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1
Q

describe the steps required in insulin binding

A
  1. insulin binds to tyrosine kinase - activated
  2. phosphorylattion of Insulin receptor on both tyrosine kinases
  3. phosphorylation of both IR substrate proteins
  4. activation of PI3K
  5. activation of PIP3
  6. recruits PDK which phosphorylates AKT and other user/thr kinases
2
Q

DNA damage noticed - what are the steps taken to stop cycle

A
  1. ATM/ATR binds to the Origin of Replication
  2. turns p53 on, turns P21 on ( a CKI)
  3. which stops G1 to S CDKs
3
Q

what controls M-CDKs and why are m-CDKs important

A

activated by cdc25
inhibited by wee1
role - to drive cell into mitosis

4
Q

role of APC and what does it cause

A

activates proteases to separate the sister chromatids

causes ubiquination of S-cyclin, Securin

5
Q

3 way cells increase proclivity of DNA replication and the basic principles of each step

A
  1. add sliding clamp - loader uses ATP hydrolysis to put clamp around DNA,causes primes to be released and triggers delta and epsilon polymerase
  2. ssDNA binding proteins - ensure no hairpins
  3. Topioisomerases - nick and reseal the backbone T1- ss no ATP , T2 ds and need ATP
6
Q

Steps to form the Pre RC and when does it occur

A

in G1

  1. origin replication complax binds to replicator sequence
  2. Cdc1 and Cdc6 bind to ORC
  3. Helicase binds to these (requires ATP hydrolysis)
7
Q

Base excision repair steps (BER) and when need

A

for pyrimidine dimers

  1. DNA glycosylases cleave
  2. AP endonuclease and phosphodiesterase remove backbone
  3. DNA polymerase
  4. Ligase seal gap

Glenda Ended Phils Polygraph lie test

8
Q

Non homologous end joining steps

A

Ku heterodimers recognise
DNA- PK and ATM protein kinases attatch
Repair synthesis and ligation

9
Q

Homologous Recombination to repair dsDNA

A

use sister as template
Digest 5’ end by nuclease
DNA ligation

10
Q

Na+ and Ca2+ channel gene

A

SLC8 family - NCX1-3 in mammals

11
Q

Nav and Cav structure

A

24TM

6SU

N + C and Intracellular

12
Q

Kir family structure

A

2TM

4SU

N and C intracellular

13
Q

CFTR cl- channel structure

A

12TM

N and C Intracellular

14
Q

Kv channel structure

A

6TM

4SU

N and C intracellular

15
Q

cyclic nucleotide gated channel

A

6TM

4SU

N and C are regulatory domains - 3 of 4 sites must be bound to

16
Q

P2X structure

A

2TM

3 SU

N and C intracellular
ATP binds

17
Q

Cys loop structure

A

4TM

5 SU

N and C extracellular

binding of ACh causes the M2 subunit to rotate and open pore

18
Q

Glutamate ionotropic structure

A

3TM

4SU

N extracellular
C intracellular

19
Q

what bind to CPY in golgi

where do they dissociate

A

Clathrin, Gga1+2 and CPY bind to Vps10 channel

dissociate in late endosome

20
Q

COP2 : GTPas, coat and cargo

A

GTPase - Sar 1
Coat - COP2
Cargo - newly synthesised proteins

21
Q

COP1 : GTPas, coat and cargo

A

GTPase - Arf 1
Coat - COP1
Cargo - retrieves and newly synthesised proteins

22
Q

Clathrin - GTPas, coat and cargo

A

GTPase - Arf 1
Coat - Clathrin
Cargo - lysosomal and endocytose material

23
Q

role of NPC proteins and what occurs if defective

A

facilitate lipid transfer from endosome and lysosome to the ER

defective - NP disease C - autosomal recessive effects liver and spleen, cells become full of cholesterol and membranes don’t have the cholesterol that they need

24
Q

3 features of the ER contact sites

A
  1. ribosomes excluded
  2. membranes are close 3-15nm
  3. long lived
25
Q

What is AP2

A

major clathrin adaptor selects material from outside cell to be brought in. adaptors recognise motifs in cargo

26
Q

What is the pathology of Xerderma Pigments

A

light sensitivity
7 different gene mutations possible
NER pathway damaged
cannot repair UV induced dimers

27
Q

Cortisol production pathway steps

A
  1. Hypothalamus signals to pituitary
  2. pituitary produces and releases ACTH
  3. ACTH to adrenal glands
  4. Stimulates production of Cortisol
  5. Cortisol released into blood
28
Q

what are the events that occur in gene conversion

A

DNA polymerase jumps to another template strand

29
Q

what percentage of genome are introns

A

20%

30
Q

what regulates monomeric signalling

A

RGS

31
Q

role of the protein coat

A

facilitates the pinching off of the vesicle

32
Q

what occurs when the unfolded protein response (UPR) is activated

A

increases the synthesis of ER chaperones and decreases protein synthesis

33
Q

what will you never find at membrane contact sites

what will you fine

A

no - hydrophillic lipids

Yes - NPC and ORP5

34
Q

2 roles of the N terminus in GPCRS

A

can direct the ligand to the site - enkephalins

block the site - adrenoreceptors

35
Q

Coated vesicle formation requires these 5 things

A

GTPases, adaptors, coat proteins, ATP and GTP

36
Q

what occurs in the ER

A

Newly made proteins are glycosylated within the ER

The lumen of the ER is rich in chaperones.

Newly-made proteins are folded within the lumen of the ER

37
Q

Small GTPases of the ras superfamily are converted to their GTP form by

A

Guanine nucleotide exchange factors

38
Q

What properties of CPY are central to its use in the screens?

A

It is glycosylated and proteolytically processed in different compartments

39
Q

what do both voltage-gated sodium channels and glutamate receptors have in common?

A

Their selectivity filter is defined by a p-loop

40
Q

what is ribophorin and p58

A

Ribophorin is a resident ER protein.

P58 is a COPII cargo protein

41
Q

Expression of Sar1GDP inhibits …..

A

COPII formation