Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BIOL 1101 > Lecture 13: Gene Expression > Flashcards

Lecture 13: Gene Expression Flashcards

1
Q

Why does the regulation of genes matter

A
  • helps us get from fertilized eggs, to a clump of non-specialized cells, to complex organisms (via cell cycle)
  • differentiation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Gene Similarity: Humans and Monkeys

A
  • explains why we have great genetic similarity with monkeys but are still very different species

i.e. Human and Gorilla are 98% genetically similar (98% of the genome is similar)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

All somatic cells are

A

are genetically identical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

So how can cells be different

A

cells express various combinations of genes
= makes them different from each other (gene expression)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How is gene expression controlled

A
  • transcriptional regulation

additional controls:
- posttranscriptional
- translational
- post translational

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Gene Expression for Prokaryotes

purpose

A

Prokaryotic gene expression reflects life history:
- rapid, reversible response to environment (hence they have to produce the appropriate proteins fast)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

The operon and what regulates it

A

Operon: A cluster of prokaryotic genes and DNA regulatory sequences

  • RNA polymerase binds at promoter for operon (cluster of genes including genes to be transcribed and regulator sites (i.e. promoter))
  • Many genes may be transcribed into 1 mRNA
  • Cluster of genes is transcription unit (transcribed all together at once)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Operator

A
  • Operator: short segment that is a binding sequence for a regulatory protein
  • regulatory DNA sequences in operon

1) Repressor proteins
2) Activator proteins

genes seperate from the operon will encode the regulatory proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Repressor Protein vs Activator Proteins

A

repressor proteins: prevent operon genes from being expression (don’t transcribe genes)

activator proteins: turn on expression of genes from operon
- activates transcription and allows it to work

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

LAC OPERON

A
  • lactose metabolism in E. coli (requires lacZ,lacY,lacA)
  • lac operon contains all three genes and regulatory sequences (prokaryotes have this)
  • Lac operon OPERATOR sequence is between the promoter and lacZ
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

where is the operon

A

between promoter and first gene of transcriptional unit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

lac Z codes for
What about Y? A?

A

Z- B-galactosidase (breaks lactose down to glucose, galactose and isomer into allolactose=regulates operon)

Y- permease (lets it in cell (transport))

A- transacetylase (lets it in the cell (transport))

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

lac repressor

A
  • codes for proteins, that, when it binds to the operator, it turns off the transcription of genes
  • lac operon: codes for metabolism of lactose

encoded by regulatory gene: lacI
- can immediately bind operator region

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

lac Operon E. coli
- not present

A
  • active lac repressor binds to the operator of the lac operon to BLOCK transcription
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what happens when lactose is absent

A
  • Lac repressor
  • stops lac operon expression (bc prokaryotes shouldn’t be making enzymes for digestion of lactose, costs them energy)
  • encoded by lacI, synthesized in active form (3D structure that can easily bind to operator sequence)
  • binds operator
  • prevents transpcription
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Purpose of binding operator
(lactose is not present)

A
  • ## lac repressor will bind to the operator to turn off RNA polymerase, prevents it from transcribing lac operon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What happens when lactose is present

A
  • ALLOCATOSE: made from lactose
  • Inducer of lac operon by binding to Lac Repressor causing a conformational change so it can’t bind to operator DNA
  • RNA polymerase can bind to promoter and transcribe 3 genes
  • Inducible operon because inducer increases expression

NEGATIVE- Unless its there its turned off

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Operon

A
  • ALLOCATOSE=MADE FROM LACTOSE
  • INDUCER: lac operon binding to Lac repressor
  • INDUCIBLE OPERON: bc inducer inreases expression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Positive regulation for lac operon

A
  • lac operon operators when lactose but not when glucose is on? Why”
  • glucose more efficient energy than source of 2n^2

however, cells express lac operon strongest w/o glucose and w/ lactose

The lac operon is considered negative regulation because its expression is primarily controlled by the lac repressor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Catatbolite Activator Protein

A
  • activator protein
  • binding site is on DNA, and it bends the DNA to make the promoter more accessible to RNA polymerase and transcription increases
  • synthesized in an inactive form that can bind to DNA only after its activated by binding with cyclic AMP

makes it positive

cylic AMP-a nucleotide that plays a role in regulating cellular processes in prokaryotic + eukyarotic cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What happens when lactose is present and glucose is absent/low

