PUBLICACIÓN

Store-operated calcium entry in differentiated C2C12 skeletal muscle cells

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ACCEDER A LA PUBLICACIÓN: Scopus Orcid

Gutierrez-Martin, Y., Henao, F., Martin-Romero, F.J.

2005 Biochimica et Biophysica Acta - Biomembranes

CITAS

41

DOI

10.1016/j.bbamem.2005.02.017

EID

2-s2.0-19444361994

ISSN

0005-2736

BIBTEX

@article { martinromero2005,title = {Store-operated calcium entry in differentiated C2C12 skeletal muscle cells},journal = {Biochimica et Biophysica Acta - Biomembranes},year = {2005},volume = {1711},number = {1},pages = {33-40},author = {Gutierrez-Martin, Y. and Martin-Romero, F.J. and Henao, F.}}

AUTORES DE LA UEX

Francisco Javier Martín Romero

OTRAS PUBLICACIONES DE INTERÉS

Inhibition Of The Sarcoplasmic Reticulum (Ca2+ + Mg2+-Atpase By Zn(Ii)
A Subset Of Orai1α And Orai1β Subunits Heteromerizes To Form Crac Channels
Stim1 Translocation To The Nucleus Protects Cells From Dna Damage
A Subset Of Orai1α And Orai1β Subunits Heteromerizes To Form Crac Channels
Stim1 Translocation To The Nucleus Protects Cells From Dna Damage
Editorial: Molecular Components Of Store-Operated Calcium Entry In Health And Disease, Volume Ii
Stim1 Translocation To The Nucleus Protects Cells From Dna Damage
Editorial: Molecular Components Of Store-Operated Calcium Entry In Health And Disease, Volume Ii
Internalized Amyloid-Β (1-42) Peptide Inhibits The Store-Operated Calcium Entry In Ht-22 Cells
Editorial: Molecular Components Of Store-Operated Calcium Entry In Health And Disease, Volume Ii
Internalized Amyloid-Β (1-42) Peptide Inhibits The Store-Operated Calcium Entry In Ht-22 Cells
Editorial: Molecular Components Of Store-Operated Calcium Entry In Health And Disease
Internalized Amyloid-Β (1-42) Peptide Inhibits The Store-Operated Calcium Entry In Ht-22 Cells
Editorial: Molecular Components Of Store-Operated Calcium Entry In Health And Disease
Stim1 Deficiency Leads To Specific Down-Regulation Of Itpr3 In Sh-Sy5y Cells
Editorial: Molecular Components Of Store-Operated Calcium Entry In Health And Disease
Stim1 Deficiency Leads To Specific Down-Regulation Of Itpr3 In Sh-Sy5y Cells
Rac1-Dependent Orai1 Translocation To The Leading Edge Supports Lamellipodia Formation And Directional Persistence
Stim1 Deficiency Leads To Specific Down-Regulation Of Itpr3 In Sh-Sy5y Cells
Rac1-Dependent Orai1 Translocation To The Leading Edge Supports Lamellipodia Formation And Directional Persistence
Fluctuation In O-Glcnacylation Inactivates Stim1 To Reduce Store-Operated Calcium Ion Entry Via Down-Regulation Of Ser621phosphorylation
Rac1-Dependent Orai1 Translocation To The Leading Edge Supports Lamellipodia Formation And Directional Persistence
Fluctuation In O-Glcnacylation Inactivates Stim1 To Reduce Store-Operated Calcium Ion Entry Via Down-Regulation Of Ser621phosphorylation
Correction To: Stim1 Deficiency Is Linked To Alzheimer’s Disease And Triggers Cell Death In Sh-Sy5y Cells By Upregulation Of L-Type Voltage-Operated Ca2+ Entry (Journal Of Molecular Medicine, (2018), 96, 10, (1061-1079), 10.1007/s00109-018-1677-Y)
Fluctuation In O-Glcnacylation Inactivates Stim1 To Reduce Store-Operated Calcium Ion Entry Via Down-Regulation Of Ser621phosphorylation
