Small Inward Rectifying K + Channels in Coleoptiles: Inhibition by External Ca 2+ and Function in Cell Elongation

1996 ◽  
Vol 149 (1) ◽  
pp. 9-20 ◽  
Author(s):  
G. Thiel ◽  
A. Brüdern ◽  
D. Gradmann
Keyword(s):  
Cell Elongation ◽  
K Channels ◽  
And Function

scholarly journals Minimal art: Or why small viral K+ channels are good tools for understanding basic structure and function relations

2011 ◽  
Vol 1808 (2) ◽  
pp. 580-588 ◽  
Author(s):  
Gerhard Thiel ◽  
Dirk Baumeister ◽  
Indra Schroeder ◽  
Stefan M. Kast ◽  
James L. Van Etten ◽  
...  
Keyword(s):  
Basic Structure ◽  
Structure And Function ◽  
K Channels ◽  
Minimal Art ◽  
And Function

Plant K+ channels: structure, activity and function

1996 ◽  
Vol 24 (4) ◽  
pp. 964-971 ◽  
Author(s):  
I. Chérel ◽  
P. Daram ◽  
F. Gaymard ◽  
C. Horeau ◽  
J.-B. Thibaud ◽  
...  
Keyword(s):  
K Channels ◽  
Structure Activity ◽  
And Function

Structure and function of two-pore-domain K channels: contributions from genetic model organisms

2005 ◽  
Vol 26 (7) ◽  
pp. 361-367 ◽  
Author(s):  
S BUCKINGHAM ◽  
J KIDD ◽  
R LAW ◽  
C FRANKS ◽  
D SATTELLE
Keyword(s):  
Genetic Model ◽  
Structure And Function ◽  
Model Organisms ◽  
K Channels ◽  
And Function ◽  
Pore Domain

scholarly journals Expression and Function of Endothelial Ca2+-Activated K+Channels in Human Mesenteric Artery

2000 ◽  
Vol 87 (6) ◽  
pp. 496-503 ◽  
Author(s):  
Ralf Köhler ◽  
Christiane Degenhardt ◽  
Meike Kühn ◽  
Norbert Runkel ◽  
Martin Paul ◽  
...  
Keyword(s):  
Mesenteric Artery ◽  
K Channels ◽  
And Function

scholarly journals Neurogenic Detrusor Overactivity Is Associated with Decreased Expression and Function of the Large Conductance Voltage- and Ca2+-Activated K+ Channels

PLoS ONE ◽  
2013 ◽  
Vol 8 (7) ◽  
pp. e68052 ◽  
Author(s):  
Kiril L. Hristov ◽  
Serge A. Y. Afeli ◽  
Shankar P. Parajuli ◽  
Qiuping Cheng ◽  
Eric S. Rovner ◽  
...  
Keyword(s):  
Detrusor Overactivity ◽  
Neurogenic Detrusor Overactivity ◽  
K Channels ◽  
And Function

scholarly journals Barttin modulates trafficking and function of ClC-K channels

2006 ◽  
Vol 103 (30) ◽  
pp. 11411-11416 ◽  
Author(s):  
U. Scholl ◽  
S. Hebeisen ◽  
A. G. H. Janssen ◽  
G. Muller-Newen ◽  
A. Alekov ◽  
...  
Keyword(s):  
K Channels ◽  
And Function

scholarly journals ACTH Inhibits bTREK-1 K+ Channels through Multiple cAMP-dependent Signaling Pathways

2008 ◽  
Vol 132 (2) ◽  
pp. 279-294 ◽  
Author(s):  
Haiyan Liu ◽  
Judith A. Enyeart ◽  
John J. Enyeart
Keyword(s):  
Hek293 Cells ◽  
Resting Membrane Potential ◽  
Zona Fasciculata ◽  
Nucleotide Exchange ◽  
Pipette Solution ◽  
K Channels ◽  
Whole Cell Patch Clamp ◽  
Dependent Protein ◽  
Secretion Inhibition ◽  
And Function

Bovine adrenal zona fasciculata (AZF) cells express bTREK-1 K+ channels that set the resting membrane potential and function pivotally in the physiology of cortisol secretion. Inhibition of these K+ channels by adrenocorticotropic hormone (ACTH) or cAMP is coupled to depolarization and Ca2+ entry. The mechanism of ACTH and cAMP-mediated inhibition of bTREK-1 was explored in whole cell patch clamp recordings from AZF cells. Inhibition of bTREK-1 by ACTH and forskolin was not affected by the addition of both H-89 and PKI(6–22) amide to the pipette solution at concentrations that completely blocked activation of cAMP-dependent protein kinase (PKA) in these cells. The ACTH derivative, O-nitrophenyl, sulfenyl-adrenocorticotropin (NPS-ACTH), at concentrations that produced little or no activation of PKA, inhibited bTREK-1 by a Ca2+-independent mechanism. Northern blot analysis showed that bovine AZF cells robustly express mRNA for Epac2, a guanine nucleotide exchange protein activated by cAMP. The selective Epac activator, 8-pCPT-2′-O-Me-cAMP, applied intracellularly through the patch pipette, inhibited bTREK-1 (IC50 = 0.63 μM) at concentrations that did not activate PKA. Inhibition by this agent was unaffected by PKA inhibitors, including RpcAMPS, but was eliminated in the absence of hydrolyzable ATP. Culturing AZF cells in the presence of ACTH markedly reduced the expression of Epac2 mRNA. 8-pCPT-2′-O-Me-cAMP failed to inhibit bTREK-1 current in AZF cells that had been treated with ACTH for 3–4 d while inhibition by 8-br-cAMP was not affected. 8-pCPT-2′-O-Me-cAMP failed to inhibit bTREK-1 expressed in HEK293 cells, which express little or no Epac2. These findings demonstrate that, in addition to the well-described PKA-dependent TREK-1 inhibition, ACTH, NPS-ACTH, forskolin, and 8-pCPT-2′-O-Me-cAMP also inhibit these K+ channels by a PKA-independent signaling pathway. The convergent inhibition of bTREK-1 through parallel PKA- and Epac-dependent mechanisms may provide for failsafe membrane depolarization by ACTH.

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