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Cell Signalling > GPCR > Flashcards

GPCR Flashcards

revision

1
Q

GPCR Receptor properties?

A

N-terminal: Extracellular
C-Terminal: Cytosolic
Integral membrane protein
Heptahelical-sepentine

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2
Q

G-Protein

A

300 amino acids

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3
Q

Membrane bound enzyme

A

Adenylyl cyclase

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4
Q

G protein

A

anchoring to memb.: Through palmitoyl group
Hetrotrimeric : α, β, γ

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5
Q

Gα

A

Largest
45 KDa
Linked Through palmitoyl group
Have GTPase action
Expose Guanine ntd. Binding site

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6
Q

Gα + GDP

A

Inactive
High affinity for β, γ

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7
Q

Gα + GTP

A

Becomes active
Affinity for β, γ decreases

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8
Q

Gβ

A

Intermediate
37 KDa

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9
Q

Gγ

A

smallest
9 Kda
lipd anchoring

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10
Q

signal transduction molecule in GPCR?

A

Adenylyl cyclase

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11
Q

secondary messengers.

A

cAMP

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12
Q

PKA

A

2 regulatory Subunit (2R) R2
2 Catalytic Subunit (2C) C2
1 AKAP

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13
Q

1 Regulatory unite has ____ Binding site for cAMP.

A

1

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14
Q

what happen once 1 cAMP binds with 1 regulatory subunit?

A

Another Binding site for cAMP get exposed on same Regulatory subunit.

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15
Q

How many cAMP is required to bind with 1 Regulatory subunit?

A

2

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16
Q

Catalytic subunit has?

A

Kinase activity

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17
Q

Catalytic subunit phosphorylate the?

A

CREB

cAMP Response element Binding

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18
Q

CREB Binds to?

A

CREB Binding Protein (CBP)

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19
Q

CREB Binding Protein (CBP) act as a?

A

Transcription Factor

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20
Q

In case of adenylyl cyclase, we get?

A

PKC

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21
Q

In case of Guanylyl cyclase, we get?

A

PKG

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22
Q

In case of PLC, we get?

A

we get PIP2: IP3 and DAG

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23
Q

Gq?

A

Gα that activates PLC

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24
Q

PLC has ____ isoforms.

A

6

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25
Q

Name 6 isoforms of PLC.

A

Beta
gamma
Delta
Epsilon
Omega
Tou

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26
Q

All isoforms has same function, i.e?

A

Hydrolysis of PIP2

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27
Q

DAG is

A

Memb. bound because glycerol is hydrophobic.

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28
Q

Inositol is

A

Sugar and hydrophilic in nature, that’s why found in cytosol.

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29
Q

IP3 Receptors present on?

A

SER membrane

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29
Q

All secondary messenger in GPCR?

A

cAMP
cGMP
IP3
DAG
Ca^2+

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30
Q

IP3 receptor is

A

Ligand Gated Ion channel

passive
along the gradient
Downhill
Ion transport
Gated- barrier
Increases the calcium concentration in cell

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31
Q

DAG provide function through?

A

PKC

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32
Q

PKC has ____ domain?

A

2

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33
Q

2 Domains of PKC binds with?

A

1 domain binds with DAG

2nd domain binds with Ca ion

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34
Q

Ca ion as secondar messenger?

A

Comes outside of the cell
G-protien directly opens the ca ion channel

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35
Q

Ligands of GPCR

A

calcitonin
PTH
Glucagon
Smatostanin
TRH - TSH
ADH
CRH-ACTH
GnRH- LH, FSH
GHRH-GIH
Oxytocin
Epinephrin
Nor-epinephrine

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36
Q

Neurotransmitter for GPCR

A

Dopamine
Serotonin
Glycine
Acetylcholine
GABA

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37
Q

Immunomodulatory for GPCR- all binds to GPCR

A

Histamine
Bradykinin

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38
Q

Sense- all binds to GPCR

A

Gustatory
Olfactory
Vision

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39
Q

Other Hormone

A

hCG
Angiotensin II

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40
Q

Ligands for cAMP

A

Calcitonin
PTH
Glucagon
Epinephrine
Nor-Epinephrine
LH, FSH, TSH
ACTH
CRH
hCG
Histamine

41
Q

Ligands for IP3

A

GnRH
Oxytocin
Angiotensin II

42
Q

Ligands for cGMP

A

Nitric Oxide
Carbon monooxide
ANP (Atrial Natreuretic Peptide)

43
Q

G-protein helps in?

