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Final Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

Describe the path of transmembrane proteins from synthesis to destination.

A

Protein synthesized in ER upon recognition of N terminal ER sequence.

  1. They will be folded correctly in the ER by chaperones
  2. modified with SS bonds and glycosylation (as needed)
  3. Then transported to the golgi for further modifications and processing
  4. Release of proteins from the cell via exocytosis
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2
Q

What happens if there is a cystic fibrosis protein

A

Protein remains in the ER because the channel is misfolded, degrading the protein inside the ER

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3
Q

What happens to protein that are not folded correctly after synthesis in the ER?

A

They will retain in the ER and eventually moved to the cytosol and degraded.

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4
Q

Describe the transport of protein into the nucleus. How is ran protein involved?

A
  1. Nuclear Transport Receptor binds to the signal sequence of protein and transport it to the nucleus.
  2. Receptor dissociates from the cargo and binds to Ran GTP
  3. Receptor exits the nucleus and Ran GTP is hydrolyzed to Ran GDP, dissociating the GDP from the receptor
  4. Cycle Repeat
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5
Q

What type of protein modification happens in the ER and Golgi?

A

In the ER, glycosylation and disulfide bond modification

In the Golgi, proteins are sorted and undergo further glycosylation if needed

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6
Q

Will a protein ALWAYS be transported to the Golgi after it has been in the ER?

A

Not all proteins move on to the golgi. Proteins with C terminal ER retention signal – stay in the ER,

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7
Q

Define Phagocytosis and Pinocytosis

A

Phagocytosis: ingesting large molecule via large vesicles

Pinocytosis: Ingestion of fluid and small molecules via small vesicles

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8
Q

What is the function of clathrin in cells?

A

Clathrin coats the outside of transport vesicles to shapes the membrane into a bud and helps capture molecules for transport

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9
Q

What is the difference between early endosome, late endosome and lysosome?

A

Early endosomes – vesicles just beneath plasma membrane
Late endosomes – vesicles closer to the nucleus
Lysosome- collection of enzyme that degrade biological polymers

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10
Q

Describe the series of events that leads to muscle contraction upon Ca2+ release from the sarcoplasmic reticulum

A

When calcium levels rise, troponin shifts the position of tropomyosin so that myosin can bind to actin, contracting it. If troponin is deleted, tropomyosin is always bound to actin, preventing myosin from binding to actin – muscle cannot contract

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11
Q

What is the likely effect on muscle contraction if the actin binding site on tropomyosin is
mutated so it no longer binds actin? Explain.

A

Muscle will not be able to relax since there is nothing stopping it from binding to actin. Muscle contraction is not coupled to calcium dependent signals

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12
Q

What is the basic function of a kinesin?

A

Kinesin is a motor protein that binds microtubules and moves cargo – vesicles, organelles along the microtubule

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13
Q

How is it different from the function of dynein?

A

Kinesin – will move cargo from the minus end to the plus end of the microtubule

Dynein is another motor protein that moves cargo from plus end to minus end

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14
Q

Define centromere, centriole, centrosome. Which of these is not a component of the cytoskeleton?

A

Centromere: Center of chromosome
Centrosome: specialized organizing centers from which microtubules form.
Centriole: Center of Centrosome

Centromere is not a component of the cytoskeleton

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15
Q

Describe the 5 different types of signaling, give examples of signals for each. which signal is the most suitable when the message needs to be broadcasted broadly throughout the organism?

A

Endocrine – insulin
Paracrine - histamine
Autocrine – any of these if cell has receptors for them
Neuronal – GABA, glutamate
Contact-dependent – delta-notch

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16
Q

What determines the response evoked in a cell to a specific signal?

A

The unique combination between the signaling molecule and the type of receptor it interacts with, in combination with intracellular signals that converge on the same pathway

17
Q

Name 3 types of cell surface receptors we discussed in class. Is this the only type of signaling (via cell surface receptors)?

A

Ligand gated ion channels, GPCRs, RTKs

Signaling can also be done via intracellular receptors (steroid hormones and nuclear receptors), or enzymes (NO)

18
Q

What is cholera toxin

A

acts on Gαs – inhibits GTP hydrolysis – constitutively active

19
Q

What is similar between nitroglycerin and sildenafil (the active ingredient in Viagra)?

A

Both modulate the effect of nitric oxide gas (NO) causing dilation of smooth muscle

Calcium activates Nos, the enzyme that generates nitric oxide gas
NO activates guanylyl cyclase to make cyclic GMP (cGMP) which ultimately causes relaxation of the smooth muscle allowing more blood to flow through the vessels
Sildenafil acts on the enzyme phosphodiesterase that breaks down cGMP, thus prolonging its effect

Calcium activates NOS. NOS generate NO which binds to guanylyl cyclase to make cGMP. This cause relaxation of smooth muscle.

