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N-Linked Glycosylation Is Required for Vacuolar H+-ATPase (V-ATPase) a4 Subunit Stability, Assembly, and Cell Surface Expression

Journal of cellular biochemistry, 2016-12, Vol.117 (12), p.2757-2768

2016

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Inhibition of Osteoclast Bone Resorption by Disrupting Vacuolar H+-ATPase a3-B2 Subunit Interaction

The Journal of biological chemistry, 2010-11, Vol.285 (48), p.37476-37490

2010

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Osteopetrosis Mutation R444L Causes Endoplasmic Reticulum Retention and Misprocessing of Vacuolar H+-ATPase a3 Subunit

The Journal of biological chemistry, 2012-08, Vol.287 (32), p.26829-26839

2012

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V-ATPase subunit interactions: the long road to therapeutic targeting

Current protein & peptide science, 2012-03, Vol.13 (2), p.164-179

2012

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COOH-Terminal Truncations Promote Proteasome-Dependent Degradation of Mature Cystic Fibrosis Transmembrane Conductance Regulator from Post-Golgi Compartments

The Journal of cell biology, 2001-05, Vol.153 (5), p.957-970

2001

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Effects of Human a3 and a4 Mutations That Result in Osteopetrosis and Distal Renal Tubular Acidosis on Yeast V-ATPase Expression and Activity

The Journal of biological chemistry, 2006-09, Vol.281 (36), p.26102-26111

2006

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Constitutive internalization of cystic fibrosis transmembrane conductance regulator occurs via clathrin-dependent endocytosis and is regulated by protein phosphorylation

Biochemical journal, 1997-12, Vol.328 ( Pt 2) (2), p.353-361

1997

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Purification and functional reconstitution of the cystic fibrosis transmembrane conductance regulator (CFTR)

Cell, 1992-02, Vol.68 (4), p.809-818

1992

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Molecular mechanisms of cutis laxa– and distal renal tubular acidosis–causing mutations in V-ATPase a subunits, ATP6V0A2 and ATP6V0A4

The Journal of biological chemistry, 2018-02, Vol.293 (8), p.2787-2800

2018

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Novel techniques in the development of osteoporosis drug therapy: the osteoclast ruffled-border vacuolar H+-ATPase as an emerging target

Expert opinion on drug discovery, 2014-05, Vol.9 (5), p.505-522

2014

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Expression of the cystic fibrosis gene in non-epithelial invertebrate cells produces a regulated anion conductance

Cell, 1991-02, Vol.64 (4), p.681-691

1991

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Novel techniques in the development of osteoporosis drug therapy: the osteoclast ruffled-border vacuolar H super(+)-ATPase as an emerging target

Expert opinion on drug discovery, 2014-05, Vol.9 (5), p.505-522

2014

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N‐linked glycosylation of a subunit isoforms is critical for vertebrate vacuolar H+‐ATPase (V‐ATPase) biosynthesis

Journal of cellular biochemistry, 2018-01, Vol.119 (1), p.861-875

2018

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Controlled bone formation using ultrasound-triggered release of BMP-2 from liposomes

Journal of controlled release, 2016-12, Vol.243, p.99-108

2016

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Detection of P-glycoprotein in multidrug-resistant cell lines by monoclonal antibodies

Nature (London), 1985-08, Vol.316 (6031), p.820-823

1985

Volltextzugriff (PDF)

Luteolin inhibition of V-ATPase a3-d2 interaction decreases osteoclast resorptive activity

Journal of cellular biochemistry, 2013-04, Vol.114 (4), p.929-941

2013

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C-terminal truncations destabilize the cystic fibrosis transmembrane conductance regulator without impairing its biogenesis. A novel class of mutation

The Journal of biological chemistry, 1999-07, Vol.274 (31), p.21873-21877

1999

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Engineering an ultrasound activated implant that provides on demand BMP-2 release for bone regeneration

Frontiers in bioengineering and biotechnology, 2016, Vol.4

2016

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cAMP-Inducible Chloride Conductance in Mouse Fibroblast Lines Stably Expressing the Human Cystic Fibrosis Transmembrane Conductance Regulator

Proceedings of the National Academy of Sciences - PNAS, 1991-09, Vol.88 (17), p.7500-7504

1991

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C-terminal Truncations Destabilize the Cystic Fibrosis Transmembrane Conductance Regulator without Impairing Its Biogenesis

