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BMS2002 stage 2 > Lecture 16 - 22 > Flashcards

Lecture 16 - 22 Flashcards

1
Q

What is diabetes mellitus?

A

The inability to regulate blood glucose

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2
Q

What is the normal levels of glucose and what is the diabetic level of glucose?

A

Normal = 5mM
Diabetes = 7mM+

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3
Q

What is the pathogenesis for type I diabetes?

A
  • caused by a failure of insulin secretion
  • character sized by low insulin and high glucose levels
  • has sudden onsets
  • caused by the destruction of beta cells
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4
Q

What is the pathogenesis of type II diabetes?

A
  • caused by insulin resistance in tissues
  • insulin present in circulation but glucose remains elevated
  • has gradual onset
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5
Q

How does insulin-dependent diabetes mellitus (type I occur)?

A

Beta cells of pancreas are destroyed by cytotoxic CD8 T cells reactive against peptides of insulin and other specific proteins which are complexed with MHC molecules and recognized by cytotoxic T lymphocytes

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6
Q

What are the symptoms of hyperglycemia?

A
  • increased fluid osmolarity in tubules
  • more water is secreted from cells into the proximal convoluted tubule
  • causes increased urine floe (dieresis)
  • water reabsorption is reduced
  • dehydration, excessive urine production and thirst
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7
Q

What is hyperglycemia?

A

When high glucose concentrations enter glomerular filtrate and overwhelms the glucose absorbing capacity of the proximal convoluted tubule

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8
Q

What are the forms of insulin used for therapy?

A
  • animal insulin (porcine/bovine)
  • human insulin
  • human insulin analogue
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9
Q

What are the types of human insulin and what are their characteristics?

A
  1. Soluble insulin
    - rapid and short lived
    - used intravenously in emergency treatment of hyperglycemic.
  2. Isophane insulin
    - tends to form precipitates = intermediate acting
  3. Insulin zinc suspension
    - tends to form precipitates = long acting
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10
Q

What are the three insulin analogues and what are their characteristics?

A
  1. Insulin Lispro
    - modified insulin obtained by switching a Lys28 and Pro29
    - very rapid and very short lived.. usually taken before a meal
  2. Insulin glaring
    - modified insulin obtained by mutating Asn21 in Gly and by adding 2 Arg at the end of the beta chain
  3. Insulin detemir
    - modified insulin obtained by mutating Thr 30 (deletion)
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11
Q

How does type 2 diabetes occur?

A

Beta cells try to compensate for peripheral resistance = beta cells become exhausted and cannot keep up with the peripheral demand of insulin = failure of insulin secretion

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12
Q

Which cell is responsible for the autoimmune reaction that destroys the beta cells of pancreas in type 1 diabetes?

A

CD8 cytotoxic T cells

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13
Q

Which of the following is NOT a feature of type 1 diabetes?

A. Sudden on-set
B. Develops early in life
C. Rare
D. Caused by failure of insulin secretion
E. Caused by peripheral insulin resistance

A

E. Caused by peripheral insulin resistance

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14
Q

Which of the following combinations of insulin forms would be normally used to control glycaemia?

A. Lispro + soluble insulin
B. Zinc suspension + Glargine
C. Soluble insulin + glargine
D. Lispro + detemir

A

C & D: Soluble insulin + glargine, Lispro + detemir

Has to be a short acting + intermediate long acting

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15
Q

What are the order of events in type 2 diabetes?

A
  1. Obesity/ sedentary life style
  2. Hyperinsulinemia
  3. Beta cells failure
  4. Hyperglycemia
  5. Retinopathy
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16
Q

What molecules can lead to insulin resistance in type 2 diabetes?

A

IL-1 & DAG

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17
Q

Which of the following drugs work by improving insulin secretion from the beta cells of the pancreas?

A. Pioglitazone
B. Beta-3 receptor agonists
C. Gliclazide
D. Metaformin
E. Insulin

A

C. Gliclazide

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18
Q

What is the role of free fatty acids in insulin resistance?