A

cell proliferation
Vesicle movement
Trafficking
RAB
Export and import from the nucleus
RAN
Translation (EF2)

44
Q

RAB Proteins

A

RAB proteins are a family of small GTPases that play key roles in the regulation of vesicle transport within cells. They help in determining the specific destination of vesicles and are crucial for processes like membrane trafficking, organelle movement, and exocytosis.

45
Q

RAN Proteins

A

RAN is another small GTPase involved in the transport of proteins and RNA across the nuclear envelope. It regulates the import of proteins into the nucleus and the export of RNA and ribosomal subunits out of the nucleus, playing a critical role in maintaining cellular function and gene expression.

46
Q

RAB and RAN proteins?

A

Both RAB and RAN are vital for cellular communication and function, facilitating the movement of materials within and between cellular compartments.

47
Q

2 photoreceptor?

A

Rods
Cones

48
Q

Cones Types?

A

Blue
Green
Red

49
Q

Rhodopsin?

A

IMP
Present in Rod cells
light absorbing pigment

50
Q

secondary messenger for Rhodopsin?

A

cGMP

50
Q

Glucagon on GPCR. Happens in?

A

in Livers cells

51
Q

cAMP acts on (Phosphorylates)?

A
  1. Phosphorylase Kinase
  2. F6P2 kinase
  3. Glycogen synthase
  4. PDE
52
Q

Role of Phosphorylase Kinase?

A

Glycogenolysis: Breakdown of Glycogen into Glucose

53
Q

Role of F6P2 kinase?

A

Gluconeogenesis: Synthesis of Glucose from Non carbohydrate source

54
Q

Role of Glycogen synthase?

A

Inactivate the synthesis of Glycogen

54
Q

Glucagon binds to GPCR when

A

Glucose level is low in Blood.

55
Q

Termination of Pathway by Ligand?

A

Concentration of Ligand

Presence or Absence of Ligand

56
Q

Termination of Pathway by GTPase?

A

GTPase hydrolyses the GTP into GDP. Once GTP is hydrolyzed, the G-protein reverts to its inactive state (GDP-bound), causing it to dissociate from the effector proteins and the GPCR.

57
Q

Desensitization?

A

Desensitization is a process by which a cell becomes less responsive to a stimulus after prolonged exposure to a signaling molecule, such as a hormone or neurotransmitter.

57
Q

RGS proteins?

A

RGS proteins accelerates process of Hydrolysis of GTP by GTPase.

58
Q

Desensitization in GPCR occurs through several mechanisms:

A
  1. Receptor Phosphorylation
  2. Receptor Phosphorylation
  3. Receptor Internalization
59
Q

Who phosphorylates beta-ARK?

A

PKA

59
Q

Receptor Internalization?

A

Desensitized receptors may be internalized into the cell, further decreasing their availability and responsiveness to the ligand.

59
Q

Receptor Phosphorylation?

A

After receptor activation, specific kinases (like GRKs) phosphorylate the receptor, which reduces its ability to activate G-proteins.

59
Q

Arrestin Binding?

A

Phosphorylated receptors can bind to arrestin proteins, preventing further G-protein activation and often leading to receptor internalization (removal from the cell surface).

59
Q

role of beta-ARK in desensitisation?

A

beta-ARK phosphorylates the activated GPCR at specific serine and threonine residues. This modification reduces the receptor’s ability to interact with and activate G-proteins.

60
Q

beta-ARK is recruited by?

A

G-βγ subunits

61
Q

beta-ARK phosphorylates the receptor at ?

A

specific serine and threonine residues at C-terminal.

62
Q

what binds at phosphorylated serine and threonine residues?

A

Cytosolic Beta-Arr-2 (Beta-arrestin)

63
Q

Disease Bcz of GPCR?

