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Metabolites of an Epac-selective cAMP analog induce cortisol synthesis by adrenocortical cells through a cAMP-independent pathway

PloS one, 2009-06, Vol.4 (6), p.e6088-e6088

2009

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Ca2+ and K+ channels of normal human adrenal zona fasciculata cells: properties and modulation by ACTH and AngII

The Journal of general physiology, 2013-08, Vol.142 (2), p.137-155

2013

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Human adrenal glomerulosa cells express K2P and GIRK potassium channels that are inhibited by ANG II and ACTH

American Journal of Physiology: Cell Physiology, 2021-07, Vol.321 (1), p.C158-C175

2021

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Curcumin inhibits bTREK-1 K + channels and stimulates cortisol secretion from adrenocortical cells

Biochemical and biophysical research communications, 2008-06, Vol.370 (4), p.623-628

2008

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Potent inhibition of native TREK-1 K+ channels by selected dihydropyridine Ca2+ channel antagonists

The Journal of pharmacology and experimental therapeutics, 2007-10, Vol.323 (1), p.39

2007

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ACTH inhibits bTREK-1 K+ channels through multiple cAMP-dependent signaling pathways

The Journal of general physiology, 2008-08, Vol.132 (2), p.279-294

2008

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Curcumin Inhibits ACTH- and Angiotensin II-Stimulated Cortisol Secretion and Cav3.2 Current

Journal of natural products (Washington, D.C.), 2009-08, Vol.72 (8), p.1533-1537

2009

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N6-Substituted cAMP Analogs Inhibit bTREK-1 K+ Channels and Stimulate Cortisol Secretion by a Protein Kinase A-Independent Mechanism

Molecular pharmacology, 2009-12, Vol.76 (6), p.1290-1301

2009

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An ACTH- and ATP-regulated Background K+ Channel in Adrenocortical Cells Is TREK-1

The Journal of biological chemistry, 2002-12, Vol.277 (51), p.49186-49199

2002

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TREK-1 K+ channels couple angiotensin II receptors to membrane depolarization and aldosterone secretion in bovine adrenal glomerulosa cells

American journal of physiology: endocrinology and metabolism, 2004-12, Vol.287 (6), p.E1154-E1165

2004

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Adrenal fasciculata cells express T-type and rapidly and slowly activating L-type Ca2+ channels that regulate cortisol secretion

American Journal of Physiology: Cell Physiology, 2015-06, Vol.308 (11), p.C899-C918

2015

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Angiotensin II inhibits native bTREK-1 K+ channels through a PLC-, kinase C-, and PIP2-independent pathway requiring ATP hydrolysis

American Journal of Physiology: Cell Physiology, 2007-08, Vol.293 (2), p.C682-C695

2007

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Caffeic Acid Esters Activate TREK-1 Potassium Channels and Inhibit Depolarization-Dependent Secretion

Molecular pharmacology, 2004-03, Vol.65 (3), p.599-610

2004

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Angiotensin II Inhibits bTREK-1 K+ Channels in Adrenocortical Cells by Separate Ca2+- and ATP Hydrolysis-dependent Mechanisms

The Journal of biological chemistry, 2005-09, Vol.280 (35), p.30814-30828

2005

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cAMP analogs and their metabolites enhance TREK-1 mRNA and K+ current expression in adrenocortical cells

Molecular pharmacology, 2010-03, Vol.77 (3), p.469-482

2010

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Corticotropin Induces the Expression of TREK-1 mRNA and K+ Current in Adrenocortical Cells

Molecular pharmacology, 2003-07, Vol.64 (1), p.132-142

2003

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ACTH Induces Cav3.2 Current and mRNA by cAMP-dependent and cAMP-independent Mechanisms

The Journal of biological chemistry, 2010-06, Vol.285 (26), p.20040-20050

2010

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Calcium-dependent inhibition of adrenal TREK-1 channels by angiotensin II and ionomycin

American Journal of Physiology: Cell Physiology, 2011-09, Vol.301 (3), p.C619-C629

2011

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Curcumin Inhibits ACTH- and Angiotensin II-Stimulated Cortisol Secretion and Ca(v)3.2 Current

Journal of natural products (Washington, D.C.), 2009-08, Vol.72 (8), p.1533-1537

2009

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Evidence for cAMP-independent bTREK-1 inhibition by ACTH and NPS-ACTH in adrenocortical cells