A
  • lead to insulin resistance in muscle and liver
  • when in excess they are transformed into secondary messenger DAG
  • DAG activates PKC which phosphorylate IRS-1 = attenuates insulin receptor signal
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19
Q

What is the role of Adipokines in insulin resistance?

A
  • released by Adipocytes
  • adiponectin is anti-hyperglycemic = improves insulin sensitivity by activating AMPK = promoting lipolysis in liver and muscle
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20
Q

What is the role of inflammation in insulin resistance?

A
  • adipocytes produce IL-6 and IL-1 which attract macrophages to fat deposits
  • experimental reduction of cytokines improve insulin sensitivity
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21
Q

What is the role of PPARgamma in insulin resistance?

A
  • promotes secretion of anti-hyperglycemic adipokines
  • mutations can cause diabetes
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22
Q

What is the role of Thiazolidinediones (Pioglitazone)?

A
  • Agonist of nuclear receptor PPAR-gamma
  • promotes expression ad secretion of anti-hyperglycemic adipokines = increases lipolysis
  • reduce insulin resistance in liver and their peripheral tissues
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23
Q

What is the role of Metformin?

A
  • suppress glucose release from liver
  • activate AMPK
  • increase lipolysis in liver and muscles = improve insulin receptor signaling
  • suppress glucose release from liver
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24
Q

What is the role of Sulphonylureas (Gliclazide)?

A
  • bind to sulhponylurea receptors expressed on membranes of beta cells
  • block ATP sensitive K+ channels in Beta cells
  • K+ accumulates inside cells = beta cells depolarize
  • Ca2+ channels open = allow insulin secretion by exocitosis
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25
Q

What are the 2 types of drugs for type 2 diabetes?

A
  1. Alpha2 adrenoreceptor antagonist
    - increase insulin secretion
  2. Selective beta3 agonists
    - beta3 adrenoreceptors control lipolysis in fat cells
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26
Q

What are the long term consequences of diabetes?

A
  • ROS = high levels of glucose in our blood cause oxidation in long term excess of glucose = reactive oxygen species
  • AGEs generation = binds to receptor and induces the production of reactive oxygen species that damage blood vessels
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27
Q

How is NF-kappaB activated in the canonical/classical pathway?

A
  • formed by a dimer of p50 and RelA
  • pathway activated by the binding of a ligand to the receptor which activates a complex of IkB kinases
  • kinases complex will phosphorylate IkB causing IkB ubiquitination and then IkB is degraded
  • p50 and RelA are free to enter the nucleus and cause the transcription of specific target genes
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28
Q

How is NF-kappaB activated in the non-canonical pathway/alternative signalling pathway?

A
  • activation of kinases NIK phosphorylate IKKAlpha which phosphorylate p100
  • processing of p100 via proteosome to form p52 = associates with RelB to cause transcription of the genes in the nucleus
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29
Q

What is the role of Rel Homology Domain (RHD)?

A

encodes the DNA binding and dimerisation functions of NF-kappaB

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30
Q

What is the role of p100 and p105?

A

contain ankyrin repeats in their C-termini that allow them to function as IkB inhibitors

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31
Q

What are TA1/TA2, TAD, SD1, SDII?

A

non-conserved transcriptional activation domains

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32
Q

What are the subunits in the canonical pathway?

A
  • p50
  • RelA
  • c-Rel
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33
Q

What are the subunits in the alternative pathway?

A
  • RelB
  • p52
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34
Q

What are the inhibitors of NF-kappaB?

A

IKBA, IKBB, IKBE and Bcl-3

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35
Q

What do the IKB proteins contain?

A

contain ankyrin repeat motifs (ANK) in their C termini. PEST, domain rich in proline (P), glutamate (E), serine (S) and threonine (T).

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36
Q

What does Bcl-3 contain?

A

nuclear coactivator for the p52 NF-κB subunit (and other transcription factors)

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37
Q

How does NF-kappaB cause cancer?

