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Mechanistic Insight into Control of CFTR by AMPK

The Journal of biological chemistry, 2009-02, Vol.284 (9), p.5645-5653

2009

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Expression of Wild-Type CFTR Suppresses NF-κB-Driven Inflammatory Signalling

PloS one, 2010-07, Vol.5 (7), p.e11598

2010

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Cystic fibrosis transmembrane regulator fragments with the Phe508 deletion exert a dual allosteric control over the master kinase CK2

Biochemical journal, 2010-01, Vol.426 (1), p.19-29

2010

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Modulation of Protein Kinase CK2 Activity by Fragments of CFTR Encompassing F508 May Reflect Functional Links with Cystic Fibrosis Pathogenesis

Biochemistry (Easton), 2008-07, Vol.47 (30), p.7925-7936

2008

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phosphorylation status of membrane-bound nucleoside diphosphate kinase in epithelia and the role of AMP

Molecular and cellular biochemistry, 2009-09, Vol.329 (1-2), p.107-114

2009

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Transglutaminase 2 and nucleoside diphosphate kinase activity are correlated in epithelial membranes and are abnormal in cystic fibrosis

FEBS letters, 2009-09, Vol.583 (17), p.2789-2792

2009

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Epithelial IgG and its relationship to the loss of F508 in the common mutant form of the cystic fibrosis transmembrane conductance regulator

FEBS letters, 2009-08, Vol.583 (15), p.2493-2499

2009

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Understanding the molecular basis of the interaction between NDPK-A and AMPK alpha 1

Molecular and cellular biology, 2006-08, Vol.26 (15), p.5921-5931

2006

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A novel physical and functional association between nucleoside diphosphate kinase A and AMP-activated protein kinase α1 in liver and lung

Biochemical journal, 2005-11, Vol.392 (1), p.201-209

2005

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Small interfering peptide (siP) for in vivo examination of the developing lung interactonome

Developmental dynamics, 2009-02, Vol.238 (2), p.386-393

2009

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Understanding the Molecular Basis of the Interaction between NDPK-A and AMPK α1

Molecular and Cellular Biology, 2006-08, Vol.26 (15), p.5921-5931

2006

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Protein kinase CK2 acts as a signal molecule switching between the NDPK-A/AMPK α1 complex and NDPK-B

The FASEB journal, 2007, Vol.21 (1), p.88-98

2007

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Protein Kinase CK2, Cystic Fibrosis Transmembrane Conductance Regulator, and the ΔF508 Mutation: F508 DELETION DISRUPTS A KINASE-BINDING SITE

The Journal of biological chemistry, 2007-04, Vol.282 (14), p.10804-10813

2007

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4α-Phorbol negates the inhibitory effects of phorbol-12-myristate-13-acetate on human cilia and alters the phosphorylation of PKC

FEBS letters, 2002-10, Vol.530 (1), p.31-36

2002

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Expression of wild-type CFTR suppresses NF-kappaB-driven inflammatory signalling

PloS one, 2010-07, Vol.5 (7), p.e11598-e11598

2010

Volltextzugriff (PDF)

Expression of Wild-Type CFTR Suppresses NF-[kappa]B-Driven Inflammatory Signalling

PloS one, 2010-07, Vol.5 (7), p.e11598

2010

Volltextzugriff (PDF)

Mechanistic Insight into Control of CFTR by AMPKS

The Journal of biological chemistry, 2009-02, Vol.284 (9), p.5645-5653

2009

Volltextzugriff (PDF)

CFTR fragments with the F508 deletion exert a dual allosteric control over the master kinase CK2

Biochemical journal, 2010-01, Vol.426 (1), p.19-29

2010

Volltextzugriff (PDF)

Inhibition of Protein Kinase CK2 Closes the CFTR Cl- Channel, but has no Effect on the Cystic Fibrosis Mutant ΔF508-CFTR

Cellular physiology and biochemistry, 2009-01, Vol.24 (5-6), p.347-360

2009

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Understanding the Molecular Basis of the Interaction between NDPK-A and AMPK α1

Molecular and cellular biology, 2008-09, Vol.28 (18), p.5827-5827

2008

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Modulation of Protein Kinase CK2 Activity by Fragments of CFTR Encompassing F508 May Reflect Functional Links with Cystic Fibrosis Pathogenesis super([dagger])