A
  • cAMP levels are high
  • cAMP binds to CAP, activating it
  • active CAP binds to the CAP site and recruits RNA polymerase (increasing gene expression) to the promoter, transcription then occurs to turn the operon ON
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

active CAP

A

cAMP-CAP complex binding to the CAP site (activated w/ cAMP)
- incerases transcription of lac operon
- RNA polymerase is more recruited and stabilized w/ increased gene expression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What happens when lactose is present and glucose is present

A
  • shift to using glucose, so turn off lac operon to prevent enzymes for lactose from being produced (very low transcription of lacZ)
  • cAMP levels are low and remains inactive because of high glucose (glucose inhibits)
  • CAP is inactive and cant bind to the CAP site, RNA polymerase is unable to bind to the promoter and no transcription occurs
  • ## not enough to produce enough enzymes to break lactose down creates a OPERON LOW LEVEL

high glucose=decreases allolactose bc lactose is low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Whenever glucose is low…

A

inhibition of lactose will be low
- cAMP will be activated and levels are high enough to activate CAP
- RNA polymerase can bind
Overall, the level of transcription is lower than when lactose is absent but higher than when lactose is present and glucose is absent

CAP is part of preferential TX of lactose over glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

trp Operon genes

A
  • five genes (trpA-E) needed for the synthesis of tryptophan by trp operon (where those 5 genes are coded for)
  • trp repressor encoded by trpR elsewhere in genome
  • Trp repressor synthesized in inactive form (default for trp repressor)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

why is trp inactive by default

A

-default state is expression bc trp repressor in inactive

trp repressor is activated by presence of tryptophan

  • trp operon is repressible operon (operon is turned off when tryptophan is available, because prokaryotes don’t want to waste energy on making it if its readily available)
  • tryptophan is the corepressor- regulatory molecule that combines w/ repressor to activate it and shut off operon

expression of trp operon ctrlled by trp repressor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

lac and trp operons both exhibit what type of gene regulation

A

negative
- opposite pathways

LAC: repressor synthesized in active form, inducer is present and binds to repressor and inactivates it
operon is then transcribed

TRP:repressor is synthesized in inactive form, when corepressor is present it binds to the repressor and activates it, the active repressor blocks transcription of the operon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what happens when tryptophan is absent

A
  • Trp repressor is inactive (default, can’t bind to initiator) in binding to the operator and transcription proceeds
  • RNA polymerase binds and transcribes operon

= OPERON ON

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what happens when tryptophan is present

A
  • the amino acids binds to and activates the Trp repressor
  • The active repressor binds to the operator and blocks transcription

Tryptophan and Trp Repressor (active)
= bind and undergo conformation change
- binding would prevent RNA polymerase from binding to operator

= OPERON OFF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Regulation of Gene Expression in Eukaryotes

A

Gene Expression in eukaryotes has more regulatory points
- more complex
- no operon
- genes are scattered (multiple linear chromosomes)
- chromatin has histones (determines level of condensation on chromosomes)
- different types of cells
- nuclear envelope
(separates chromosomes with genes from rest of cell)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

review: site of transcription and translation

A

transcription: in nucleus
translation: cytoplasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Increased condensation

A

No transcription

31
Q

4 Levels of regulation of gene expression in eukaryotes

A

1) during transcription:
MOST IMPORTANT
Transcription regulation (during transcription)
- chromatin remodelling to make genes accessible for transcription
- regulation of transcription initiation
= determines which genes are translated

2) Post-transcriptional regulation (after transcription, during translation)
- variations in pre-mRNA processing
- removal of masking proteins
- variations in rate of mRNA breakdown
- RNA interference
= determines type and availability of mRNA to ribosomes

3) Translational Regulation (during translation)
- variations in rate of initiation of protein synthesis
= determines rate at which proteins are made

4) Postttranslational regulation (after translation)
- variations in rate of protein processing
- removal of masking segments
- variations in rate of protein breakdown
= determines availability of finished proteins

