Brainscape's Knowledge GenomeTM

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


See full index

Health Disease Therpeutics 1.1 > Cell processes > Flashcards

Cell processes Flashcards

1
Q

Steroid hormone pathway for cell communication (e.g testosterone)

A

Testosterone + carrier protein (prevents it disintegration as hydrophobic and lipophilic)
- reaches target - detatches from carrier protein- crosses PM an NM- SH (testo)+ Receptor on promoter (TESTOSTERONE TESTOSTERONE RECEPTOR COMPLEX) - recruits TF and TA for translation and transcription

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

AIS treatment and cause

A
  • defective testosterone receptor
    -X linked recessive disorder
  • Female cannot
    -Treatment:
    Complete- vagionoplasty, estrogen
    Mild: Androgen, hypospadius repair
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Flutamide what does it do

A

potent inhibitor of testosterone

  • non streoidal anti androgen
  • no 4 ring structure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are anti estrogens used for

A
  • breast cancer

- BC often caused by excessive estrogen

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

intracellular transduction pathway (inside the cell)

A
  • extracellular signal + receptor - intracellular signalling proteins - splits to metabolic enzyme (altered metabolism) or gene regulatory (altered gene expression)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Extracellular responses diagram (on the surface of cells)

A

Extracelluar signal+ cell surface receptor- slow (Transcription)- altered protein synthesis OR fast (intracellular signalling) lead to altered protein function
- BOTH lead to altered cell behaviour

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

cAMP endocrine pathway

A

signal molecule+ G protein coupled receptor– a of HT G protein complex activated– activates adenylyl cyclase– Convertes ATP to cAMP- activates PKA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Phosphorylation of of protein kinase

A
  • transfer of phosphate of ATP to SER, THR, TYR (of target protein)
  • this activates target protein or inactivate sometimes = REVERSIBLE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What response phosphorylation give

A

PKA– [phosphorylates TARGET PROTEINS] –which are metabolic. enzyme (altered metabolism) or gene regulatory protein (Altered gene expression)

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

How does glycogen turn to glucose with the trigger of PKA

A

adrenaline(SM) — PKA– phosphorylase kinase active– acts as signal for Glugogen phosphorylase to activate– glycogen cleaved onto muscle cell receptors and onto glucose making it active for muscle action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How is adrenaline also involved in the fight or flight response

A
  • adrenaline (produced my adrenal medulla) + GPCR on muscle cell (b adrendenic receptor) - glucose then made as a store of energy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What do beta blockers do

(altering pathway to stop metabolic action) FAST RESPONSE

A
  • blocks interaction of adrenaline with receptor- treats hypertension (high BP), stops heart muscle contraction by stopping glucogenlysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How can we alter the triggering pathway to alter gene expression (SLOW RESPONSE)

A
  • CREB activated by PKA (transcription factor)– binds to CRE of promotor of somatostain gene– recruits CBP (creb binding protein) [transcriptional co activator] – transcription and translation– new protein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How are signals from outside the cell converted to inside

A
  • Extracellular signal delivered through blood stream/ adjacent cell
  • receptor picks this up and converts it to intracellular signals
  • determines the cell needs to be replicated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do the amount and type of signal determine cell behaviour

A
  • cell respond to multiple of signals
  • many signals together of different combinations result in different survival behaviour
  • all have independent factors and protein receptors in how they will convert extracellular signals to intracellular events that will ultimately control cell behaviour
  • absesnce of signals mean cell enters apoptosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do transmembrane receptors relay signals to intracellular signals and alter cell behaviour

A

EC signal membrane bound receptors—- intracellular signals—- metabolic enzyme (altered metabolism), (cytoskeletal protein) altered cell shape, (transcription regulator) altered gene response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How can we turn enzyme activity on or off

A 
ADDING PHOSPHATE (kinase)
REMOVING PHOSPHATE (phosphatase)
- adding phosphate by ATP= confirmational change in enzyme = active
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does an epidermal growth factor lead to cell proliferation

A
  • epidermal growth factor+ receptor tyrosine kinase (two halves)– two halves come together (dimer)– phosphate by ATP adds to protein such as RAS – GTP will also add to RAS to activate it too
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the stages of the cell cycle G0,G1, S, G2 (interphase

