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MABS Physiology > lecture 2 > Flashcards

lecture 2 Flashcards

1
Q

the two different types of cell death?

A

apoptotic and necrotic pathway

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2
Q

describe the cell cycle? 3 points

A

1) cell growth and chromosome replication
2) chromosome segregation
3) cell division

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3
Q

how many phases is the cell cycle? what are they?

A

4 phases;M, G1, S, G2

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4
Q

describe each of the phases

A

M for mitotic phase, G1 (or G1 capable) can remain in this state or proceed with cell replication and G2 are cell growth, and S is for synthesis/replication. Understand that G1 also contains a G0 phase like neurons can never come to G1 phase and not replicate

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5
Q

what happens between each of the phases during the cell cycle?

A

checkpoints to prevent replication of errors through use of own cyclins

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6
Q

what are cyclin dependent protein kinases?

A

phosphorylates cyclins to facilitate the progression through the cell cycle.

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7
Q

what happens if M-cyclin levels are always high?

A

usually indicative of cancer cell growth leading to uncontrolled growth

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8
Q

With respect to the abundance of cyclins, how are they regulated?

A

ubiquitination which deactivates m-cyclins and are destroyed by proteosomes mediated by anaphase promoting complex (APC) also inactivating M-Cdk. Remember this happens at the end of each phase because each phase has their own cyclins

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9
Q

why is the cell cycle so effective?

A

Because you have checkpoints proofreading for errors, surveillance proteins and enzymes that can remove errors from the genetic material to prevent replication and cyclins are used to proceed the cell into its next phase and at anytime the cell cycle progression can stop if errors are found.

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10
Q

what is significant about G1 cells with respect to going into the G0 phase?

A

G1 cells can go into G0 and remain or out. Like a hepatocyte, these cells are in G0 phase and can come into G1 phase and replicate. Or a neuron, which remains in G0 phase all its life.

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11
Q

how do cyclins promote the progression of the cell cycle?

A

cyclin receives signal that phase is to be initiated and so CDK binds with cyclin allowing for elongation factor to promote cellular activity like cell growth or replication of genetic material. Once finished, cyclin dependent inhibitory protein (phosphorylase) binds with cdk complex and inhibits further activity and cell can move onto next phase.

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12
Q

what are the genes encoding cyclin D and CDK4 called?

A

oncogenes

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13
Q

what are proto-oncogenes?

A

mainly encode proteins involved in a cell’s normal growth control pathway

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14
Q

what controls cell growth and division?

A

growth factors

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15
Q

what are oncogenes?

A

these are genes that facilitate continued growth potentially becoming uncontrolled and cancerous generally surveilled by tumor suppressor genes if proto-oncogenes are damaged, even just one.

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16
Q

why are tumor suppressor genes important?

A

they control cell growth

17
Q

what is xeroderma pigmentosm?

A

mutation in genes of the nucleotide excision repair pathway. Squamous cell carcinoma and metastatic malignant melanoma develops in patients with XP

18
Q

what is hereditary nonpolyposis colorectal cancer (HNPCC)?

A

mutation in mismatch repair genes like when nucleotide base pairs are mismatched

19
Q

how are oncogenes documented if they are cellular in origin?

A

“c”-designation

20
Q

how are oncogenes documented if they are viral?

A

“v”-designation

21
Q

what is Burkitt’s Lymphoma?what gene is affected?

A

cancer of B lymphocytes where myc gene is translocated from chromosome 8 to 14 which can result in the movement of the gene to a strong promoter where this would result in over expression

22
Q

what is Burkitt’s Lymphoma an example of?

A

gene translocation

23
Q

what is gene translocation?

A

DNA sequences may move from one position in the genome to another.

24
Q

what is philadelphia chromosome?

A

Usually occurs in bone marrow cells where the DNA changes between chromosomes 9 (ABL) and 22 (BCR) creating a fusion protein that increases tyrosine kinase activity and promotes uncontrolled growth of leukemic cells (chronic myelogenous leukemia) and apoptotic control is lost because BCR controls it and here we see it is affected

25
Q

How is Burkitt’s lymphoma written?

A

T(8,14)

26
Q

How is Philadelphia Chromosome written?

A

T(9,22)

27
Q

how are tumor suppressor genes affected that allow for the development of cancer?

A

both copies of the gene have to be affected

28
Q

what is p53 gene?

A

stops replication in cells that have DNA damage and targets unprepared cells for apoptosis

29
Q

how is p53 protein stimulated?

A

DNA damage

30
Q

how does p53 gene work?

A

simulates production of p21 which inhibits cyclin/CDK complexes and stops cell cycle progression and proliferation and also stimulates the production of DNA repair enzyme GADD to fix DNA problems

31
Q

If p53 cannot fix the DNA damage through primary means then what does it do?

A

it stimulates two genes for apoptosis: max and IGF-BP3 and if this fails than cancer can result because there is no more regulation. IT IS PRO APOPTOTIC

32
Q

what is necrotic process?

A

cell death, messy, major inflammatory reaction in the cell

33
Q

what is apoptotic process?

A

cytochrome c from mitochondria will start caspace cascade, a controlled form of programmed cell death that is used for removing unwanted or damaged cells. Very regulated and caspace 1 activates caspace 2 all the way to 13. Initiated by BCL-2 protein

34
Q

how many phases is apoptosis?

A

three: initiation, signal integration, execution

35
Q

during apoptosis, if an unwanted part of the cell needs to be removed how does it happen?

A

After apoptosis, the unwanted portion of the cell is cut into pieces and put into a vesicle marked so that it can be engulfed and disposed by macrophages through phagocytosis.

36
Q

what gene initiates apoptotic process?

A

BCL-2 gene

37
Q

why are T-cells important?

A

They undergo specializations and have to be able to know what is foreign in the body and what isn’t. 95% of immature T cells die, leaving 5% to work

38
Q

how the apoptotic process aid in our development.

A

1) epithelial cells must die to allow to fusion of palates
2) cells of mullein ducts die in males to aid in proper gender development
3) prostate cells die when deprived of hormone
4) cells of interdigital webbing die

39
Q

telomeres?

A

these shorten and cause aging, telomerase act to lengthen telomeres but usually not active in our cells, telomeres get shorter and shorter whenever genetic material is replicated. However in cancer cells, telomerase can be activated without regulation and uncontrolled cell growth occurs

MABS Physiology (57 decks)

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