Correction To: Stim1 Deficiency Is Linked To Alzheimer’s Disease And Triggers Cell Death In Sh-Sy5y Cells By Upregulation Of L-Type Voltage-Operated Ca2+ Entry (Journal Of Molecular Medicine, (2018), 96, 10, (1061-1079), 10.1007/s00109-018-1677-Y)
Role Of Stim1 In Neurodegeneration
Correction To: Stim1 Deficiency Is Linked To Alzheimer’s Disease And Triggers Cell Death In Sh-Sy5y Cells By Upregulation Of L-Type Voltage-Operated Ca2+ Entry (Journal Of Molecular Medicine, (2018), 96, 10, (1061-1079), 10.1007/s00109-018-1677-Y)
Role Of Stim1 In Neurodegeneration
Stim1 Deficiency Is Linked To Alzheimer’s Disease And Triggers Cell Death In Sh-Sy5y Cells By Upregulation Of L-Type Voltage-Operated Ca2+ Entry
Role Of Stim1 In Neurodegeneration
Stim1 Deficiency Is Linked To Alzheimer’s Disease And Triggers Cell Death In Sh-Sy5y Cells By Upregulation Of L-Type Voltage-Operated Ca2+ Entry
The Interplay Between Cytoskeleton And Calcium Dynamics
Stim1 Deficiency Is Linked To Alzheimer’s Disease And Triggers Cell Death In Sh-Sy5y Cells By Upregulation Of L-Type Voltage-Operated Ca2+ Entry
The Interplay Between Cytoskeleton And Calcium Dynamics
Store-Operated Calcium Entry Is Dispensable For The Activation Of Erk1/2 Pathway In Prostate Cancer Cells
The Interplay Between Cytoskeleton And Calcium Dynamics
Store-Operated Calcium Entry Is Dispensable For The Activation Of Erk1/2 Pathway In Prostate Cancer Cells
Regulation Of Membrane Ruffling By Polarized Stim1 And Orai1 In Cortactin-Rich Domains
Store-Operated Calcium Entry Is Dispensable For The Activation Of Erk1/2 Pathway In Prostate Cancer Cells
Regulation Of Membrane Ruffling By Polarized Stim1 And Orai1 In Cortactin-Rich Domains
Phospho-Stim1 Is A Downstream Effector That Mediates The Signaling Triggered By Igf-1 In Hek293 Cells
Regulation Of Membrane Ruffling By Polarized Stim1 And Orai1 In Cortactin-Rich Domains
Phospho-Stim1 Is A Downstream Effector That Mediates The Signaling Triggered By Igf-1 In Hek293 Cells
Stim1 Phosphorylation Triggered By Epidermal Growth Factor Mediates Cell Migration
Phospho-Stim1 Is A Downstream Effector That Mediates The Signaling Triggered By Igf-1 In Hek293 Cells
Stim1 Phosphorylation Triggered By Epidermal Growth Factor Mediates Cell Migration
Thymbra Capitata Essential Oil Prevents Cell Death Induced By 4-Hydroxy-2-Nonenal In Neonatal Rat Cardiac Myocytes
Stim1 Phosphorylation Triggered By Epidermal Growth Factor Mediates Cell Migration
Thymbra Capitata Essential Oil Prevents Cell Death Induced By 4-Hydroxy-2-Nonenal In Neonatal Rat Cardiac Myocytes
Apoptotic Cell Death In Cultured Cardiomyocytes Following Exposure To Low Concentrations Of 4-Hydroxy-2-Nonenal
Thymbra Capitata Essential Oil Prevents Cell Death Induced By 4-Hydroxy-2-Nonenal In Neonatal Rat Cardiac Myocytes
Apoptotic Cell Death In Cultured Cardiomyocytes Following Exposure To Low Concentrations Of 4-Hydroxy-2-Nonenal
Phosphorylation Of Stim1 At Erk1/2 Target Sites Regulates Interaction With The Microtubule Plus-End Binding Protein Eb1
Apoptotic Cell Death In Cultured Cardiomyocytes Following Exposure To Low Concentrations Of 4-Hydroxy-2-Nonenal
