Biol 430 W22 Final Exam 100 pts.
You may use your notes, textbook, PowerPoints, old quizzes, assignments, assigned articles,
handouts, etc. Do NOT use the web especially Wikipedia, everything you need was covered
in lecture or is in the text. I will only consider the answer correct if it is based on the book
or material I presented or provided not information directly from the internet.
Please read the question carefully so you do not misread what I am asking. To receive full
credit, try and only answer the question I am asking not everything related. It will shorten
the amount of writing and time needed to answer the questions.
Also check your answers to make sure they are complete, and you have answered all the
parts.
Question 1 (10 pts.) This is for the overall quality and thoughtfulness in answering the
questions which consists of: 1. Directly answering the specific question I asked so please
read carefully the question2. Framing and synthesizing it in your own words (not directly
copying large pieces of information word for word from my lecture transcription and/or
book). You don’t have to perfect in this regard but the effort in doing this is what I am
looking for.
Question 2 (8 pts.)
We covered a great of information regarding cell biology and its relevance to understanding
organismal well-being and function at the cellular level. Please provide a short self-reflection on
a topic that you personally found interesting and why? What else you would like to have learned
about that topic. I am looking for 4-6 sentences here (if you are compelled to write more that is
OK too).
My favorite topic from this unit was definitely cancer related genes, and the labs we did with the
HER2 cell cultures. Also, something that fascinated me was the Philadelphia chromosome
lectures we had and maybe I like it because my team presented on this, so I have a deep
understanding about the BCR/ABL genes. Don’t know if you are looking for a short summary of
what we learned but I will give a tiny, summarized version anyway.
The Philadelphia chromosome is the abnormality and the translocation of the genes 9 and 22 in
our bodies. This mutation causes TK receptors to be activated (abnormally) and tells the myeloid
cells of the body to divide, causing cancer.
I don’t think there is anything else I wished to learn in this topic! It was a fun class, and I am
glad I took it .
Question 3 (30pts). Cancer is a result of disruption of important regulatory pathways.
a) 10 pts. Describe the steps of the pathway that starts with a growth factor binding a
receptor tyrosine kinase (RTK) and leads to the synthesis or transcription of genes that
activate the cell cycle and entry into the restriction point and onto the S phase).
1) The cell cycle is initiated in the MAP kinase pathway which starts with the growth factor.
2) The extracellular domain of TK (Tyrosine Kinase) is where the growth factor binds to
3) The dimerization is what the product is of the binding of the growth factor.
, 4) Then, the autophosphorylation of TK (Tyrosine Kinase) takes place
5) The intracellular TK is binded with the SH2 domain of the GEF protein
5) The activation of GEF proteins takes place.
6) The exchange of GDP to GTP on Ras takes place in the GEF protein
7) The activation of Ras takes place
8) Ras initiates the activation of Raf
9) Raf activates MEK due to the hydrolyzation of ATP to ADP,
10) Activation of ERK kinase takes place
11) The translocation of ERK from the cytosol to the nucleus occurs
12) The activation of transcription factors SRF and SRE begin to allow transcription from ERK.
b) 5 pts. suppose there is DNA damage detected before entry into S (DNA replication)
phase in the form of a mismatch of an G to A in this phase. Describe DNA Repair pathway
the cell would use in this case
Base Excision Repair would be the DNA repair pathway since there is a mismatch of a single
nucleotide. The nitrogenous base of the repair would be removed first by the Glycosylase. The
sugar from the misplaced nucleotide would be removed by the AP endonuclease, and the ester
bond would be broken down by phosphodiesterase. Allowing entering and binding with the
correct nucleotides’ subsequent bases – which are C or T.
c) 10 pts. I have described the transcription factor, p53, as “the decider” in the cell cycle
check points.
1) What are the two pathways it (p53) is deciding between at the check pts.?
The two pathways are freezing the cell cycle through the inhibition of p21 of Cdk2/Cyclin E and
allow for repair to take place or cell death.
So, at checkpoint, p53 either goes through the continuation of the cell cycle or apoptosis (cell
death)
2) How is p53 activated? Which pathway/protein are involved?
P53 is stabilized and activated by the P’n, it regulates the production of P21 (CDk) inhibitor. The
damage activates and is recognized by the ATM kinases and Chk2 which then phosphorylates
P53.
3) What are the two main protein(s) that are transcribed/expressed by p53 order to
regulate the decision being made and what are their function?
PUMA is the protein that p53 initiates the transcription of, which then diminishes the two
proteins that allow BAX/BAX to form in these channels. This then releases the cytochoromosone
C, and this activates caspase 9 - these all lead to apoptosis/cell death.
P53 leads to cell cycle arrest and causes transcription of the P53 gene Cdk inhibitor p21. This
inhibits Cdk2 and cyclin E, which stops the cell cycle at G1.
You may use your notes, textbook, PowerPoints, old quizzes, assignments, assigned articles,
handouts, etc. Do NOT use the web especially Wikipedia, everything you need was covered
in lecture or is in the text. I will only consider the answer correct if it is based on the book
or material I presented or provided not information directly from the internet.
Please read the question carefully so you do not misread what I am asking. To receive full
credit, try and only answer the question I am asking not everything related. It will shorten
the amount of writing and time needed to answer the questions.
Also check your answers to make sure they are complete, and you have answered all the
parts.
Question 1 (10 pts.) This is for the overall quality and thoughtfulness in answering the
questions which consists of: 1. Directly answering the specific question I asked so please
read carefully the question2. Framing and synthesizing it in your own words (not directly
copying large pieces of information word for word from my lecture transcription and/or
book). You don’t have to perfect in this regard but the effort in doing this is what I am
looking for.
Question 2 (8 pts.)
We covered a great of information regarding cell biology and its relevance to understanding
organismal well-being and function at the cellular level. Please provide a short self-reflection on
a topic that you personally found interesting and why? What else you would like to have learned
about that topic. I am looking for 4-6 sentences here (if you are compelled to write more that is
OK too).
My favorite topic from this unit was definitely cancer related genes, and the labs we did with the
HER2 cell cultures. Also, something that fascinated me was the Philadelphia chromosome
lectures we had and maybe I like it because my team presented on this, so I have a deep
understanding about the BCR/ABL genes. Don’t know if you are looking for a short summary of
what we learned but I will give a tiny, summarized version anyway.
The Philadelphia chromosome is the abnormality and the translocation of the genes 9 and 22 in
our bodies. This mutation causes TK receptors to be activated (abnormally) and tells the myeloid
cells of the body to divide, causing cancer.
I don’t think there is anything else I wished to learn in this topic! It was a fun class, and I am
glad I took it .
Question 3 (30pts). Cancer is a result of disruption of important regulatory pathways.
a) 10 pts. Describe the steps of the pathway that starts with a growth factor binding a
receptor tyrosine kinase (RTK) and leads to the synthesis or transcription of genes that
activate the cell cycle and entry into the restriction point and onto the S phase).
1) The cell cycle is initiated in the MAP kinase pathway which starts with the growth factor.
2) The extracellular domain of TK (Tyrosine Kinase) is where the growth factor binds to
3) The dimerization is what the product is of the binding of the growth factor.
, 4) Then, the autophosphorylation of TK (Tyrosine Kinase) takes place
5) The intracellular TK is binded with the SH2 domain of the GEF protein
5) The activation of GEF proteins takes place.
6) The exchange of GDP to GTP on Ras takes place in the GEF protein
7) The activation of Ras takes place
8) Ras initiates the activation of Raf
9) Raf activates MEK due to the hydrolyzation of ATP to ADP,
10) Activation of ERK kinase takes place
11) The translocation of ERK from the cytosol to the nucleus occurs
12) The activation of transcription factors SRF and SRE begin to allow transcription from ERK.
b) 5 pts. suppose there is DNA damage detected before entry into S (DNA replication)
phase in the form of a mismatch of an G to A in this phase. Describe DNA Repair pathway
the cell would use in this case
Base Excision Repair would be the DNA repair pathway since there is a mismatch of a single
nucleotide. The nitrogenous base of the repair would be removed first by the Glycosylase. The
sugar from the misplaced nucleotide would be removed by the AP endonuclease, and the ester
bond would be broken down by phosphodiesterase. Allowing entering and binding with the
correct nucleotides’ subsequent bases – which are C or T.
c) 10 pts. I have described the transcription factor, p53, as “the decider” in the cell cycle
check points.
1) What are the two pathways it (p53) is deciding between at the check pts.?
The two pathways are freezing the cell cycle through the inhibition of p21 of Cdk2/Cyclin E and
allow for repair to take place or cell death.
So, at checkpoint, p53 either goes through the continuation of the cell cycle or apoptosis (cell
death)
2) How is p53 activated? Which pathway/protein are involved?
P53 is stabilized and activated by the P’n, it regulates the production of P21 (CDk) inhibitor. The
damage activates and is recognized by the ATM kinases and Chk2 which then phosphorylates
P53.
3) What are the two main protein(s) that are transcribed/expressed by p53 order to
regulate the decision being made and what are their function?
PUMA is the protein that p53 initiates the transcription of, which then diminishes the two
proteins that allow BAX/BAX to form in these channels. This then releases the cytochoromosone
C, and this activates caspase 9 - these all lead to apoptosis/cell death.
P53 leads to cell cycle arrest and causes transcription of the P53 gene Cdk inhibitor p21. This
inhibits Cdk2 and cyclin E, which stops the cell cycle at G1.