A

Cardiovascular disorders
Blindness
Cholera
Pertussis

64
Q

Toxin in Cholera?

A

AB Type

65
Q

AB5

A

A is 1 in no.
B is 5 in no.

66
Q

A is

A

enzymatic
ADP Ribosyl transferase: ADP ribosylation

67
Q

Toxins reach to?

A

RER.

68
Q

B is

A

Non enzymatic

helps toxins to enter in host.
B allow to select the host cell

69
Q

In RER ____

A

A and B gets separated.

A is cleaved into A1 and A2

70
Q

A2 is _____

A

enzymatic

71
Q

A2 perform?

A

ADP Ribosylation

72
Q

action of ADP Ribosylation on G-alpha in case of cholera (GPCR)

A

Cholera toxin transfers an ADP ribose group to a specific amino acid (typically an arginine) on the G-alpha subunit of Gs, preventing it from hydrolyzing GTP to GDP.

73
Q

Constitutive Activation

A

This modification locks the G-alpha subunit in its active GTP-bound state, causing continuous stimulation of adenylate cyclase.

74
Q

Effect of prolonged activation of protein kinase A, in intestinal cells?

A

In intestinal cells, this results in excessive secretion of chloride ions and water into the intestinal lumen, causing severe diarrhea, a hallmark symptom of cholera.

74
Q

Effect of Constitutive Activation?

A

cAMP level Increases
prolonged activation of protein kinase A

75
Q

Effect of prolonged activation of protein kinase A?

A

Acts on CFTR
Disrupts normal cellular functions.

76
Q

CFTR?

A

Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) is a protein that functions as a chloride channel in epithelial cells, playing a crucial role in maintaining the balance of salt and water across cell membranes.

77
Q

Receptor for Cholera Toxin?

A

GM1

78
Q

GPCR in Diptheria?

A

Caused by “Corny Bacterium”

79
Q

Role of GM1?

A

The binding of cholera toxin to GM1 triggers endocytosis, allowing the toxin to enter the cell where it can exert its effects.

80
Q

Nature of Toxin?

A

AB Type

81
Q

AB Type does

A

ADP Ribosylation at His-Residues of Elongation Factor-2.

82
Q

Pertussis caused by ?

A

ADP ribosylation of G-protein at 16 a.a of Respiratory cells.

Results in no exchange of GDP to GTP. G-protein remains Inactive

82
Q

GPCR in Pertussis?

A

Caused by “Bordetella Pertussis”

Gram negative

Infect Respiratory Tract

83
Q

The Walker motif plays a critical role in ?

A

this nucleotide exchange process, enabling the G-protein to transmit the signal downstream.

83
Q

which residues in the toxin are crucial for ADP Ribosylation in Pertussis?

A

Cysteine

83
Q

The cysteine residues are involved in ?

A

The cysteine residues are involved in the structural integrity and function of the toxin, allowing it to effectively enter host cells and disrupt normal GPCR signaling by inhibiting Gi protein activity.

83
Q

Walker motif’s sequence with a consensus pattern ?

A

GXXXXGKS/T

83
Q

Stimulatory G-Protein (Gs)?

A

When GHRH binds to its receptor on somatotrophs, Gs is activated, stimulating adenylate cyclase to increase cAMP levels. This cascade enhances GH synthesis and secretion.

83
Q

Walker motif?

A

It refers to a specific sequence of amino acids found in G-proteins and some other ATP-binding proteins, crucial for their function. Walker motif is involved in the binding of guanine nucleotides (GTP and GDP).

84
Q

GPCR in somatotroph?

A

somatotrophs are regulated by the opposing actions of GHRH and somatostatin, which interact with GPCRs linked to stimulatory and inhibitory G-proteins, respectively.

84
Q

Guanine interact with only?

A

K,S/T by Hydrogen Bond

84
Q

Walker motif is essential for?

A

GTP binding

84
Q

Inhibitory G-Protein (Gi)?

A

When somatostatin binds to its receptor, Gi is activated, inhibiting adenylate cyclase and reducing cAMP levels. This inhibition decreases GH release.

Cell Signalling (8 decks)

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