Phosphorylation Of Stim1 At Erk1/2 Target Sites Regulates Interaction With The Microtubule Plus-End Binding Protein Eb1
The Regulation Of Stim1 By Phosphorylation
Phosphorylation Of Stim1 At Erk1/2 Target Sites Regulates Interaction With The Microtubule Plus-End Binding Protein Eb1
The Regulation Of Stim1 By Phosphorylation
Inhibition Of Stim1 Phosphorylation Underlies Resveratrol-Induced Inhibition Of Store-Operated Calcium Entry
The Regulation Of Stim1 By Phosphorylation
Inhibition Of Stim1 Phosphorylation Underlies Resveratrol-Induced Inhibition Of Store-Operated Calcium Entry
Intracellular Cyclophilin A Is An Important Ca2+ Regulator In Platelets And Critically Involved In Arterial Thrombus Formation
Inhibition Of Stim1 Phosphorylation Underlies Resveratrol-Induced Inhibition Of Store-Operated Calcium Entry
Intracellular Cyclophilin A Is An Important Ca2+ Regulator In Platelets And Critically Involved In Arterial Thrombus Formation
Extended Embryo Culture Supplementation
Intracellular Cyclophilin A Is An Important Ca2+ Regulator In Platelets And Critically Involved In Arterial Thrombus Formation
Extended Embryo Culture Supplementation
2,3,7,8-Tetrachlorodibenzo-P-Dioxin Induces Apoptosis By Disruption Of Intracellular Calcium Homeostasis In Human Neuronal Cell Line Shsy5y
Extended Embryo Culture Supplementation
2,3,7,8-Tetrachlorodibenzo-P-Dioxin Induces Apoptosis By Disruption Of Intracellular Calcium Homeostasis In Human Neuronal Cell Line Shsy5y
Calcium Signaling In Mouse Oocyte Maturation: The Roles Of Stim1, Orai1 And Soce
2,3,7,8-Tetrachlorodibenzo-P-Dioxin Induces Apoptosis By Disruption Of Intracellular Calcium Homeostasis In Human Neuronal Cell Line Shsy5y
Calcium Signaling In Mouse Oocyte Maturation: The Roles Of Stim1, Orai1 And Soce
Role Of Store-Operated Calcium Entry During Meiotic Progression And Fertilization Of Mammalian Oocytes
Calcium Signaling In Mouse Oocyte Maturation: The Roles Of Stim1, Orai1 And Soce
Role Of Store-Operated Calcium Entry During Meiotic Progression And Fertilization Of Mammalian Oocytes
Inhibition By 4-Hydroxynonenal (Hne) Of Ca2+ Transport By Serca1a: Low Concentrations Of Hne Open Protein-Mediated Leaks In The Membrane
Role Of Store-Operated Calcium Entry During Meiotic Progression And Fertilization Of Mammalian Oocytes
Inhibition By 4-Hydroxynonenal (Hne) Of Ca2+ Transport By Serca1a: Low Concentrations Of Hne Open Protein-Mediated Leaks In The Membrane
Erratum: Inhibition By 4-Hydroxynonenal (Hne) Of Ca2+ Transport By Serca1a: Low Concentrations Of Hne Open Protein-Mediated Leaks In The Membrane (Free Radical Biology & Medicine (2011) 50 (323-336))
Inhibition By 4-Hydroxynonenal (Hne) Of Ca2+ Transport By Serca1a: Low Concentrations Of Hne Open Protein-Mediated Leaks In The Membrane
Erratum: Inhibition By 4-Hydroxynonenal (Hne) Of Ca2+ Transport By Serca1a: Low Concentrations Of Hne Open Protein-Mediated Leaks In The Membrane (Free Radical Biology & Medicine (2011) 50 (323-336))
Inhibition By 4-Hydroxynonenal (Hne) Of Ca 2+ Transport By Serca1a: Low Concentrations Of Hne Open Protein-Mediated Leaks In The Membrane