A

G0- cyclin-dependent kinases disappear- cell remain in the G0 phase until there is a reason for them to divide

G1- cell grows- most proteins made for DNA replication and mitosis (monitor intra+extra environ to check if conditions correct)

S-DNA replicates chromosomes perfectly (ensures double genetic material)

g2- more checks that genome fully replicated and more growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the main regulators of the cell cycle and how are they activated

A
  • Cyclin- cyclin dependent kinase
  • activated with cyclin attached to it (heterodimer)
  • to deactivate cyclin breaks down
  • main regulators
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How does S phase get triggered to start replication

A 
- G1 forms a pre replicative complex preparing s phase
containing Cdc6 (which inhibits it proceeding to s phase)
  • Scdk phosphorylate cdc6– degration of Pcdc6— enables replication to proceed– assembly of replication fork– DNA replication
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What factors does p53 check for in damaged DNA in G1

A
  • sees if there is UV ionizing radiation. lack of nucleotides, oncogene signalling (genes that can cause cancer), lack of oxygen)hypoxia)
  • p53 fixes it - cell cycle arrest (stopping) or cell death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How does Rb check for extracellular unfavourable environments in the cell cycle

A
  • active Rb and inactivates transcription factor = NO TF binding- NO CELL GROWTH
  • when Growth factor released– upregulate cyclin– cyclin cdk phosphorylate Rb- cant bind to TF= cell proliferation
24
Q

When can you see chromosomes and when can you not

A
  • cannot see chromosomes in interphase as DNA is decondensed (being sileced by heterochromatin)
  • in mitosis – chromosome condense- chromosomes seen
25
Q

What are the stages of mitosis

A

prophase- chromosome condense, centrosomes apart
Prometaphase - nuclear membrane breaks down, microtubules attach to keinetochores

meta- chromosomes allign centre, keintochores attach to opposite poles

Ana- sister chromatids separate, keinochore shorten, spindle poles move apart

TELA- chromosomes arrive opposite poles, nuclear envolope reassemples, two new nuclei

CYTOKINESIS- contractile ring formes- divides the two cells

26
Q

Steps during apoptosis

A
  • mitro release cytochrome C + free radicals break down protein site in cell membrane
  • nuc mem break down
  • chromatin consence
  • phagocytosis of apoptotic bodies
27
Q

What chemical reactions lead to damaged DNA

A
  • depurination
  • free radicals
  • deamination
28
Q

What does UV radiation cause

A
  • thymidine dimer: two adjacent thymine bonded - prevent correct hydrogen bond- distorts DNA
29
Q

how does dna repair DNA mutations

A
  • phosphodiester backbone recognised by DNA mismatch repair protein
  • removes the region thats wrong
  • fills gap with dna polymerase and ligase
30
Q

What are the different types of DNA mutations

A
  • deletion / insertion of one or more nucleotides
  • substution of nucleotides
  • point mutations
  • –alteration of single base pair position
  • consequences depend on position of mutation
31
Q

What causes Sickle cell anaemia

A
  • point mutation of B goblin gene (change in one nucelotide)
  • haemaglobin cannot form normal shape + polymerises
  • goes through capilaries- capillaroes block
  • no oxygen delivery (muscle weekness)
32
Q

When does translocation of chromosomes occur

A
  • chromosomal abnormality - chromosome breaks and reattaches to another- fewer alleles for genes- misconjunction - impacts heterocho (inactive) and euchro (active)
33
Q

What does CML (chronic myelogenous leukaemia) show

A
  • inappropiate number of blast cells in myeloid pathway (too many white cells in blood)
  • unregulated myeloid in bone barrow and accumulation in blood
  • translocation of chromosome 9 and 22
34
Q

How is cancer caused

A
  • multiple mutations at multiple genes (multi step process)

- mutations in proteins involved in cell cycle checkpoints

35
Q

How does an adenoma go from benign to malignant

A
  • adenoma (adrenal gland in bowel)– accumulation of more mutations expands – malignant so invade epithelial cell and move around the body
36
Q