Sildenafil enhances NO, promoting relaxation

20
Q

What is the difference between paracrine and autocrine signaling?

A

In autocrine signaling, a cell signals to itself, releasing a ligand that binds to receptors on its own surface. Paracrine cannot do this.

21
Q

What are second messengers? What are examples?

A

molecules that are activated following receptor activation

cAMP, calcium, IP3, DAG

22
Q

What is the advantage for utilizing second messengers in a signaling pathway?

A

The advantage of utilizing second messengers is to be able to amplify
Or relay the signal to multiple different targets, intersect with other signaling pathways

Ex:
IP3 relay signal to AKT
cAMP relay signal to promote glyogen breakdown
Calcium relay signal that leads to cGMP
DAG relay signal to PKC

23
Q

What is the pathway that activates PKA?

A

GPCR -> Gprotein alpha s -> adenylyl cyclase -> cAMP -> PKA

24
Q

What is the pathway that activates PKC from GPCR

A

GPCR -> G protein alpha q -> phospholipase C -> DAG -> PKC

25
Q

What is the pathway that activate MAP Kinase

A

RTK - > Ras GEF - > MAP KKK -> MAP KK - > MAP K

26
Q

What is the pathway that activates PKC from RTK

A

RTK -> Phospholipase C -> DAG -> PKC

27
Q

What is the pathway that activates CaMK

A

RTK - > Phospholipase C -> IP3 -> Calcium -> Calmodulin -> PKC

28
Q

What is the difference between a cell in G1, Go or terminally differentiated? Why is there a need for so many different states of cell cycle?

A

G1- Growth Phase; metabolic rate increase

G0 - cell cycle machinery is inhibited, the cell is not going to divide

Terminally differentiated – cell cycle machinery is mostly dismantled, the cell will not be able to divide

Cells need multiple stages to enhance control over their division. Abnormal division can lead to cancer

29
Q

How are cdk-cyclin regulating cell cycle?

A

When activated, the complex is enabling cell’s transition to the next stage of cell cycle

S cdk-cyclins promote recruitment of replication machinery to the origin of replication to drive DNA replication step
M cdk-cyclins promote chromosome segregation and cell division into two daughter cells by phosphorylating downstream targets

30
Q

What regulate cdk-cyclin activity?

A

CDK does positive feedback to increase cdc 25, which remove phosphate cdk to activate it

CDK does negative feedback by activation of APC/C which promotes ubiquitinoylation and degradation of cyclins

31
Q

What process enables the rapid activation and inhibition of the Cdk-cyclin complexes?

A

Phosphorylation

32
Q

What is the difference between intrinsic and extrinsic apoptotic induction?
Give an example when each would be used by a cell/organism.

A

Signal for apoptosis can arrive from outside, or inside the cell

Inside: release of cytochrome C from mitochondria

During neuronal development – lack of survival signal for neurons that did not make connections with targets will induce apoptosis

DNA damage that cannot be repaired – high stress, apoptosis can be induced by p53

33
Q

What is angiogenesis, and why would blocking angiogenesis be useful to treat cancer?

A

Angiogenesis – the process of generation of new blood vessels.

As cancerous tumor grows and expands, it needs oxygen and nutrients, or else it cannot expand. Cancer cells secrete factors that promote new blood vessel sprouting.

34
Q

Mutations in p53 are often found in cancers. Why can deletion of p53 be beneficial to
cancer cells?

A

. p53 stops a cell from dividing if a damage in DNA is detected. If it is mutated, cells can continue to divide even with mutations, such as what occurs in cancer cells

35
Q

What are the differences between benign, malignant and invasive tumors?

A

Benign – cannot invade
Malignant – can invade
Metastasis (invasive) – pieces break off, and invade other tissues

36
Q

Apoptosis plays a major role in cancer. Describe the mechanism of apoptosis, name key proteins involved, and give examples of processes in which apoptosis occurs normally.

A

Apoptosis – programmed cell death.

  1. Bax and Bak are activated
  2. Cytochrome c is released
  3. Cytochrome c activates procaspases
  4. Apoptosis forms
37
Q

What are three basic ways to convert a proto-oncogene to an oncogene?

A
  1. Mutation in coding sequence creating a hyperactive protein

2.Gene duplication causing generation of multiple copies of the protein

  1. Chromosomal rearrangement, causing regulatory element to induce activation of gene, or fusion to gene that promotes formation of hyperactive protein
38
Q

. Explain 1) the role of telomerase in a cell and,
2) why increased telomerase activity is often observed in tumor cells.

A

Telomerase replicates the ends of chromosomes to enable accurate replication of the lagging strand. It is highly active during development, then is silenced
With each division of adult cells, the telomere sequences become shorter, until cells stop dividing
Reactivation of telomerase will ensure division in adult cells that shouldn’t divide – increasing risk of mutations or replication errors and instability, promoting cancer

Biology (20 decks)

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