scholarly journals Dominant negative effects of a Gβ mutant on G-protein coupled inward rectifier K+channel

FEBS Letters ◽  
2006 ◽  
Vol 580 (16) ◽  
pp. 3879-3882 ◽  
Author(s):  
Qi Zhao ◽  
Abla M. Albsoul-Younes ◽  
Peng Zhao ◽  
Tohru Kozasa ◽  
Yasuko Nakajima ◽  
...  
Keyword(s):  
G Protein ◽  
Inward Rectifier ◽  
Dominant Negative ◽  
K Channel ◽  
Negative Effects ◽  
G Protein Coupled

scholarly journals Subunit Stoichiometry of a Heteromultimeric G protein-coupled Inward-rectifier K+Channel

1996 ◽  
Vol 271 (48) ◽  
pp. 30524-30528 ◽  
Author(s):  
Scott K. Silverman ◽  
Henry A. Lester ◽  
Dennis A. Dougherty
Keyword(s):  
G Protein ◽  
Inward Rectifier ◽  
K Channel ◽  
Subunit Stoichiometry ◽  
G Protein Coupled

scholarly journals Functional and Physical Interactions among Saccharomyces cerevisiae α-Factor Receptors

2012 ◽  
Vol 11 (10) ◽  
pp. 1276-1288 ◽  
Author(s):  
Austin U. Gehret ◽  
Sara M. Connelly ◽  
Mark E. Dumont
Keyword(s):  
Saccharomyces Cerevisiae ◽  
G Protein ◽  
Dominant Negative ◽  
Negative Effects ◽  
Content Type ◽  
Functional Interactions ◽  
Wide Range ◽  
Physical Interactions ◽  
Mutant Receptors ◽  
G Protein Coupled

ABSTRACT The α-factor receptor Ste2p is a G protein-coupled receptor (GPCR) expressed on the surface of MAT a haploid cells of the yeast Saccharomyces cerevisiae . Binding of α-factor to Ste2p results in activation of a heterotrimeric G protein and of the pheromone response pathway. Functional interactions between α-factor receptors, such as dominant-negative effects and recessive behavior of constitutive and hypersensitive mutant receptors, have been reported previously. We show here that dominant-negative effects of mutant receptors persist over a wide range of ratios of the abundances of G protein to receptor and that such effects are not blocked by covalent fusion of G protein α subunits to normal receptors. In addition, we detected dominant effects of mutant C-terminally truncated receptors, which had not been previously reported to act in a dominant manner. Furthermore, coexpression of C-terminally truncated receptors with constitutively active mutant receptors results in enhancement of constitutive signaling. Together with previous evidence for oligomerization of Ste2p receptors, these results are consistent with the idea that functional interactions between coexpressed receptors arise from physical interactions between them rather than from competition for limiting downstream components, such as G proteins.

scholarly journals Primary structure and functional expression of a mouse inward rectifier K+ channel and rat G-protein-coupled muscarinic K+ channel.

1995 ◽  
Vol 15 (2) ◽  
pp. 106-113
Author(s):  
Yoshihiro Kubo ◽  
Eitan Reuveny ◽  
Paul A Slesinger ◽  
Timothy J Baldwin ◽  
Yuh Nung Jan ◽  
...  
Keyword(s):  
G Protein ◽  
Primary Structure ◽  
Functional Expression ◽  
Inward Rectifier ◽  
K Channel ◽  
G Protein Coupled

scholarly journals Interaction Sites of the G Protein β Subunit with Brain G Protein-coupled Inward Rectifier K+Channel

2001 ◽  
Vol 276 (16) ◽  
pp. 12712-12717 ◽  
Author(s):  
Abla M. Albsoul-Younes ◽  
Pamela M. Sternweis ◽  
Peng Zhao ◽  
Hiroko Nakata ◽  
Shigehiro Nakajima ◽  
...  
Keyword(s):  
G Protein ◽  
Inward Rectifier ◽  
K Channel ◽  
Β Subunit ◽  
Interaction Sites ◽  
G Protein Coupled

Single-channel properties of a G-protein-coupled inward rectifier potassium channel in brain neurons

1996 ◽  
Vol 75 (1) ◽  
pp. 318-328 ◽  
Author(s):  
J. J. Grigg ◽  
T. Kozasa ◽  
Y. Nakajima ◽  
S. Nakajima
Keyword(s):  
G Protein ◽  
Single Channel ◽  
Inward Rectifier ◽  
Equilibrium Potential ◽  
K Channel ◽  
Open Probability ◽  
K Concentration ◽  
Inwardly Rectifying ◽  
G Protein Coupled ◽  
Cytoplasmic Side

1. In cultured rat locus coeruleus neurons, somatostatin or met-enkephalin induces an inwardly rectifying K+ conductance. This inward rectifier was analyzed at the single-channel level. 2. Using the inside-out patch-clamp, guanosine 5'-triphosphate (GTP) application to the cytoplasmic side in the presence of somatostatin or met-enkephalin in the pipette produced a large increase in channel activity, which disappeared on switching from GTP to guanosine 5'-diphosphate. 3. The unitary conductance was approximately 30 pS at -95 mV with an extracellular K+ concentration of 156 mM and an intracellular K+ concentration of 124 mM at 23 degrees C. The channel showed burst behavior, and the closed time histogram was fit by two exponentials, with the fast time constant being 0.4 ms. The burst time histogram was also fit by two exponentials, with time constants of 0.24 and 2.0 ms (at 10 nM somatostatin). When the somatostatin concentration was changed from 500 to 1 nM, the kinetic behavior of the channel did not change, except that the open probability of the patch was decreased. 4. The current-voltage relation of the unitary channel current showed inward rectification. The reversal potential coincided with the K+ equilibrium potential, and it shifted according to a change in the K+ equilibrium potential. 5. In the presence of external somatostatin, the application of guanosine 5'-O-(3-thiotriphosphate) to the cytoplasmic side induced an irreversible activation of this channel. 6. These results indicate that this K+ channel is the microscopic counterpart of the somatostatin- or met-enkephalin-induced inwardly rectifying K+ current in whole cell recording, and that the channel is activated by a G protein without a diffusible second messenger. Thus this channel is identified as a neuronal G-protein-coupled inward rectifier K+ channel. 7. Analysis of the burst behavior, based on a close-close-open kinetic model, revealed that there are at least four states in the K+ channel, a short gap, a longer closing, a short opening, and a long opening, and that the neuronal inward rectifier is activated at faster rates than the atrial inward rectifier.

Assignment of Human G-Protein-Coupled Inward Rectifier K+Channel Homolog GIRK3 Gene to Chromosome 1q21–q23

Genomics ◽  
1995 ◽  
Vol 29 (3) ◽  
pp. 808-809 ◽  
Author(s):  
F. Lesage ◽  
M. Fink ◽  
J. Barhanin ◽  
M. Lazdunski ◽  
M.-G. Mattéi
Keyword(s):  
G Protein ◽  
Inward Rectifier ◽  
K Channel ◽  
G Protein Coupled ◽  
Chromosome 1Q21
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