Molecular and cellular endocrinology, 2012-01, Vol.348 (1), p.305-312

2012

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8-Phenylthio-adenines stimulate the expression of steroid hydroxylases, Cav3.2 Ca²⁺ channels, and cortisol synthesis by a cAMP-independent mechanism

American journal of physiology: endocrinology and metabolism, 2011-11, Vol.301 (5), p.E941-E954

2011

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Modulation of native T-type calcium channels by ω-3 fatty acids

Biochemical and biophysical research communications, 2005-02, Vol.327 (2), p.485-493

2005

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Neuroprotective agent riluzole dramatically slows inactivation of Kv1.4 potassium channels by a voltage-dependent oxidative mechanism

The Journal of pharmacology and experimental therapeutics, 2001-10, Vol.299 (1), p.227

2001

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Mibefradil Potently Blocks ATP-Activated K+ Channels in Adrenal Cells

Molecular pharmacology, 1999-12, Vol.56 (6), p.1192-1197

1999

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Adrenal fasciculata cells express T-type and rapidly and slowly activating L-type Ca^sup 2+^ channels that regulate cortisol secretion

American Journal of Physiology: Cell Physiology, 2015-06, Vol.308 (11), p.C899

2015

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Metabolites of an Epac-selective cAMP analog induce cortisol synthesis by adrenocortical cells through a cAMP-independent pathway

Ca2+ and K+ channels of normal human adrenal zona fasciculata cells: properties and modulation by ACTH and AngII

Human adrenal glomerulosa cells express K2P and GIRK potassium channels that are inhibited by ANG II and ACTH

Curcumin inhibits bTREK-1 K + channels and stimulates cortisol secretion from adrenocortical cells

Potent inhibition of native TREK-1 K+ channels by selected dihydropyridine Ca2+ channel antagonists

ACTH inhibits bTREK-1 K+ channels through multiple cAMP-dependent signaling pathways

Curcumin Inhibits ACTH- and Angiotensin II-Stimulated Cortisol Secretion and Cav3.2 Current

N6-Substituted cAMP Analogs Inhibit bTREK-1 K+ Channels and Stimulate Cortisol Secretion by a Protein Kinase A-Independent Mechanism

An ACTH- and ATP-regulated Background K+ Channel in Adrenocortical Cells Is TREK-1

TREK-1 K+ channels couple angiotensin II receptors to membrane depolarization and aldosterone secretion in bovine adrenal glomerulosa cells

Adrenal fasciculata cells express T-type and rapidly and slowly activating L-type Ca2+ channels that regulate cortisol secretion

Angiotensin II inhibits native bTREK-1 K+ channels through a PLC-, kinase C-, and PIP2-independent pathway requiring ATP hydrolysis

Caffeic Acid Esters Activate TREK-1 Potassium Channels and Inhibit Depolarization-Dependent Secretion

Angiotensin II Inhibits bTREK-1 K+ Channels in Adrenocortical Cells by Separate Ca2+- and ATP Hydrolysis-dependent Mechanisms

cAMP analogs and their metabolites enhance TREK-1 mRNA and K+ current expression in adrenocortical cells

Corticotropin Induces the Expression of TREK-1 mRNA and K+ Current in Adrenocortical Cells

ACTH Induces Cav3.2 Current and mRNA by cAMP-dependent and cAMP-independent Mechanisms

Calcium-dependent inhibition of adrenal TREK-1 channels by angiotensin II and ionomycin

Curcumin Inhibits ACTH- and Angiotensin II-Stimulated Cortisol Secretion and Ca(v)3.2 Current

Evidence for cAMP-independent bTREK-1 inhibition by ACTH and NPS-ACTH in adrenocortical cells

8-Phenylthio-adenines stimulate the expression of steroid hydroxylases, Cav3.2 Ca²⁺ channels, and cortisol synthesis by a cAMP-independent mechanism

Modulation of native T-type calcium channels by ω-3 fatty acids

Neuroprotective agent riluzole dramatically slows inactivation of Kv1.4 potassium channels by a voltage-dependent oxidative mechanism

Mibefradil Potently Blocks ATP-Activated K+ Channels in Adrenal Cells

Adrenal fasciculata cells express T-type and rapidly and slowly activating L-type Ca^sup 2+^ channels that regulate cortisol secretion

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