Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Biochem > Signal receptors > Flashcards

Signal receptors Flashcards

1
Q

Hormones

A

produced by glands and act on external bodies

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

polypeptide growth facotors

A

act locally, in the area in which they are produced

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

Ionotropic receptors

A

‐ ionchannel (gate through which ions can transfer)
‐ receptor, binding spot for ligand.
‐ Synapsis in central nervous system
‐ Acetylcholine receptor; nicotine acetylcholine receptor
- bound by neurotransmitters (acetylochine - nicotonic)
- binding results in changes in ion transport
- extra cellular lignand binding domain, intercellular domain with enzymatic function

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

G protein coupled receptors

A

‐ Bound by hormones and slow transmission
‐ 7 transmembrane helices
‐ Bound to G‐proteins which hydrolyse guanosine triphosphate (GTP)
to GDP

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

Kinase receptors

A

‐ Extracellular ligand binding domain
‐ Intracellular domain with enzymatic function
‐ Transfer phosphate from ATP to target peptide

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

nuclear receptors

A

‐ Present in cytoplasm
‐ After binding of ligand migrate into cell nucleus and bind DNA
‐ Estrogen receptor (often high expressed in breast cancer)
- present in cytoplasm
- migrate after lignand binding to nucleus and and bind DNA

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

estrogen receptor signaling

A

protein molecule found inside cells that are targets for estrogen

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

agonist

A

activates receptor and results in a strong biological effect; the maximum
respons by a natural ligand = full agonist

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

partial agonist

A

activates the receptor but not to its fullest capacity, even not after
maximum binding

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

antagonist

A

binds but does not activate

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

inverse agonist

A

results after binding in opposite effect (for example instead of activation
it gives repression)

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

tyrosine kinase receptors

A

‐ Phosphorylate tyrosine residues in proteins (not serine/threonine)
‐ Transfer phosphate from ATP to target peptide
‐ Extracellular ligand binding domain
‐ Intracellular domain with enzymatic function
‐ critical role in the development and progression of many types of cancer

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

ErbB 1

A

Upon ligand binding the receptor undergoes a conformational change
 The ligand binding domains are brought together and the cystein rich
region 1 is exposed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

ErbB 2

A

no binding ligands, always in open configuration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

ErbB 3

A

does not have tyrosine kinase domain

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

ErbBs

A

have different affinity for ligands

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

EGFR:EGFR

A

normal signal

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

ErbB3:ErbB3

A

no signal

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

ErbB4:ErbB4

A

normal signal

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

ErbB2:EGFR/ErbB3/ErbB4

A

strong signal

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

pertuzmab

A

antibody prevents dimerization by blocking CR1

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

cancer removal

A

‐ Surgical removal of tumors
‐ Chemotherapy: use cytostatic/cytotoxic drugs to remove tumors
‐ Radiotherapy: use radiation to remove tumors

