15-13. You are working in a laboratory on an independent study project. You have some epithelial cells from a human growing in a bottle. These cells normally divide throughout life. Before spring break, you replaced the medium (fluid surrounding the cells) with fresh medium and forgot to include any growth factors. Then you went home for spring break. A-1. Now that you have come back after vacation, you will probably find that the cells have (grown normally) (arrested at G1/S) (arrested at S/G2) (arrested at G2/M) (grown much more than usual) AND A-2. When you add the missing growth factor to the medium, the cells will probably start to synthesize (p53) (growth factor receptor) (MPF) (cyclin) (cdk = cyclin dependent kinase) (none of these).

Biochemistry
9th Edition
ISBN:9781319114671
Author:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.
Publisher:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.
Chapter1: Biochemistry: An Evolving Science
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15-13. You are working in a laboratory on an independent study project. You have some epithelial cells from a
human growing in a bottle. These cells normally divide throughout life. Before spring break, you replaced the
medium (fluid surrounding the cells) with fresh medium and forgot to include any growth factors. Then you went
home for spring break.
A-1. Now that you have come back after vacation, you will probably find that the cells have (grown normally)
(arrested at G1/S) (arrested at S/G2) (arrested at G2/M) (grown much more than usual) AND
A-2. When you add the missing growth factor to the medium, the cells will probably start to synthesize (p53)
(growth factor receptor) (MPF) (cyclin) (cdk = cyclin dependent kinase) (none of these).
B. Ink proteins bind to and inhibit one of the cdk's in the cell cycle. (Ink = INhibitor of Kinase.) Many cancer cells
have mutations in the INK gene(s). (For clarity, the protein name is given in lower case and the gene name in upper
case.) Some cancer cells have normal INK genes but have mutation(s) in the corresponding CDK gene(s) that
eliminate cdk-ink protein binding. (Other aspects of cdk function are normal.) Given this information, what would
you expect?
B-1. Levels of ink activity in tumor cells with mutations in the INK gene should be (normal) (above normal)
(below normal) (can't predict).
B-2. Levels of ink activity in tumor cells with mutations in the CDK gene should be (normal) (above normal)
(below normal) (can't predict).
Transcribed Image Text:15-13. You are working in a laboratory on an independent study project. You have some epithelial cells from a human growing in a bottle. These cells normally divide throughout life. Before spring break, you replaced the medium (fluid surrounding the cells) with fresh medium and forgot to include any growth factors. Then you went home for spring break. A-1. Now that you have come back after vacation, you will probably find that the cells have (grown normally) (arrested at G1/S) (arrested at S/G2) (arrested at G2/M) (grown much more than usual) AND A-2. When you add the missing growth factor to the medium, the cells will probably start to synthesize (p53) (growth factor receptor) (MPF) (cyclin) (cdk = cyclin dependent kinase) (none of these). B. Ink proteins bind to and inhibit one of the cdk's in the cell cycle. (Ink = INhibitor of Kinase.) Many cancer cells have mutations in the INK gene(s). (For clarity, the protein name is given in lower case and the gene name in upper case.) Some cancer cells have normal INK genes but have mutation(s) in the corresponding CDK gene(s) that eliminate cdk-ink protein binding. (Other aspects of cdk function are normal.) Given this information, what would you expect? B-1. Levels of ink activity in tumor cells with mutations in the INK gene should be (normal) (above normal) (below normal) (can't predict). B-2. Levels of ink activity in tumor cells with mutations in the CDK gene should be (normal) (above normal) (below normal) (can't predict).
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