A

control of NF-kappaB is lost = NF-kappaB in cytoplasm causes the transcription of genes = uncontrolled proliferation of cells

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38
Q

What is the structure of p53?

A
  • N-terminal domain contains a sub-transactivation domain and a proline-rich domain which is involved in regulation of apoptosis.
  • Core domain bind to specific DNA sequences
  • C-terminal domain contains the tetramerization domain
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39
Q

What is the p53 signalling pathway?

A
  1. p53 binds to an inhibitor HDM2
  2. stimuli activates p53 and is recognised as an oncosurpressor
  3. when activated p53 the inhibitors are degraded so p53 is free
  4. p53 can repair DNA or induce apoptosis if the DNA cannot be repaired
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40
Q

What is the difference between NF-kappaB and p53?

A

NF-kappaB = tumor-promoting functions
p53 = tumour suppressing functions

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41
Q

What needs to happen to carry out a cell cycle?

A
  • chromosomes need to be duplicated
  • other organelles need to be copied
  • cells need to grow
  • chromosomes need to be segregated accurately
  • cell needs to physically divide
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42
Q

What drives the cell cycle?

A

cyclin-dependent kinases (Cdks)

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43
Q

What are Cdks?

A

protein kinase that transfer a phosphate onto their substrates = act as master regulators

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44
Q

What makes cyclin levels oscillate?

A

Mechanisms controlling synthesis = changes in transcription and translation rate

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45
Q

What is the role of the APC/C signal?

A

signals degradation of M-cyclin to end mitosis and initiate cell division

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46
Q

What is the role of the SCF signal?

A

signals degradation of CKIs to promote G1-S transition

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47
Q

How is cell cycle fidelity maintained?

A
  • cyclin oscillations provide timing for the successive phases of the cell cycle = checkpoints monitoring the cell cycle to make sure everything is in place
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48
Q

How do checkpoints in the cell cycle work?

A

act by promoting Cdk activation or inactivation

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49
Q

What are mitogens and their role in the cell cycle?

A

proteins that signal the cell to proliferate = promotes G1/S synthesis

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50
Q

What is the role of DNA damage in the cell cycle?

A

inhibits M phase cyclin activity by phosphoregulation or CKI

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51
Q

What is the role of unattached chromosomes in the cell cycle?

A

prevents M phase cyclin destruction = cell stays in M phase until chromosomes are attached

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52
Q

What does the G1 checkpoint check?

A
  • if nutritional conditions are stable
  • if the cell is receiving proliferation signals
  • if damaged DNA has been repaired
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53
Q

What does the G2 checkpoint check?

A
  • if damaged DNA has been repaired
  • if DNA replication is complete
  • if the cell is big enough
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54
Q

What does the mitotic/spindle assembly checkpoint check?

A
  • of the chromosomes are properly attached to the spindle
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55
Q

What happens if a checkpoint cannot be satisfied?

A

Cells will resume the cell cycle if errors or damage can be fixed.

if not

Cells can withdraw from the cell cycle (senescence)
-Terminal exit from cell cycle
-Allows cell to remain part of tissue but it will not proliferate

Or:
Cells can undergo programmed cell death (apoptosis)
- Removes cell from organism

56
Q

How can cells trigger the transcriptions of G1-S cyclins?

A

Early G1 genes (Myc) can react to mitogens and bind to cell-surface = activates and increases the transcription of several genes

57
Q

What genes are activated and increased in G1/S transition?

A
  • cyclin D
  • SCF ubiquitin ligase (for protein proteolysis)
58
Q

What are temperature sensitive mutants?

A

Mutants that allow gene products to function at low temperature but not higher temperature

59
Q

Why do we use temperature sensitive mutants?

A

To track cell cycle by size and budding

60
Q

What triggers the degradation of M-cyclin?

A

APC/C

61
Q

What is the role of the poly ubiquitin chain on cyclins?

A

Chains of ubiquitin form a tag that the cell recognizes as a destroy signal = cyclin moves to proteosme to be destroyed

62
Q

What are the 4 groups of Cdks?