Erratum: Inhibition By 4-Hydroxynonenal (Hne) Of Ca2+ Transport By Serca1a: Low Concentrations Of Hne Open Protein-Mediated Leaks In The Membrane (Free Radical Biology & Medicine (2011) 50 (323-336))
Inhibition By 4-Hydroxynonenal (Hne) Of Ca 2+ Transport By Serca1a: Low Concentrations Of Hne Open Protein-Mediated Leaks In The Membrane
Phosphorylation Of Stim1 At Erk1/2 Target Sites Modulates Store-Operated Calcium Entry
Inhibition By 4-Hydroxynonenal (Hne) Of Ca 2+ Transport By Serca1a: Low Concentrations Of Hne Open Protein-Mediated Leaks In The Membrane
Phosphorylation Of Stim1 At Erk1/2 Target Sites Modulates Store-Operated Calcium Entry
Role Of Transforming Growth Factor Β In Cancer Microenvironment
Phosphorylation Of Stim1 At Erk1/2 Target Sites Modulates Store-Operated Calcium Entry
Role Of Transforming Growth Factor Β In Cancer Microenvironment
Relocalization Of Stim1 In Mouse Oocytes At Fertilization: Early Involvement Of Store-Operated Calcium Entry
Role Of Transforming Growth Factor Β In Cancer Microenvironment
Relocalization Of Stim1 In Mouse Oocytes At Fertilization: Early Involvement Of Store-Operated Calcium Entry
Clustering Of Plasma Membrane-Bound Cytochrome B5 Reductase Within 'lipid Raft' Microdomains Of The Neuronal Plasma Membrane
Relocalization Of Stim1 In Mouse Oocytes At Fertilization: Early Involvement Of Store-Operated Calcium Entry
Clustering Of Plasma Membrane-Bound Cytochrome B5 Reductase Within 'lipid Raft' Microdomains Of The Neuronal Plasma Membrane
Store-Operated Calcium Entry In Human Oocytes And Sensitivity To Oxidative Stress
Clustering Of Plasma Membrane-Bound Cytochrome B5 Reductase Within 'lipid Raft' Microdomains Of The Neuronal Plasma Membrane
Store-Operated Calcium Entry In Human Oocytes And Sensitivity To Oxidative Stress
Reduction Of Ascorbate Free Radical By The Plasma Membrane Of Synaptic Terminals From Rat Brain
Store-Operated Calcium Entry In Human Oocytes And Sensitivity To Oxidative Stress
Reduction Of Ascorbate Free Radical By The Plasma Membrane Of Synaptic Terminals From Rat Brain
Contribution Of Culture Media To Oxidative Stress And Its Effect On Human Oocytes
Reduction Of Ascorbate Free Radical By The Plasma Membrane Of Synaptic Terminals From Rat Brain
Contribution Of Culture Media To Oxidative Stress And Its Effect On Human Oocytes
Hydrogen Sulfide Raises Cytosolic Calcium In Neurons Through Activation Of L-Type Ca2+ Channels
Contribution Of Culture Media To Oxidative Stress And Its Effect On Human Oocytes
Hydrogen Sulfide Raises Cytosolic Calcium In Neurons Through Activation Of L-Type Ca2+ Channels
Sarcoplasmic Reticulum Calcium Atpase Is Inhibited By Organic Vanadium Coordination Compounds: Pyridine-2,6-Dicarboxylatodioxovanadium(V), Bmov, And An Amavadine Analogue
Hydrogen Sulfide Raises Cytosolic Calcium In Neurons Through Activation Of L-Type Ca2+ Channels
Sarcoplasmic Reticulum Calcium Atpase Is Inhibited By Organic Vanadium Coordination Compounds: Pyridine-2,6-Dicarboxylatodioxovanadium(V), Bmov, And An Amavadine Analogue
Vanadate Induces Necrotic Death In Neonatal Rat Cardiomyocytes Through Mitochondrial Membrane Depolarization
Sarcoplasmic Reticulum Calcium Atpase Is Inhibited By Organic Vanadium Coordination Compounds: Pyridine-2,6-Dicarboxylatodioxovanadium(V), Bmov, And An Amavadine Analogue