The Journal of biological chemistry, 1999-07, Vol.274 (31), p.21873-21877

1999

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Conformational maturation of CFTR but not its mutant counterpart (delta F508) occurs in the endoplasmic reticulum and requires ATP

The EMBO journal, 1994-12, Vol.13 (24), p.6076-6086

1994

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The delta F508 mutation decreases the stability of cystic fibrosis transmembrane conductance regulator in the plasma membrane. Determination of functional half-lives on transfected cells

The Journal of biological chemistry, 1993-10, Vol.268 (29), p.21592-21598

1993

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Mislocalization of ΔF508 CFTR in cystic fibrosis sweat gland

Nature genetics, 1992-08, Vol.1 (5), p.321-327

1992

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The V-ATPase a3 subunit: Potential therapeutic target for osteoporosis

Bone (New York, N.Y.), 2008-10, Vol.43, p.S98-S98

2008

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Protein kinase A (PKA) still activates CFTR chloride channel after mutagenesis of all 10 PKA consensus phosphorylation sites

The Journal of biological chemistry, 1993-05, Vol.268 (15), p.11304-11311

1993

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N-Linked Glycosylation Is Required for Vacuolar H+-ATPase (V-ATPase) a4 Subunit Stability, Assembly, and Cell Surface Expression

Inhibition of Osteoclast Bone Resorption by Disrupting Vacuolar H+-ATPase a3-B2 Subunit Interaction

Osteopetrosis Mutation R444L Causes Endoplasmic Reticulum Retention and Misprocessing of Vacuolar H+-ATPase a3 Subunit

V-ATPase subunit interactions: the long road to therapeutic targeting

COOH-Terminal Truncations Promote Proteasome-Dependent Degradation of Mature Cystic Fibrosis Transmembrane Conductance Regulator from Post-Golgi Compartments

Effects of Human a3 and a4 Mutations That Result in Osteopetrosis and Distal Renal Tubular Acidosis on Yeast V-ATPase Expression and Activity

Constitutive internalization of cystic fibrosis transmembrane conductance regulator occurs via clathrin-dependent endocytosis and is regulated by protein phosphorylation

Purification and functional reconstitution of the cystic fibrosis transmembrane conductance regulator (CFTR)

Molecular mechanisms of cutis laxa– and distal renal tubular acidosis–causing mutations in V-ATPase a subunits, ATP6V0A2 and ATP6V0A4

Novel techniques in the development of osteoporosis drug therapy: the osteoclast ruffled-border vacuolar H+-ATPase as an emerging target

Expression of the cystic fibrosis gene in non-epithelial invertebrate cells produces a regulated anion conductance

Novel techniques in the development of osteoporosis drug therapy: the osteoclast ruffled-border vacuolar H super(+)-ATPase as an emerging target

N‐linked glycosylation of a subunit isoforms is critical for vertebrate vacuolar H+‐ATPase (V‐ATPase) biosynthesis

Controlled bone formation using ultrasound-triggered release of BMP-2 from liposomes

Detection of P-glycoprotein in multidrug-resistant cell lines by monoclonal antibodies

Luteolin inhibition of V-ATPase a3-d2 interaction decreases osteoclast resorptive activity

C-terminal truncations destabilize the cystic fibrosis transmembrane conductance regulator without impairing its biogenesis. A novel class of mutation

Engineering an ultrasound activated implant that provides on demand BMP-2 release for bone regeneration

cAMP-Inducible Chloride Conductance in Mouse Fibroblast Lines Stably Expressing the Human Cystic Fibrosis Transmembrane Conductance Regulator

C-terminal Truncations Destabilize the Cystic Fibrosis Transmembrane Conductance Regulator without Impairing Its Biogenesis

Conformational maturation of CFTR but not its mutant counterpart (delta F508) occurs in the endoplasmic reticulum and requires ATP

The delta F508 mutation decreases the stability of cystic fibrosis transmembrane conductance regulator in the plasma membrane. Determination of functional half-lives on transfected cells

Mislocalization of ΔF508 CFTR in cystic fibrosis sweat gland

The V-ATPase a3 subunit: Potential therapeutic target for osteoporosis

Protein kinase A (PKA) still activates CFTR chloride channel after mutagenesis of all 10 PKA consensus phosphorylation sites

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