32
Q

Transcriptional regulation

A

1) initiation of transcription
2) methylation of DNA
3) chromatin structure

33
Q

Transcription initiation

A
  • PROMOTER
    includes the TATA BOX that binds transcription factors (once they bind, RNA polymerase can bind to transcription factors to begin)
  • PROMOTER PROXIMAL REGION
    =upstream of promoter
    DNA-nucleotide sequences that regulate gene expression
  • contains promoter proximal elements, (activator = proteins can bind to enhance transcription)
  • increases transcription rates
  • ENHANCER further upstream
    to determine maximum transcription rate
34
Q

Transcription initiation regulation

A

general transcription factors initiate transcription
- bind to TATA box area
- recruit RNA polymerase 2
- transcriptional initiation complex
= low rate (basal level)

ACTIVATORS- bind to promoter proximal elements and increase transcription rate

35
Q

Transcription complex on the promoter

A

1) TATA Box- first general transcription factor
recognizes and binds to TATA box of a protein coding gene’s promoter

2) Additional general transcription factors and then RNA polymerase add to the complex
- general transcription factor unwinds promoter DNA and then transcription begins (once all bound together)
= TRANSCRIPTION COMPLEX

= LOW LEVEL OF TRANSCRIPTION

36
Q

DNA-binding and activation of activators

A
  • activators are protein with 2 distinct domains
  • 3D arrangement of proteins produces highly specialized regions called MOTIFS
  • DNA binding activators have 3 MOTIFS
    1) helix-turn-helix
    2) zinc finger
    3) leucine zipper

2 domains: DNA BINDING DOMAIN, ACTIVATON DOMAIN

37
Q

3 Motifs

A

1) Helix turn helix
- part of a protein bound to DNA, one of the alpha-helixes bind to base pairs in groove of DNA, looped region of protein connects to a second alpha-helix that holds the first one in place

2) Zinc Finger
- parts of proteins, bind to specific base pairs in grooves of DNA

3) Leucine zipper
- proteins are monomers consisting alpha-helical segments
hydrophobic interactions between leucine resides within the leucine zipper motif hold onto monomers together
- other a-helices bind to DNA base pairs in major groove

38
Q

transcription initiation regulation

A
  • coactivators: bridge enhancers and promoters, come together to bind to activators in both regions
    = increase transcription to maximal rate using activators and repressor proteins
  • repressors oppose effect of activators
    = decrease transcription

a) bind to specific site in DNA near activator and interact w/ it so it cant bind
b) bind to same regulatory sequence as activators

Transcription rate depends on balance between activation and repression signals (to determine amount of gene expression and transcription, we then create differences in cells w/ regards to regulation)

39
Q

interactions btwn activators at the enhancer, coactivator, and proteins at the promoter and promoter proximal region

A
  • form a transcriptional complex that facilitates RNA polymerase II recruitment and stabilization, leading to maximized transcription rates.

-gene is looped to make a bridge which increases rates of transcription

40
Q

Combinatorial gene regulation

A
  • high gene regulation with low numbers of activators
    = used in different combos so we can have diff levels of regulation w/o needing many
  • therefore, a unique combo of activators ctrl gene A and B
41
Q

What does combinatorial regulation allow
- and role of hormones

A
  • allows for genes with related functions to response to one signal

HORMONES
- signal molecules activate all cells with specific hormone receptors
- all gene regulated by a specific hormone contain a steroid hormone response element
=EFFICIENCY

42
Q

Steroid hormone regulation

A
  • found in all genes regulated by the same steroid
  • increases transcription and therefore translation
43
Q

Methylation of DNA

A

a) add methyl groups to cytosine
- gene silencing occurs when DNA methylation is located in promoters, meaning RNA polymerase can’t attach=silence

b) Genomic imprinting
- permanent silencing of a maternal/paternal allele
- inherited methylated allele is silenced
- methylation maintained as DNA is replicated

44
Q

Chromatin Structure

A

Eukaryotic DNA + histones = nucleosomes
- promoters inaccessible

Chromatin Remodelling (relax vs highly coiled)
1) activators recruit remodelling complexes that displace nucleosomes

2) Activators recruit histone acetyltransferase enzyme (transfers acetyl group to histones) that acetylates and loosens histones association with DNA

= Makes gene promoters more accessible (once they’re loose)

45
Q

What does chromatin remodelling do to histones?

