Genes Flashcards

(40 cards)

1
Q

spearman/pearson test

A

correlation coefficient AND looking for correlation between two variables

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2
Q

mutation in transcription factor

A

dna of cell changed
tertiary structure change
TF not complementary to gene
cannot bind - little mRNA for gene produced and translated
less available for drug/something else to bind to

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3
Q

mutation in cells that prevent cell division

A

mRNA transcription change
change in protein structure - non-functioning/faulty
uncontrollable division

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4
Q

samples

A

ethical = death/suffering

large number = improve reliability

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5
Q

tumours measured in volume

A

have varying depth

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6
Q

standard deviation

A

spread of distribution around the mean/degree of variation from the mean

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7
Q

SD overlap

A

difference is statistically insignificant
not conclusive
could be down to chance/equal results

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8
Q

change in sequence of DNA bases

A

change in primary structure
change in hydrogen bonds
alters tertiary structure
substrate cannot bind - no ES complexes

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9
Q

DNA structure

A
  1. Sugar-phosphate back bone = provides strength
  2. Long molecule = store lots of information
  3. Helix = compact
  4. Base sequence = transcription
  5. Double stranded = replication occur semi-conservatively
  6. Hydrogen bonds = stable
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10
Q

human vs bacterium

A

different enzymes

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11
Q

tumour suppressor genes mutation

A
abnormal methylation as a mutation
inactive
methyl groups added
tertiary structure altered
genes don't produce mRNA so not transcribed
proteins that slow division not produced
uncontrollable cell division
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12
Q

control groups

A

same conditions without trialled/independent variable

unethical to deny treatment

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13
Q

percentages

A

to compare

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14
Q

promoter regions

A

where RNA-polymerase binds to DNA
mutation = “ “ unable to bind to promoter
no mRNA made so no transcription of gene

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15
Q

siRNA

A

specific tertiary structure and shape
complementary so binds to mRNA only
mRNA cut - prevents translation
gene inhibited so protein not made

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16
Q

sample size

A

small = not representative
big = reliable
repeats in lab experiment

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17
Q

cancer

A

much higher rate of cell division? cancer IS uncontrollable cell division

18
Q

hormone oestrogen therapy not always cancerous

A

genetic differences with TSG
bodies may have little OE and hrt restores it
body already has processes to remove cancer

19
Q

getting rid of main source

20
Q

conclusion

A

lowest/most COMPARED TO ….
SD overlap = results by chance and not conclusive need stat test
lab study = repeats needed
drugs - side effects, human vs mice differences
small sample size = not rep or reliable
does it cure/stop?
results with little effect

21
Q

tumour develops

A

advanced cancer investigated

22
Q

in transcription, not all genes are expression - this is controlled by….

A

transcription factors

bind to specific DNA sites (promoters)

23
Q

TF’s control expression by controlling….?

A

rate of transcription
ACTIVATORS - incr rate by helping enzyme bind to DNA
REPRESSORS - decr rate by binding w/ start of target gene so preventing RNA Polymerase

24
Q

OESTROGEN

A

binds to TF called OE receptor
lipid-soluble
receptor-hormone complex binds to specific DNA site and stimulates transcription

25
miRNA
translation of target mRNA blocked
26
epigenetics
heritable change in gene function without change to the base sequence of DNA
27
acetylation
COCH3 binds to histone proteins chromatin = less condensed protein separated from DNA= more exposure gene switched on - transcribed!
28
hypermethylation
CH3 attaches to DNA bases at CpG site change in tertiary structure no transcription - gene switched off
29
hypomethylation
too little CH3 proto-oncogenes act as oncogenes incr. prod of proteins that encourage cell / = uncontrollable cell /
30
cell division controlled by 2 genes
proto-oncogenes = stimulate cell division | tumour suppressor genes = slow cell division
31
PROTO-ONCOGENES
proteins produced BUT mutation...? p-o = oncogene gene is overactive cell divides uncontrollably
32
TUMOUR SUPPRESSOR GENES
mutation...? gene is inactivated protein not produced - uncontrollable dividision
33
benign vs malignant
slow vs fast | covered in fibrous tissue vs invades other tissues
34
TRANSCRIPTION + TRANSLATION
1) DNA strands separate by DNA helicase nucleotides join to DNA template strand Uracil binds to Adenine RNA polymerase joins to nucs = mRNA 2) mRNA to ribosome mRNA codon binds with tRNA's comp anti-codon amino acid attached to each tRNA formation of peptide bonds between aa's
35
mutagenic agents
increase rate of mutations e.g. UV or ionising radiation, chemicals/viruses -alter bases or act as base or change DNA structure
36
same protein produced if mutation in dna?
genetic code is degenerate and mutations could occur in introns
37
mutation definition
alteration to DNA base sequence - often arises spontaneously during replication
38
frameshift
amino acid sequence produced is different
39
scatter graph
relationship between two independent variables
40
genome
organisms complete set of DNA