 5
You observe that a particular protein is modified by Glucosidase II and UDP-glucose-glycoprotein glucosyl transferase, but not Mannosidase I if otherwise normal mammalian cells are incubated at 40°C. However, this same protein is modified by Glucosidase II, Mannosidase I and N-Acetylglucosamine phosphotransferase if these cells are incubated at 32°C. Identify the protein.
A. The protein is the allele of Mdr1 present in drug-resistant tumor cells.
B. The protein is an allele of BiP in which KDEL has been replaced with REDV.
C. The protein is the M6P receptor.
D. The protein is the ΔF508 allele of CFTR.
E. The protein is an allele of a lysosomal enzyme with a missense mutation.
Question 2 of 5
The lysosomes in cells from individuals with Tay-Sachs (T-S) disease are deficient in hexosaminidase A (HEXA). However, cells from some individuals with T-S exhibit normal lysosomes containing functional HEXA if they are incubated with a small molecule that resembles N-Acetylgalactosamine. Based on this observation, which of the following is the most likely cause of the HEXA deficiency in these particular T-S individuals?
A. T-S cells lack the M6P receptor.
B. T-S HEXA misfolds in the ER and is ERADicated.
C. T-S HEXA lacks recognition sites for NAGPT.
D. T-S cells lack NAGPT.
E. T-S cells lack NAG glycosylation in the medial-golgi.
Question 3 of 5
What causes the conversion of macrophage to foam cells?
A. Macrophage within blood vessels, differentiate into foam cells in response to inflammation.
B. Macrophage within the intima, accumulate excess HDL particles and become foam cells.
C. Macrophage within the intima import LDL particles, accumulate lipid droplets & differentiate into foam cells.
D. Undifferentiated monocytes within the intima import LDL particles, accumulate lipid droplets & differentiate into macrophage which are also called foam cells.
E. Undifferentiated monocytes within the bloodstream import LDL particles, accumulate lipid droplets & differentiate into macrophage which are also called foam cells.
Question 4 of 5
Why is the majority of cholesterol in the LDL particle esterified to linoleic acid?
A. To increase the fluidity of the LDL particle so it’s less prone to clog an artery.
B. To increase the amount of cholesterol packaged inside the LDL particle.
C. To reduce the concentration of linoleic acid in the bloodstream.
D. To reduce the amount of cholesterol packaged inside in the LDL particle.
E. To reduce fluidity of the LDL particle so it’s more compact.
Question 5 of 5
Which of the following describes the relationship between the level of a cell surface endocytic receptor (e.g., the LDL receptor) and the concentration of its corresponding ligand (e.g., the LDL particle)?
A. Receptor level is proportional to intracellular ligand concentration.
B. Receptor level is proportional to extracellular ligand concentration.
C. Receptor level is inversely proportional to intracellular ligand concentration.
D. Receptor level is inversely proportional to extracellular ligand concentration.
E. There is no relationship between receptor level and its ligand concentration.
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