A
  • displaces histones
  • exposes genes promoter
  • promoter not accessible to proteins for transcription initiation (RNA polymerase can’t get to promoter)

SO…

  • use activator and remodelling complex which requires ATP and produces ADP + Pi

AND…

  • loosening the bond, allows w/ RNA polymerase to bind + transcribe = we can now express those genes
46
Q

Effect of adding acetyl group for chromatin remodelling

A
  • loosens up the charge
  • attractive forces between DNA and histones decrease, loosening up the DNA

= acetylation by histone acetyltransferase
- DNA (-q) allows us to form nucleosome complex (+q)

= deacetylation by histone decetylase
- removes acetyl groups from histones

47
Q

Posttranscriptional Regulation
- after transcription
- before translation.

A
  • posttranscriptional regulation controls availability of mRNA to ribosomes

= pre-mRNA processing changes which proteins are made
- alternative splicing of introns and exons
- regulatory proteins: ctrl abundance of mRNA

48
Q

alternative mRNA splicing

A
  • controlled by regulatory proteins specific to each of these cells
    = ctrl whether we go smooth or striated muscle for example (diff groups of regulatory proteins for either muscle)
49
Q

Posttranscriptional Regulation
- masking proteins

A

Masking proteins binds to mRNA to prevent translation
- signal for mRNA activation removes masking proteins during development
= you don’t usually translate mRNA right away, we use masking proteins until we are ready for translation, this is common for eggs when they will translate once fertilization takes place to allow for organism to form

  • mRNA breakdown rates (degradation) are variable depends on 5’ UTR nucleotide sequences (determine speed of breakdown)
50
Q

CASEIN mRNA

A

(posstranscriptional regulation)
- breakdown is slower during lactation and faster w/o lactation

51
Q

miRNA and posttranscriptional regulation

A

mIRNA- cell made it itself, and it interferes with gene expression by blocking translation coded by a non-coding gene
- regulates gene expression through RNA interference (RNAi)
- miRNA binds to any complementary mRNA sequence and silences it

  • Small interfering RNA (siRNA)- form RNA encoded outside the cells genome
  • often used by viruses
52
Q

RNA interference

A
  • enzymes will clip off loop of 3’ miRNA and bind to it
  • imperfect pairing=block translation

miRNA-induced silencing complex: enzyme in protein complex degrades 1 strand of RNA and leaves the miRNA
-miRNA in miRISC binds to target mRNAs that have a complementary or nearly complementary base sequence in 3’UTRs leading to imperfect/perfect pairing

perfect: every nucleotide matches=blocks translation to destroy DNA
imperfect: some nucleotides don’t match (bulge)
- miRNA will block translation but won’t destroy mRNA

53
Q

Translational regulation

A
  • controls rate at which mRNAs are used in protein synthesis (w/ translation regulatory proteins)
  • increasing length of poly(A) tail increases translation of mRNA
54
Q

Posttranslational regulation

A
  • controls functional proteins
  • chemical modification alters activity of protein
  • processes inactive precursors to active proteins
  • rate of degredation=UBIQUITIN
55
Q

Protein Degradation

A

1) addition of ubiquimtin to a protein (requires ATP)
- signalling molecules bind to ubiquimtin are proteins that will tell proteasome that it needs to be degraded
= creates lack of expression of a gene

2) proteasome recognizes ubiquimtin tagged protein and unfolds it, enzymes that are part of core digest protein to small peptides (requires ATP)

3) Released peptides are degraded to amino acids by cytosolic enzymes

= PROTEASOME AND UBIQUINTIN ARE RECYCLED

56
Q

Epigenetic Regulation

A

Epigenetic gene regulation
- persists through cell or organismal generation
- doesn’t result from chances in DNA nucleotide sequence
(+inherits that expression later)

Two Epigenetic Mechanism
1. Feedback Loops
- self-sustaining regulatory loop (eg phage lambda, comes back to further regulate it)
2. Chromatic packaging
- regulation of packaging of DNA and its associated proteins (e.g. List noncoding RNA)
= gene makes protein and RNA to turn it off

57
Q

Cancer

A

Loss of regulatory controls
Tumour: a mass of cells due to dedifferentation
- opposite of differentiation, therefore take specialized cells and make them unspecialized