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

targeted drugs

A

small organic molecules or biologicals, specific

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

active immunization

A

vaccination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
passive immunization
rastuzumab  temporal immunization with antibodies that are biologically made, generally used for treatment
26
general activation of t cells
he tumor generates molecules that deactivate T‐cells, so these T‐cells will not target the tumor cells.
27
IGF1
produced in liver, enhances growth during puberty
28
IGF2
produced in liver, embyonal important, Scavenger receptor (opruim receptor), Everything that binds on the extracellular domain will be recruited in the cell and degraded
29
insulin
produced by beta cells of pancreas, important for sugar and fat metabolism, diabetes - sugar/ fat metabolism
29
IGF1R and insulin receptor featurs
+ 3 S‐S bridges and dimeric structure with L1, CR, L2 + 4 chains: 2x alpha chain, 2x beta chain + activation by ligand binding, not by dimerization (as happens for EGF) -cell growth
30
IGF2 features
+ Many extracellular domains to which ligands can bind:  IGF2 binding  Mannose‐6‐phosphate binding + No kinase activity - everything that binds will be recruited in cell and degraded
31
measure of DNA synthesis
labeled thymidine is added and amount of thymidine incorporated in newly synthesized DNA can be measured
32
TGFB receptors
homodimer connected by disulfate bridge, no tyrosine kinase activity but serine/theonine kinases,Serine/Threonine Kinase (STK) domain of type II receptor: constitutive active, Joining two type II receptors does not change activity in terms of signaling, can inhibit growth of poliferation cells but stimulates growth of of fiberblasts
33
active TGFB
‐ Growth stimulation for non‐transformed fibroblasts (muscle and bone cells) ‐ Growth inhibition for most cells, including cancer cells! also shuts down system so not ideal! -TGFB induces genes for extracellular matrix proteins like collagen and fibronectin via receptor signaling
34
TGFB type 2
stk domains which phosphorilate he GS box in type 1
35
TGFB 1
is activated by phosphorylation of Glycine/serine box (GS) afterwards the stk (phosphorylation) domain of type 1 receptors activate, signal sent
36
trastuzumab
temporal immunization with ab that are biologically made
37
ipilimumab
developed for treatment of melanoma and ab that prevents deactivation of T cells
38
phosphatidylcholines PC
class of phospholipids that incorporate choline as a headgroup. They are a major component of biological membranes
39
enzymes that process PC
+ Phospholipase I will split the fatty acid a the first carbon atom of glycerol + Phospholipase II will do the same for the second carbon atom + PLC cuts at the polar head + PLD cut after the phosphate group glycerophospholipid molecules: phosphatidylcholine negative OH and positive N, so neutral
40
PL1
splits the fatty acids a the first carbon atom of glycerol
41
PL 2
splits the fatty acids at the second carbon atom of glycerol
42
PLC
cuts the polar head of PC
43
PLD
cuts after the phosphate group
44
proteins with an SHw domain that can bind
‐ PLC: phospholipase C‐gamma ‐ PI3K: phosphatidyl‐inositol‐3‐kinase ‐ SHC: adaptor protein
45
PI3K
converts PIP2 to PIP3 by phosphorelation of C3
46
PLC gamma
converts PIP2 in DAG and IP3
47
PIP 3
activates PKB/AKT (cytoplasmic STK) which inhibits aptosis
48
DAG
activates PKC (cytoplasmic STK)
49
STK
serine/theonin kinase
50
PTEN
phosphatase, converts PIP3 back to PIP2
51
PKB
protein kinase B
52
PKC
protein kinase C
53
IP3
increases ca+, temporal increase in cell division, muscle contraction
54
RAS
G protein, needs GTP as energy and then converts it to GDP, when activated binds to RAF and activates STK activity, RAF will phosphorylate the kinase MEK, which phosphorylates ERK
55
GEF (SOS) for RAS
GTP exchange factor, removes GDP and adds GTP
56
GAP
GTPase activating protein, regulates activity of GTP ase -> RAS, catalyses the convertion into GDP
57
GRB2
+ adaptor molecule between SHC and SOS + GRB2‐SOS complex in cytoplasm + After SHC activation recruitment to membrane and activation of RAS
58
ERK
in a complex with MEK, ERk goes into the nucleus to activate genes, phosphorylates SRF
59
nuclear recptors
‐ Present in cytoplasm ‐ After binding of ligand migrate into cell nucleus and bind DNA ‐ Estrogen receptor (often high expressed in breast cancer)
60
promoter
+ Contains DNA binding elements for transcription factors (TF) + There is variation in DNA sequences, so not all transcription factors can bind the same DNA element + A specific sequence that is bound by a specific transcription factor upon an extracellular signal is called a response element (e.g. the estrogen response element, ERE)
61
SRF
phosphorylated by ERk, results in transcription of FOS and JUN, recruits RNA polymerase
62
FOS and JUN
genes for cell division g0 to g1 phase, transcription factors which form a complex AP-1
63
TPA
tumor-promoting agents, resembling DAG, can enter the cell easily because its apolar, it activates PKC
64
growth factors
essential for cell growth, multiple gene programs need to be activated, present for up to 8 hours,ErbB, Ins PGF -> all have tyrosine tail phosphorilation
65
PDGF
stimulates all three pathways too much, cell growth very harsh, growth factor
66
EGF + Insuline
EGF and Insulin can stimulate downstream pathways independently, but when together they stimulate parallel pathways and give synergistic effect
67
GPCR
- Bound to G‐proteins which hydrolyze guanosine triphosphate (GTP) to GDP ‐ Activate many different pathways (dependent on which GPCR is stimulated), cross membrane 7x, After ligand binding the complex becomes a GEF: GTP exchange factor, activator of G‐ proteins. The GEF removes GDP from GDP and replace it with GTP
68
Gs alpha/beta-gamma
+ stimulatory + stimulates ATP conversion to cAMP (cyclic AMP; a derivation of adenosine monophosphate; its decay is inhibited by caffeine/red bull) + cAMP activates many processes, such as glycogen to glucose process + adrenergic receptors: adrenaline
69
Gi alpha/beta-gamma
+ inhibitory + inhibits ATP conversion to cAMP + Cannabinoid receptors: cannabis
70
Gq alpha/beta-gamma
+ activates PLC + converts PIP2 to DAG and IP3 + Bradykinine receptors: bradykinine (lowers blood pressure)  GPCRs can activate similar pathways as Tyrosine Kinase receptors
71
SMAD2-SMAD4 complex
binds to promoters of genes with SBE (SMAD binding element) + matrix genes (fibronectin, collagen) + genes for growth(inhibition)
72
SMAD2
phosphorylated by STK box in TGFB receptors, binds to SMAD4 and the complex enters the nucleus
73
cytokines
especially important for the immune system, interleukins, interferon ‐ Cytokines are bound by receptors without tyrosine or serine‐threonine kinase activity ‐ However, the receptors are associated with the tyrosine kinase JAK: Just Another Kinase; Janus Kinase
74
JAK
when cytokines activate it activates and phosphorilates the receptor at tyrosine residues, this recruits STAT proteins form cytoplasm
75
STAT
signal transducer and activator of transcription STAT proteins have SH2 domain which bind phosphorylated tyrosines,phosphorylated STAT proteins will move to nucleus, bind STAT Response Elements and activate gene transcription
76

Biochem (11 decks)

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