Biochemistry (Easton), 2008-01, Vol.47 (30), p.7925-7936

2008

Volltextzugriff (PDF)

Protein Kinase CK2, Cystic Fibrosis Transmembrane Conductance Regulator, and the ΔF508 Mutation

The Journal of biological chemistry, 2007-04, Vol.282 (14), p.10804-10813

2007

Volltextzugriff (PDF)

Protein kinase CK2 acts as a signal molecule switching between the NDPK-A/AMPK 1 complex and NDPK-B

The FASEB journal, 2007-10, Vol.21 (12), p.3398-3398

2007

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Retraction notice to ‘NDPK-A (but not NDPK-B) and AMPK α1 (but not AMPK α2) bind the cystic fibrosis transmembrane conductance regulator in epithelial cell membranes’ [Cell. Signal 18 (2006) 1595–1603]

Cellular signalling, 2008-12, Vol.20 (12), p.2370-2370

2008

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Protein kinase CK2, cystic fibrosis transmembrane conductance regulator, and the deltaF508 mutation: F508 deletion disrupts a kinase-binding site

The Journal of biological chemistry, 2008-09, Vol.283 (36), p.25103-25103

2008

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Mechanistic Insight into Control of CFTR by AMPK

Expression of Wild-Type CFTR Suppresses NF-κB-Driven Inflammatory Signalling

Cystic fibrosis transmembrane regulator fragments with the Phe508 deletion exert a dual allosteric control over the master kinase CK2

Modulation of Protein Kinase CK2 Activity by Fragments of CFTR Encompassing F508 May Reflect Functional Links with Cystic Fibrosis Pathogenesis

phosphorylation status of membrane-bound nucleoside diphosphate kinase in epithelia and the role of AMP

Transglutaminase 2 and nucleoside diphosphate kinase activity are correlated in epithelial membranes and are abnormal in cystic fibrosis

Epithelial IgG and its relationship to the loss of F508 in the common mutant form of the cystic fibrosis transmembrane conductance regulator

Understanding the molecular basis of the interaction between NDPK-A and AMPK alpha 1

A novel physical and functional association between nucleoside diphosphate kinase A and AMP-activated protein kinase α1 in liver and lung

Small interfering peptide (siP) for in vivo examination of the developing lung interactonome

Understanding the Molecular Basis of the Interaction between NDPK-A and AMPK α1

Protein kinase CK2 acts as a signal molecule switching between the NDPK-A/AMPK α1 complex and NDPK-B

Protein Kinase CK2, Cystic Fibrosis Transmembrane Conductance Regulator, and the ΔF508 Mutation: F508 DELETION DISRUPTS A KINASE-BINDING SITE

4α-Phorbol negates the inhibitory effects of phorbol-12-myristate-13-acetate on human cilia and alters the phosphorylation of PKC

Expression of wild-type CFTR suppresses NF-kappaB-driven inflammatory signalling

Expression of Wild-Type CFTR Suppresses NF-[kappa]B-Driven Inflammatory Signalling

Mechanistic Insight into Control of CFTR by AMPKS

CFTR fragments with the F508 deletion exert a dual allosteric control over the master kinase CK2

Inhibition of Protein Kinase CK2 Closes the CFTR Cl- Channel, but has no Effect on the Cystic Fibrosis Mutant ΔF508-CFTR

Understanding the Molecular Basis of the Interaction between NDPK-A and AMPK α1

Modulation of Protein Kinase CK2 Activity by Fragments of CFTR Encompassing F508 May Reflect Functional Links with Cystic Fibrosis Pathogenesis super([dagger])

Protein Kinase CK2, Cystic Fibrosis Transmembrane Conductance Regulator, and the ΔF508 Mutation

Protein kinase CK2 acts as a signal molecule switching between the NDPK-A/AMPK 1 complex and NDPK-B

Retraction notice to ‘NDPK-A (but not NDPK-B) and AMPK α1 (but not AMPK α2) bind the cystic fibrosis transmembrane conductance regulator in epithelial cell membranes’ [Cell. Signal 18 (2006) 1595–1603]

Protein kinase CK2, cystic fibrosis transmembrane conductance regulator, and the deltaF508 mutation: F508 deletion disrupts a kinase-binding site

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