A
  1. G1-Cdks = Cdk 4 & 6
  2. G1/S Cdks = Cdk2
  3. S- Cdks = Cdk2 & Cdk1 (CDC2)
  4. M-Cdk = Cdk 1 ( CDC2)
63
Q

What are the 3 groups of cyclins?

A
  1. G1 cyclins = Cyclin D
  2. G1/S cyclins = Cyclin D, cyclin E, cyclin A
  3. G2/M cyclins = cyclin B
64
Q

What type of division occurs in mitosis?

A

Equational division = each of the daughter cells have the same numbers of chromosomes that we started with (in parental cell)

65
Q

What type of division occurs in meiosis?

A

Two division steps

  1. Reductional division = start with 2 sets of chromosomes San end up with one set
  2. Equational division = start with one set of chromosomes and end with one set of chromosomes
66
Q

What needs to happen in PROPHASE (mitosis)?

A
  • chromosomes begin to condense
  • centerosomes (which organize microtubules) move apart = form a bipolar spindle
  • nuclear membrane breaksdown
67
Q

What needs to happen in PRO-METAPHASE (mitosis)?

A
  • chromosomes attach to spindles/microtubules
68
Q

What needs to happen in METAPHASE (mitosis)?

A
  • chromosomes align in the middle of the cell (metaphase plate)
  • microtubules teach onto chromosome centromeres
69
Q

What needs to happen in ANAPHASE (mitosis)?

A
  • chromosomes are separated onto opposite poles via spindle fibers
70
Q

What needs to happen in TELOPHASE (mitosis)?

A
  • chromosomes decondense
  • nuclear envelope reforms
  • process of cell division begins
71
Q

What needs to happen in CYTOKINESIS (mitosis)?

A
  • cell pinches into 2 separate cells
71
Q

What needs to happen in CYTOKINESIS (mitosis)?

A
  • cell pinches into 2 separate cells
72
Q

What is the role of M-Cdk?

A

Regulates cell entry into mitosis

73
Q

How does M-Cdk work?

A

Directly phosphorylate key substrate proteins to change the cell into a mitosis state.

  • regulates downstream mitotic kinase (aurora B and Cyclin B kinases) which phosphorylate additional substrates
74
Q

What is the kinetochore?

A

The microtubules binding site on a chromosome

75
Q

How does assembly of microtubules occur in prophase?

A
  • Phosphorylation of M-cyclin and Aurora B recruit new proteins to assemble microtubules in early mitosis
76
Q

What is the structure of the kinetochore?

A
  • large macromolecular complex that assembles on the centromere
77
Q

What proteins/kinases are needed in the kinetochore?

A
  • M-Cdk (Cyclin B-Cdk1) & Aurora B required to recruit kinetochore proteins in early mitosis
78
Q

What is the role of cohesion rings?

A

Cohesion rings entrap two pieces of DNA = brings 2 pieces of DNA together and force cohesion

79
Q

What happens when chromosomes condense in prophase?

A
  • Cohesin is removed
  • condensing are recruited
  • interphase chromosome structure is lost
  • mitotic structure is gained
80
Q

What is the structure of microtubules?

A

Alpha and beta tubule dimmers that have a minus an d plus end

81
Q

What does gamma-TuRC do?

A

Nucleates proteins at the minus end of microtubules to trigger the assembly of tulip into polymers

82
Q

What are the different types of microtubules and what do they do?

A
  1. INTRAPOLAR MICROTUBULES = interact with each other across the spindle
  2. ASTRAL MICROTUBULES = project away from the centrosome and contact the cell cortex
  3. KINETOCHORE = microtubules that bind to chromosome
83
Q

What are the roles of Microtubules adapter proteins (MAPs)?

A

Allow cell components to bind microtubules = modulate the stability of microtubules (whether they grow or shrink)

84
Q

What is the role of Ndc80/Nuf2?

A

Modulates the stability of microtubules at kinetochores

85
Q

What is the roll of motors?

A

Allow cell components to move along microtubules (moves chromosomes around)

86
Q

What is the role of Kinesin-5?

A

Walks to the plus end of the microtubules

87
Q

What is the role of Dynein?

A

Walks to the minus end of the microtubules

88
Q

How do Kinesin motors function?

A

Use ATP energy to “walk” along chromosomes

89
Q

How does Kinesin-5 carry cargo?

A

Forms dimmers and cross-links microtubules ( cargo is another kinesin-5 molecule)

90
Q

How does CENP-E carry cargo?

A

Binds to kinetochores (cargo is a kinetochore)

91
Q

How does mitotic spindle assembly occur?

A
  • nucleation of microtubules at centrosomes (minus end)
  • formation of interpolar microtubules and sliding moves centrosomes apart
  • nuclear envelope breakdown allows microtubules to capture kinetochores
92
Q

What is the role of conversion of lateral attachment?

A

conversion of lateral attachment to end on attachment is a critical part in getting to a bi-orientated state.

93
Q

How does conversion of later to end-on attachments occur?

A

Once a kinetochore reaches the + end of a microtubule, the means of attachment changes.
End-on attachments require the Ndc80 complex (Ndc80 and Nuf2)

94
Q

What is the role of the kinase Aurora B?

A

Detects bi-orientation by localizing to centromeres and phosphorylates Ndc80 to remove microtubules from kinetochores

95
Q

What does the spindle checkpoint check for?

A

Detects any unattached kinetochores

96
Q

What do unattached kinetochores produce?

A

Produce the mitotic checkpoint complex (MCC)

97
Q

What is the role of the MCC?

A

MCC inhibits the APC/C by acting as a stop signal = prevents M-cyclin degradation which keeps cells in mitosis

98
Q

What happens when all kinetochores are occupied with microtubules?

A

MCC is no longer produced and M-cyclin is degraded, cell exits mitosis

99
Q

What is securin?

A

Inhibitor of protease named separase = cleaves cohesin in the centromere and removes the attachments between the two sister chromatids

100
Q

What happens in anaphase A?

A

Chromosomes moves towards the spindle poles
- driven largely by microtubules depolymerization at the plus end of kinetochore microtubules

101
Q

What happens in Anaphase B?

A

Spindle poles move apart.
- Driven largely by microtubules motors e.g kinesin-5

102
Q

What happens in telophase?

A
  • nuclear envelope reforms and nuclear pores are inserted
  • chromosomes decondense
  • condensins dissociate
  • cohesin re-associate and enable the formation of chromosome looping structures needed for correct gene expression
103
Q

What is the importance of asymmetric cell division in development?

A

Critical for multicellular organisms to differentiate from a single cell into many tissue types

104
Q

What is the role of ACD in normal stem cells?

A

ACD balances proliferation and self-renewal with cell-cycle exit and differentiation

105
Q

What is the difference between the two types of asymmetric cell division?

A

INTRINSIC:
- relies on internal factors within the cell to divide
- when cell divides, factors will be inherited by one daughter cell only

EXTRINSIC:
- don’t rely on intrinsic factors within the cell to divide
- promotes the self-renewal/proliferation capacity of stem cells
- mitotic spindle is orientated prior to division

106
Q

How does asymmetric cell division of germ cells support their immortality?

A
  • forms 2 cells = one with “junk” of the cell and one that becomes a sex cell
  • germ cells allow for the preserve cells of the genome that is passed from parents into offspring.
107
Q

How is cell polarity established?

A

Established through PARs

108
Q

What does the polar axis show?

A

Polar axis within the cell indicates that one side of the cell is different from the other

109
Q

What are the 2 ways that centrosomes signal polarity?

A
  1. Regulating the myosin cytoskeleton
  2. Pathway that depends on the microtubules that are emanating from the centrosome
110
Q

What happens in regulating the myosin cytoskeleton?