What does Darwinian model of cancer progression sugges

A
  • more mutations you accumulate the faster cells grow– more they invade – faster lead to tumor– malignance
37
Q

What is the process of clonal mutation

A

1 mutation= hyperplasia
2nd mutation=more aggressive rapid growth
3rd mutation=increase growth and metastasis spread (invade tissues – dangerous tumors– invade other tissues– proliferate in other tissues)

38
Q

What is an onco gene and how does it work

A

oncogene upregulates cell growth leading to proliferation
proto-oncogene promote entry into cell cycle– becomes oncogene
- RTK= PO – mutate (O)– recognises growth factors– upregulate cell growth as it will always be proliferation
- RAS= PO– mutate - always active- upregulation

39
Q

What 2 things do we need for cancer

A
  • oncogenes to upregulate genes

- proteins such as RB and p53 to mutate to not check cell cycle

40
Q

what are the 3 stem cell stages of what it can become

A

pluripotent- gives rise to many different cell types in body

Multipotent- in progenitor state number of choices becomes fewer of which cell type

Unipotent - gives rise to only one cell type

41
Q

What is haemopoiesis

A
  • BLOOD DIFFERENTIATION
  • pathway depends on conditions of body and signals
  • can either go to myeloid progenitor (many diff cell types)
  • Lymphoid progenitor(either B cell or T cell)
42
Q

What makes cells different to one another

A
  • proteins defining cell type features
  • metabolic proteins
    -structural proteins
    REGULATORY PROTEIN such as histone shared by every cell
43
Q

How do genes control cell differentiation

A
  • gene expression defines the cell that is
  • stem cells = different pattern of gene expression
  • stem cell genes will be switched off
  • genes needed for the differentiated cell will be switched on during progenitor stage
44
Q

How is gene regulation controlled

A

by transcription factor and enhancers = transcriptional regulatory sequences - lets RNA polymerase to activate gene or silence gene for cell differentiation- each cell have specific pattern of gene expression

45
Q

What is an example of specific transcriptional factors in control of red blood cell or platelet differentiation

A

RBC- TF 4,2,1 expressed in early progenitor stage – turn on red blood cell specific genes
PLA– TF 8– pl specific gene

TF3 common in both cells

46
Q

How are gene signals determined from environment

A
  • environment factors talk to stem cells/ early progenitor to up regulate cells we need
47
Q

What is EPO signalling and how does it work

A

Low O2 in body– EPO binds to EPO receptor on CM on progenitor cell— up regulation of TF for RBC– TF binds to promotor– red blood cells made

48
Q

What happens to patients with B cell acute lymphoblastic leukaemia

A
  • stem cells–precursor (on way to becoming B cells)
    • something goes wrong with differentiated pathway – blasts (b cell presucors) made instead of B cells – blast tumour in the blood
49
Q

How can we use cell based therapies to treat diseases

A

1st way: convert differentiated cell into another differentiated cell by inserting cell specific proteins (transcription factors) for that cell

2nd way: differentiated cell– step cell by stem cell transcriptional factors–turn it into patient specific cell

50
Q

Why is in vitro transcription inefficient

A
  • general transcription factors (basal machinary) (TFIID) – TATA binding protein and TBF assosiated factors and RNA polymerase – minimal factors for pre initiation complex– makes small amount of MRNA– inefficient
51
Q

What is a gene promoter

A
  • promote transcription - when TF bind to promoter, RNA polymerase activated
  • promoter= binding site for basal transcription, RNA polymerase and co factors (minimal required for transcription)
52
Q

What distorts the promoter DNA

A

TATA binding proteins (TBP) bend the DNA promoter

53
Q

Why is Activated transcription more efficient

A
  • more protein sequences and more transcription factors– higher level of transcription activity – more mRNA made
54
Q

What do we use in addition to TFIID in cell specific transcription

A
  • multiple enhancers (act like switches and make TC specific)
  • multiple transcription activators (up regulate gene activity and tell RNA P and BM to make mRNA)
55
Q

How do gene regulatory proteins communicate with RNA polymerase

A
  • by touching and bending the flexible DNA to bind and twist to the promoter to communicate whether gene is active or not

Health Disease Therpeutics 1.1 (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions