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Cell Bio > Cell Bio Old Exam 4 Questions > Flashcards

Cell Bio Old Exam 4 Questions Flashcards

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1
Q

Which of the following is NOT required for sorting and synthesis of proteins destined for the lumen of the ER?

A

Stop transfer sequence

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2
Q

______ normally inhibits passage through cell cycle checkpoints, but through “loss of function” mutations can cause cancer

A

Tumor suppressor genes

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3
Q

Which of the following structurally mimics the (+) end of a microtubule and acts as a nuclear ion site for polymerization from the centrosomes?

A

Y-Tubulin ring complex

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4
Q

Which of the following events does NOT usually occur during interphase?

Cells grow in size
Cell checks for damaged DNA
DNA is replaced
The nuclear envelope breaks down

A

The nuclear envelope breaks down

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5
Q

Necessary and sufficient to target proteins to organelles is a true statement about what?

A

Protein signal sequences

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6
Q

Which cytoskeletal filaments lack polarity?

A

Intermediate filaments

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7
Q

Levels of Cdk activity changes during the cell cycle, in part, because __________

A

cyclin levels change during the cell cycle

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8
Q

which of the following is not a mechanism that results in the production of oncogenes

A

gene deletion

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9
Q

the random ingestion of fluid and small molecules by vesicles less than 150 nm in diameter is called

A

pinocytosis

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10
Q

which of the following binds to G-actin and prevents the monomer from being added to an actin filament?

A

profilin

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11
Q

cells in G0 state ________

A

do not divide

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12
Q

enzymes secreted by cancer cells that digest extracellular matrix components are called

A

metalloproteases

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13
Q

N-Pro-Pro-Lys-Lys-Lys-Arg-Lys-Arg-Lys-Arg-C

A

signal sequence that would be used to target a protein to the nucleus

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14
Q

the process of removing DNA from an egg and injecting the nucleus from an adult somatic cell in order to generate embryonic stem cells is called

A

Somatic cell nuclear transfer

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15
Q

thebasic contractile unit of muscle that is composed of myosin-II bipolar filaments and actin filaments that slide past each other is called a

A

sarcomere

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16
Q

which of the following components in the receptor mediated endocytosis pathway is responsible for recycling the receptor back to the plasma membrane?

A

endosome

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17
Q

Myc and ras^D are two proto-oncogenes that, when mutated, can cause tumor formation. Which would you expect to result in the greatest chance that a tumor will actually form?

A

Mutated Myc and mutated ras^D combined

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18
Q

true or false: the nuclear envelope re-forms in anaphase?

A

false

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19
Q

gtp-binding protein that utilizes the hydrolysis of gtp to pinch vesicles off from the membrane during endocytosis?

A

dynamin

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20
Q

adult cells that have been reprogrammed to become pluripotent stem cells?

A

iPS induced pluripotent stem cells

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21
Q

_______ normally promotes cell survival and cell proliferation, but can cause cancer after a “gain of function” mutation

A

protooncogenes

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22
Q

at the end of DNA replication, the sister chromatids are held together by _______

A

cohesins

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23
Q

_______ is a microtubule motor protein that moves towards the (+) end of the filament, and ________ is a microtubule motor protein that moves towards (-) end of the filament

A

kinesin, dynein

24
Q

in the process of protein transport into the ER, which of the following is responsible for cleaving the ER signal sequence from the polypeptide after translation

A

Signal peptidase

25
Q

which of the following description is consistent with the behavior of a cell that lacks a protein required for a checkpoint mechanism that operates in G2?

A

the cell would enter M phase under conditions when normal cells would not

26
Q

during initial translation of a protein destined for the ER, the ER signal sequence is exposed on the polypeptide. which of thefollowing binds to the mRNA/ribosome/polypeptide ER signal sequence complex and halts translation until it can dock to the ER membrane?

A

signal recognition particles SRP

27
Q

what is not a use of cholesterol

A

used by the ribosome during translation

28
Q

which of the following is not required for cilica movement

microtubules
dynein
nexin
myosin-II

A

myosin-II

29
Q

place the following steps of nuclear import in the order that they occur, starting with a cargo protein that has been synthesized in the cytoplasm

A
  1. Nuclear transport receptor binds to the nuclear localization signal on the cargo protein
  2. cargo protein and NTR move into the nucleus
  3. Ran-GTP binds to NTR and releases cargo protein
  4. Ran-GTP and NTR move out of the nucleus
  5. Ran-GTP hydrolyzes GTP–>GDP+Pi and releases the nuclear transport receptor.
30
Q

monomer that binds and hydrolyzes ATP

A

actin filaments

31
Q

includes keratin and nuclear lamins

A

Intermediate filaments

32
Q

important for formation of the contractile rings during cytokinesis

A

actin filaments

33
Q

supports and strengthens the nuclear envelope

A

Intermediate filaments

34
Q

their stability involves a GTP cap

A

Microtubule filaments

35
Q

directly involved in muscle contraction

A

actin filaments

36
Q

can be connected through desmosomes

A

intermediate filaments

37
Q

a component of the mitotic spindle

A

microtubule filaments

38
Q

explain how statins can treat high cholesterol. what is their function and how does the cell respond to these treatments to lower cholesterol levels?

A

statins inhibit the cells ability to synthesize its own cholesterol by inhibiting the HMG coA reductase enzyme which will stimulate the cells to take in more cholesterol from the blood stream lowering the levels in the blood.

39
Q

explain how fiber can treat high cholesterol. what is its function and how does fiber lead to lower cholesterol levels?

A

fiber binds to bile acids and prevents intestinal cells from recycling them. stimulating the cells to create more bile acids from free cholesterol to lower the levels.

40
Q

cancer cells exhibit six general cellular properties. please list three of the 6

A 
sustained angiogenesis
self-sufficiency in growth signals
insensitivity to antigrowth signals
tissue invasion and metastasis
limitless replicative potential
evasion of apoptosis
41
Q

totipotency definition

A

can develop into any type of cell in the human body, including the placenta

42
Q

pluripotent definition

A

more limited developmental potential, can develop into any cells of the fetus but NOT placental cells

43
Q

unipotency definition

A

stem cells that are committed and can only develop into specialized types of cells, like blood cells

44
Q

describe the role of the GTP-cap in regulating the dynamic instability of microtubules

A

gtp-cap regulates microtubule dynamics because it promotes microtubule polymerization. If the rate of polymerization is greater than the rate of GTP hydrolysis, the end of the microtubule will have a GTP- cap and will continue to grow. if, however the rate of gtp hydrolysis is faster than the rate of addition the gtp cap is lost and the microtubule will disassemble

45
Q

taxol and cholchicine are commonly used chemotherapy drugs. describe the function of either taxol or colchicine and how they are effective at killing cancer cells. -explain how they inhibit cellular functions

A

colchicine binds to tubulin heterodimer and prevents microtubule polymerization. taxol binds to the microtubule and prevents depolymerization. both are used to treat cancer because both will inhibit the mitotic spindle needed for cell division. cancer cells divide at a must faster rate than mormal cells so the inhibition will be effective at killing cancer cells.

46
Q

one example of a cancer forming gene is retinoblastoma (Rb). describe the function of Rb and how mutations in this gene can potentially lead to cancer formation.

A

Rb is a tumor suppresing gene. its function is to inhibit the transcription factor E2F. in response to mitogens Rb is phosphorylated by G1/S-Cdk complex and is inactivated thus releasing E2F to transcribe genes required for cell division. Loss of the Rb gene will result in the inability for cells to inhibit cell division and can lead to cancer development because they have lost that checkpoint.

47
Q

describe the function of Cdks. how are they activated and inhibited?

A

Cdks are kinases that rgulate progression through cell cycle. first they must bind to their corresponding cyclin. then Cdks are phiosphorylated at both activating and inhibiting Amino acid sites. finally, phosphotases dephosphorylates inhibitory amino acid on the Cdk which allows kinases to be active and stimulate cell cycle progression.

they are inhibited by two mechanisms: specific proteins called cdk inhibitor proteins which bind to the kinases and prevent them from functioning. also the cyclins are targeted for degradation through ubiquitylation and this will inactivate Cdks

48
Q

one example of cancer forming gene is p53. describe the function of p53 and how mutations in this gene can potentially lead to cancer formation.

A

p53 is a protein that normally unstable and turns over rapidly, however in the presence of DNA damage is stabilized. p53 regulates the transcription of p21 which is a cyclin/cdk inhibitor and inhibits the G1/G-Cdk complex to stop the cell from entering the S phase until the DNa damage is corrected. if cells are allowed to replicate in the presence of damaged DNA this can lead to cancer formation. so loss of p53 checkpoint mechanisms is a hallmark of cancer formation .

49
Q

describe one type of mutation of the LDL receptor and how it can cause familial hypercholestermia

A

LDL mutations can be in the synthesis of the receptor, the transport of the receptor to the plasma membrane, or mutations in the cytoplasm tail of the receptor or LDL binding. Mutations in the LDL receptor prevent cells from taking LDL out of the blood stream and this results in increased blood cholesterol levels which can lead to hypercholestermia.

50
Q

what are the steps for receptor mediated endocytosis of the LDL receptor

A

the LDL receptor in plasma membrane binds to LDL in the blood stream.Adaptin binds to the cytoplasmic tail of the receptor and clathrin binds to adaptin. this forms a vesicle, which is the pinched off from the plasma membrane by the GTPase dynamin. after the vesicle is fillu endocytosed, the clathrin and adaptin proteins uncoat from the vesicle. the vesicle fuses with the endosome where the receptors are recycled back to the plasma membrane and the LDL is kept in the lumen. Then this fuses with the lysosome which degrades the LDL and provides free cholesterol for use by the cell.

51
Q

chromosomes condense, centrosome duplicate and start to form the spindle poles

A

prophase

52
Q

nuclear envelope breaks down, chromosomes attach through their kinetochores to microtubules

A

prometaphase

53
Q

chromosomes allign at the metaphase plate

A

metaphase

54
Q

sister chromatids separate, spindle poles move away from each other and separate

A

anaphase

55
Q

new nuclear envelope starts to form and contractile ring starts to assemble

A

telophase

56
Q

actin-myosin II contractile ring separate the daughter cells

A

cytokinesis

Cell Bio (30 decks)

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