  1. benign tumours single mass
  2. malignant tumors cancer invade other tissue by metastasis=spread to other parts of the body
    - tumor repressor gene function lost (code for proteins cells turning into cancer)
58
Q

Oncology

A

branch of medicine for the study, treatment, and prevention of cancer

59
Q

Classification of Cancers

A

a) CARCINOMA- tumor in cells of epithelial origin (breast, prostate, lung, colon)

b) SARCOMA- tumour in cells of connective tissue (bone, cartilage, fat)

c) LEUKEMIA- tumour in cells of blood systems and cells (bone marrow)

d) LYMPHOMA- cells of the immune system (white blood cells)

60
Q

Cancer progression

A
  • tumour grade (1-3)
    resemblance of tumour to normal tissue
  • looking to see cellular organization of tumours= cells in tumour are unorganized *
  • tumour stage (1-4)
    degree of tumour invasion (how far the tumour has gone)
    ex. stage 4: full metastasis to secondary site, left its primary site
  • prognosis
    probability of survival 5 years after diagnosis (5 is standard, 10 is also common)
61
Q

Commonly Diagnosed Cancers

A

Male:
Prostate
Lung
Colon
Bladder

Female:
Breast
Lung
Colon
Uterus

62
Q

Most deadliest Cancers

A

Male:
Lung
Colon
Prostate
Pancreas (organ that’s hidden so symptoms are found later on (at this point the cancer is in stages 3-4))

Female:
Lung
Breast
Colon
Pancreas

63
Q

Cancer and Gene Controls

IDENTIFY CLASSES OF CANCER

A
  • 3 main classes of genes are implicated in cancer
    1. Proto-oncogenes
    = genes that can become oncogenic (cancer-causing genes)
    2. Tumour Suppressor Genes
    = genes that prevent cancer from happening
    3. miRNA genes
    = find and bind to mRNA
64
Q

Proto-Oncogenes

A
  • originally normal genes
  • encode proteins that stimulate cell division
    NORMALLY
  • tell the cell to grow and divide, loss of ctrl = over expression, porto-oncogene can go out of ctrl and since it’ll keep telling the cell to grow to divide w/o ctrl

ONCOGENE
- altered proto-oncogene that cause a cell to be cancerous

= deregulation of the cell cycle

65
Q

Mechanisms of Oncogene Formation

A

Several ways:

  • mutations in promoter or other control sequences (may lead to cancer, not definite)
  • Mutations in coding segment may produce abnormally active protein
  • altering a.a. sequence and can result in a protein that’s ALWAYS ON, continuous growth and division
  • Segment of chromosome translocation gated to area near promoter or enhancer (chromosomes that shouldn’t be recombining but they are: proto-oncogene is carried on
  • viral infection of gene that regulates cell cycle
    leads to alteration in protooncogene
    = loose ctrl of cell division and growth
66
Q

Tumor Suppressor Genes

A
  • encode proteins that inhibit cell division (prevent cancer)
  • In cancer, tumour suppressor genes can be mutated, alteration in nucleotide sequence = a.a. sequence

EX. p53- guardian of the genome
= over 50% of cancers=mutations in p53
- mutation causes gene to not be transcribed/translated properly
Regulates cell cycle by:
- holding cells at G1-S checkpoint by inhibiting CDKs
- initiate apoptosis

PREVENTS GENE MUTATIONS
-activation of DNA repair proteins (enzymes will be triggered to fix DNA)

67
Q

BRCA1 AND BRAC2

A
  • both are tumour suppressor genes
  • involved in DNA damage and repair (they trigger enzymes to do this)
  • mutated genes are risk factors for breast cancer
  • 60% of breast cancers have BRAC1/2 mutation
  • up to 85% if both are involved

NOT ONLY WOMEN!

a) SPORADIC
- 2 independent mutations of BRAC1 tumour suppressor
=60%

b) FAMILIAL
- individual has predisposition of breast cancer because of inherited mutated BRAC1 allele
= 60%

68
Q

cancer + mi-RNA genes

A
  • Encode for miRNAs
  • In cancer:
    1) OVEREXPRESSION of miRNA genes that encodes miRNA that prevent translation of tumour suppressor mRNA
    2) Inactivation of mi-RNA genes that encode mi-RNA that prevent translation of porto-oncogenes