A
  • as centrosomes mature, they emanate Aurora A kinase factor = impacts the organization of the myosin cytoskeleton
  • advection
  • foci assemble and disassemble
111
Q

What is the structure of myosin cytoskeleton?

A

Network of actin filaments interfering with myosin motors

112
Q

What is advection?

A

PAR proteins are being moved without contact

113
Q

What happens in the pathway that depends on the microtubules that are emanating from the centrosomes?

A
  • microtubules prevent kinase from the anterior pass to act upon posterior parts and remove them from the membrane.
  • domains are maintained by mutual antagonism
114
Q

In fruit fly asymmetric division what happens when the embryo delaminates?

A

Polarity is inherited by the epithelium it was residing in

115
Q

What happens when PARs are removed?

A

Both spindle poles migrate to the exterior

116
Q

What doe LGN promote?

A

Promotes the formation of complex on the apical membrane = important for the rotation of the mitotic spindle

117
Q

What are the steps for centrosome stereotypical positioning?

A
  1. Centrosome is recruited to the apical crescent
  2. Daughter centrosome remains apical and presents more microtubules polymerization activity = mother centrosome shreds PCM
  3. Favoring the orientation of the forming spindle
  4. Mother centrosome will be inherited by the cell undergoing differentiation
118
Q

What is PAR1 and what is its function?

A

PAR1 = a posterior PAR protein = phosphorylates MEX-5 which leads to segregation of MEX-5 to the anterior

119
Q

What are P-granules?

A

A condensate of proteins and RNAs that mix from the cytoplasm without the need for a membrane

120
Q

What is the difference between P-granules and MEX-5?

A

P-granules become enriched in the posterior
MEX-5 become enriched in the anterior

121
Q

What do APC targets promote?

A

Promote differentiation and inhibit cell renewal

122
Q

In what ways do aPKCs inhibit cell renewal?

A
  1. NUMB = inhibitor of Notch signaling
  2. MIRANDA = directs the localization of..
    - Staufen = mRNA binding protein
    - Prospero = transcription factor
    - Brat = protein translation inhibitor
123
Q

How does cell fate specification occur?

A

Through aPKC phosphorylation

  • when aPKC encounters Miranda it phosphorylates it and removes it from the membrane
124
Q

How does the division of the two cells occur in cytokenisis?

A

Through the action of the contractile ring = formed by actin filaments and myosin motors.

Upon pulling the myosin motors = constriction of ring = division of the two cells

125
Q

What are the 4 groups of CDKs?

A
  1. G1-CDK: CDK4 & 6
  2. G1/S-CDK: CDK2
  3. S-CDK: CDK2 & CDK1 (CDC2)
  4. M-CDK: `cdk1 (CDC2)
126
Q

What are the 4 groups of cyclins?

A
  1. G1-cyclin: cyclin D
  2. G1/S cyclin: cyclin E
  3. S-cyclin: cyclin A
  4. G2/M cyclin: cyclin B
127
Q

What are the 3 main checkpoints that coordinate cell cycle progression?

A
  1. restriction point (START in yeast)
  2. G2/M (DNA damage) checkpoint
  3. Mitotic checkpoint
128
Q

How does chromosome duplication occur in the cell cycle?

A

Chromosome is replicated in S phase and are held together in G2 (cohesion).

129
Q

How does centrosome duplication occur in the cell cycle?

A

Happens in S phase along with DNA replication.

130
Q

How does the golgi, ER and mitochondria duplication occur in the cell cycle?

A

disassemble and then vesiculate as cells go into mitosis.

131
Q

What is the role of SCF?

A

signals degredation of CKIs to promote G1-S transition

132
Q

What is SCF?

A

it is a ubiquitin ligase

133
Q

What is the role of APC/C?

A

signals degradation of M-cyclin

134
Q

What is the role of ubiquitinylation?

A

it is a tag for protein degredation

135
Q

How do checkpoints act?

A

act by promoting Cdk activation or inactivation

BMS2002 stage 2 (4 decks)

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