Cell biology Flashcards

1
Q

What is the function of telomerase?

A

Stabilise telomeres leading to immortalisation.

Cancer cells pathologically activate telomerase.

Telomeres are structures at the end of chromosomes which progressively shorten with each cell division.

When telomerase is suppressed (normal physiology) shortened telomeres cause cell-growth arrest = normal ageing and tumour suppression.

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2
Q

What is Kennedy Disease?

A

AKA “X-Linked bulbospinal neuronopathy”.

A tri-nucleotide repeat disorder which presents with gradual onset of limb and bulbar muscle weakness.

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3
Q

Which lab technique is used to identify the presence of specific DNA sequences?

A

Southern Blotting

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3
Q

What is the typical age onset of Kennedy disease?

A

Age 40-60 but with repeat expansion can appear as early as the 20s.

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4
Q

What is the function of a Western blot?

A

Used to identify specific proteins.

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5
Q

Function of proteosomes?

A

Peptide degradation.

Cellular stress leads to damage of intracellular proteins which are then identified by the ubiquitin proteasome system for degradation.

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6
Q

What conditions may be caused by disordered proteasome function?

A

Degenerative disorders such as Parkinson’s or cancer.

In Parkinson’s disease you get protein aggregates and Lewy body formation.

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7
Q

Function of the Golgi apparatus?

A

Post-translational modifications of proteins e.g addition of lipid or carbohydrate moieties.

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8
Q

Function of endoplasmic reticulum?

A

Manufacture of proteins

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9
Q

Function of mitochondria?

A

Driving oxidative metabolism.

Mitochondrial dysfunction therefore leads to syndromes with features of defective energy utilisation e.g leading to muscle weakness.

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10
Q

Function of peroxisomes?

A

Break down of long-chain fatty acids.

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11
Q

Describe the stages involved in the phase of accute inflammation.

A

1) The initiating factor originates from platelets activated by mature collagen exposed in a wound

2) Platelets aggregate and then release a variety of active agents including lysosomal enzymes, ATP, serotonin and wound cytokines

3) A fibrin clot develops, which completes homeostasis and provides strength and support to the wound

4) The surface dries to form a scab

5) Platelets and macrophage factors cause local vasodilation which produces warmth and increased capillary permeability, allowing serum and white blood cells to accumulate and cause swelling.

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12
Q

What happens following the initial acute inflammation phase?

A

Demolition: macrophages become active and remove unwanted fibrin, dead cells and bacteria and create fluid-filled spaces for granulation tissue.

Macrophages also release factors that stimulate the formation of new capillary buds during this phase and later they initiate and control fibroblast activity during repair.

Within the connective tissue, randomly orientated collagen begins to form after a few days, reaching a peak of activity after 5-7 days.

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12
Q

Function of riboflavin?

A

Riboflavin is involved in redox processes involving the hydrogen-transfer chain in the mitochondria and profuction of ATP.

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13
Q

Which immune cells carry out degranulation?

A

Basophils, eosinophils and mast cells

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14
Q

What does the process of degranulation involve?

A

Intracellular lysosomes fuse with the plasma membrane and discharged their contents. This allows attack against larger infecting organisms such as protozoa and helminths which cannot be engulfed by phagocytosis.

15
Q

What processes are involved in phagocytosis?

A

Chemotaxis, ingestion within a phagosome, intracellular enzymatic degradation and exocytosis.

16
Q

In which process is endocytosis involved in?

A

Antigen presentation

17
Q

Stages of mitosis?

A

Prophase: chromatin condenses

Metaphase: chromosomes become attached to the spindle fibre

Anaphase: microtubular shortening

Telophase: chromatids move to opposite ends of the cell and two nuclei are formes

18
Q

What is apoptosis and how does it happen?

A

Apoptosis= programmed cell death.

Occurs via two ways:
1) The intrinsic pathway: driven by mitochondrial dysfunction
2) Extrinsic pathway: cell-receptor mediated cell-death

19
Q

What is senescence defined by?

A

Arrest of mitosis

20
Q

What is endothelin-1?

A

A 21- amino acid polypeptide which is a highly potent vasoconstrictor and plays a part in the modulation of vascular toe.

21
Q

Two examples of conditions that endothelin plays a role in?

A

Pulmonary hyertension and Raynauds.

22
Q

Role of VCAM-1?

A

A vascular cell adhesion molecule which facilitates the passage of white cells into the extravascular space

23
What triggers heat-shock proteins?
Tissue stress and underlying inflammation or hypoxia
24
What is ICAM-1?
An intracellular adhesion molecule which is upregulated during inflammation
25
What would you expect to find in a biopsy of sarcoid granulomas?
Asteroid bodies
26
Which white cells are commonly found in granulomas?
Macrophages
27
How is a resting neurone charged?
At rest: Inside of neurone: rich in chloride ions and therefore negatively charged. Outside of neurones: rich in sodium ions and therefore positively charged. Net result= the neurone is positively charged- "the rsting potential".
28
What is the function of MMP9?
Gellatinase
29
What is the function of p53?
Promotes growth arrest at the G1/S regulation point in the presence f DNA damage. It is therefor a target of cancer therapy.
30
Which syndrome does a congeintal mutation in p53 cause?
Li-Fraumeni syndrome
31
Marfan's is caused by a mutation in which gene?
FBN1
32
Function of FBN1 gene?
Responsible for the formation of microfibrils which provide strength and stability to connective tissue.
33
What is HLA?
HLA is the genetic code on the short arm of chromosome 6, codes for important aspects of the immune system.
34
Most common HLA and disease assciations?
HLA-A: Haemochromatosis (A3) HLA-B: Behcet syndrome (B5) Ank spond (B27) Reactive arthritis (B27) HLA-C: Psoriasis (cW6) HLA-DR Goodpasture syndrome (DR2) MS (DR2) Addison's (DR3) Rheumatoid disease (DR4)
35
What is the process of DNA splicing?
Excision of introns and the joining of exons which ultimately results in production of a peptide.
36
How is aciclovir activated?
Aciclovir is a guanine analogue pro-drug that s used primary in herpes zoster and herpes simplex infections. The key step in activating it is conversion into a triphosphate form by host cel kinases, hich eventually allows it to incorporate into viral DNA resulting in chain termination. Viral DNA polymerase is then unable to function and replication of the herpes virus is terminated.
37
How long does it take to achieve peak plasma concentration after oral administration of aciclovir?
1-2 hours