What we want vs Cancer

We want:
- oncogene mRNA to not be translated because it can cause cancer
- tumour suppressor mRNA to be translated to prevent cancer

= in cancer, it wants and does the opposite, silences tumour sup. and not oncogene

69
Q

Cancer Develops Gradually

A
  • multiple genes must be modified to develop cancer
  • Explains why carcinogens may cause cancer years later
  • age is the greatest risk factor (2 rzns)
  • Removal of carcinogen may halt multistep progression oncogene

a) As you age, you undergo cell cycle so many times, cells can make mistakes that go unnoticed and passed on, which can accumualte=CANCER

b) environment risk factors
- greater potential of exposure to potential carcinogens

70
Q

Developmental of colorectal cancer

A

NORMAL COLON CELLS
Loss of APC tumour-suppressor gene and other DNA changes
= reduced number of cancer preventing proteins

  • SMALL ADENOMA (benign growth)
    = benign: non-cancerous tumour

ras oncogene activation; loss of DCC tumour suppressor gene
PROTO-ONCOGENE=ONCOGENE

  • LARGE ADENOMA (benign growth)
    loss of TP53 tumour-suppressor, (can cause adenoma to become cancerous) gene and other mutations
  • CARCINOMA (malignant tumour with metastasis)
71
Q

process for most cancers

A
  • detect early
  • early treatment for prevention
72
Q

Normal cells are … what by cancer cells

A

recruited by cancer cells using signals that benefit the cancer cells
- signal transduction

73
Q

Tumour Angiogenesis

A

Tumour cells signal the formation of new blood vessels
- you want this
1) as you grow
2) when you’re have to help repair

CANCER CELLS:
3) use it to provide blood supply to get it to be a fast growing tumour
tumours will need ATP, need a lot of glucose and O2 (final e- acceptor)
= they send signals to endothelial cells to grow and form towards tumours allowing for increased growth

The cells providing the signal=NORMAL
The cells sending the signal=CANCEROUS

74
Q

Metastasis

A

Intravasation- cancer cells ENTER blood vessels
Transported to other parts of the body
Extravasation- cancer cells EXIT the blood vessels
Metastasis=secondary site

75
Q

Tx of Cancer

A

a) Surgery-removal of tumour and lymph nodes
- part of lymphatic system that cancer cells may be collected in

b) Chemotherapy- chemical that are selective and non-selective to cancer cells
- systemic: drugs go around whole body
- killing all cells that grow fast
- side effects of chemotherapy (hair loss, WBC loss=immunocompromised)

c) Radiotherapy- radiation Tx of cancer
- will kill all cells that grow quick but in only one part of the body
- kills normal and cancer cells

d) Targeted Therapy- specific to cancer cells
- Tx will only affect cancer cells
- less damage to normal cells

Need to know patients genetics beforehand to determine form of Tx that’s best

76
Q

Breast Cancer Genes

A

Her2/neu
- tyrosine receptor kinase (membrane-bound)
- epidermal growth factor receptor (adds PO4)
- involved in signal transduction pathways leading to increased cell growth (signal molecule, epidermal growth factors, tells cell to grow and divides, PROTO-ONCOGENE)
- encoded by proto-oncogenes
- 15-20% of breast cancer HER2 is over expressed

HERCEPTIN- drug targeted therapy against HER2, specifically binds HER2 receptor and stops cell division
- blocks signals from binding to receptor=no cell growth and division

GROWTH FACTORS BIND TO HER2 RECEPTOR

  • triggers immune system to destroy cell so its not passed on, role 1 of Herceptin
  • Herceptin binds to HER2 and blocks signalling=role 2 of hereceptin
77
Q

ranking the transcription levels for lac operon

A

1) Lactose present, glucose absent – Highest transcription because CAP binds with cAMP, enhancing RNA polymerase binding and initiating transcription.

2) Lactose present, glucose present – Medium transcription, CAP is not activated due to low cAMP, but lactose prevents the repressor from binding.

3) Lactose absent, glucose absent – Low transcription, as the repressor binds the operator and blocks transcription.

4) Lactose absent, glucose present – Lowest transcription because the repressor is bound and CAP is inactive due to high glucose (low cAMP).

BIOL 1101 (18 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions