导图社区 G proteins
在结构上不同于前述的G蛋白,分子量较小,在20-30kDa之间,不是以α、β、γ三聚体方式存在,而是单体分子,因此被称为小G蛋白(small G proteins)。如ras表达产物为一种小G蛋白。小
编辑于2022-06-14 21:44:51G proteins
Superfamilies
Trimeric G protein
adrenergic signaling
Gs
Gi
vision
transducin
Small G proteins
insulin signaling(Ras)
Vesicle trafficking
ARF
Rab
Transport into and out of the nucleus
Ran
Timing of the cell cycle
Rho
Protein synthesis
initiation factor
IF2
Elongation factors
EF-Tu
EF-G
differences
200 genes
differ in
size
subunit structure
intracellular location
function
common
timers
inactivate themselfs after short period of activation
Same core structures
active conformation when GTP is bound
inactive conformation when GDP is bound
many are covalently bond lipids
give them an affinity for membranes and dictate their locations in the cell
Ras as a standard
Ras is mutated in 25% of all cancers
The mutition site is critical residues around the GTP binding site or in the P loop
eliminate the GTPase activity
The Swiches
switch I
Thr 35
switch II
Gly 60
P loop
interactes with the γ phosphate of GTP
form hydrogen bonds by the phosphate's oxygen with switches I/II
So the switch I and II is hided after the γ phosphate is hydrolized
Specificity
Ala 146 hydrogen-bonds to the guanine oxygen, allowing GTP, but not ATP, to bind
Interact with the down stream signals
Buried when GDP is bonded
Intrinsic GTPase
cleaves the γ phosphate
Ras
GTPase activator proteins(GAPs)
Increase the intrinsic GTPase activity for 10^5 folds
The tumor suppressor gene NF1 encodes a GAP that enhances the GTPase activity of normal Ras.
so the mutation of it will only live Ras with its intrisic GTPase activity and cause cancer
heterotrimeric G proteins
regulators of G protein signaling (RGSs)
Disease causeing mutations
Activating mutations in Gs
permanently active Ga
continueous increase of [AMP]
found in about 40% of putuitary tumors(adenomas)
Inactivating mutations in Ga
unresponsive to hormones
such as thyroid hormone
Mutations in Transducin α subunit (Tα)
involved in visual signaling
night blindness
due to defective interaction between the activated Tα subunit and the phosphodiesterase of the rod outer segment
A sequence variation in the gene encoding the β subunit of a heterotrimeric G protein is commonly found in individuals with hypertension (high blood pressure)
this variant gene is suspected of involvement in obesity and athrosclerosis
response for the timming
They contribute a critical Arg residue that reaches into the G-protein GTPase active site and assists in catalyst
Intrinsic replacing bond GDP with GTP
Slow
Swiching the protein on
Catalyzed by guanosine nucleotide exchange factor(GEFs)
locates in the upstream signals
Toxins agains G proteins
Cholera toxin
secreted by Vibrio cholerae in the intestine of an infected person
Heterodimeric protein
1. Entry the cell
subunit B recognizes and binds to specific gangliosides on the surface of intestinal epithelial cells and provides a route for subunit A to enter these cells.
2. After entry
After intry, subunit A is brocken into two pieces: the A1 fragment and A2 fragment.
A1 associates with ADP-ribosylation factor ARF6 (a small G protein) through residues in its swich I and swich II regions.
ARF6 is only accessible in its active(GTP bound form)
The association with ARF6 activates A1, which catalyzes the transfer of ADP-ribose from NAD+ to critical Arg residue in the P loop of the α subunit of Gs.
ADP-ribosylation blocks the GTPase activity of Gs and thereby renders Gs permanently active.
This results in
continous activation of the adenylyl cyclase of intestinal epicelial cells
chronically high [cAMP]
chronically active PKA.
PKA phosphprylates the CFTR Cl- channel and a Na+-H+ echanger in the intestinal epithelial cells.
It results in efflux of NaCl
It triggers massive water loss through the intestine
To ensuring osmotic imbalance
severe dehydration
severe electrolytes lost
Pertussis toxin
Produced by Bordetella pertussis
catalyzes ADP-ribosylation of the α subunit of Gi
Prevents GDP-GTP exchange
Blocks the inhibition of adenylyl cyclase by Gi
The bacteria infects the respiratory tract
it destroys the ciliated epithelial cells that normally sweep away mucus.
Without this ciliary action, vigorous coughing is needed to clear the tract.
Gasping cough and spreads the bacteria to others