Vanadate Induces Necrotic Death In Neonatal Rat Cardiomyocytes Through Mitochondrial Membrane Depolarization
Blood Micromolar Concentrations Of Kaempferol Afford Protection Against Ischemia/reperfusion-Induced Damage In Rat Brain
Vanadate Induces Necrotic Death In Neonatal Rat Cardiomyocytes Through Mitochondrial Membrane Depolarization
Blood Micromolar Concentrations Of Kaempferol Afford Protection Against Ischemia/reperfusion-Induced Damage In Rat Brain
Regionalization Of Plasma Membrane-Bound Flavoproteins Of Cerebellar Granule Neurons In Culture By Fluorescence Energy Transfer Imaging
Blood Micromolar Concentrations Of Kaempferol Afford Protection Against Ischemia/reperfusion-Induced Damage In Rat Brain
Regionalization Of Plasma Membrane-Bound Flavoproteins Of Cerebellar Granule Neurons In Culture By Fluorescence Energy Transfer Imaging
Inhibition Of Skeletal Muscle S1-Myosin Atpase By Peroxynitrite
Regionalization Of Plasma Membrane-Bound Flavoproteins Of Cerebellar Granule Neurons In Culture By Fluorescence Energy Transfer Imaging
Inhibition Of Skeletal Muscle S1-Myosin Atpase By Peroxynitrite
Transfemoral Selective Intraluminal Wiring Technique For Transient Middle Cerebral Artery Occlusion In Rats
Inhibition Of Skeletal Muscle S1-Myosin Atpase By Peroxynitrite
Transfemoral Selective Intraluminal Wiring Technique For Transient Middle Cerebral Artery Occlusion In Rats
Store-Operated Calcium Entry In Differentiated C2c12 Skeletal Muscle Cells
Transfemoral Selective Intraluminal Wiring Technique For Transient Middle Cerebral Artery Occlusion In Rats
Store-Operated Calcium Entry In Differentiated C2c12 Skeletal Muscle Cells
Alteration Of Cytosolic Free Calcium Homeostasis By Sin-1: High Sensitivity Of L-Type Ca2+ Channels To Extracellular Oxidative/nitrosative Stress In Cerebellar Granule Cells
Store-Operated Calcium Entry In Differentiated C2c12 Skeletal Muscle Cells
Alteration Of Cytosolic Free Calcium Homeostasis By Sin-1: High Sensitivity Of L-Type Ca2+ Channels To Extracellular Oxidative/nitrosative Stress In Cerebellar Granule Cells
Modulation Of Sarcoplasmic Reticulum Ca2+-Atpase By Chronic And Acute Exposure To Peroxynitrite
Alteration Of Cytosolic Free Calcium Homeostasis By Sin-1: High Sensitivity Of L-Type Ca2+ Channels To Extracellular Oxidative/nitrosative Stress In Cerebellar Granule Cells
Modulation Of Sarcoplasmic Reticulum Ca2+-Atpase By Chronic And Acute Exposure To Peroxynitrite
Kaempferol Blocks Oxidative Stress In Cerebellar Granule Cells And Reveals A Key Role For Reactive Oxygen Species Production At The Plasma Membrane In The Commitment To Apoptosis
Modulation Of Sarcoplasmic Reticulum Ca2+-Atpase By Chronic And Acute Exposure To Peroxynitrite
Kaempferol Blocks Oxidative Stress In Cerebellar Granule Cells And Reveals A Key Role For Reactive Oxygen Species Production At The Plasma Membrane In The Commitment To Apoptosis
Fluorescence Measurements Of Steady State Peroxynitrite Production Upon Sin-1 Decomposition: Nadh Versus Dihydrodichlorofluorescein And Dihydrorhodamine 123
Kaempferol Blocks Oxidative Stress In Cerebellar Granule Cells And Reveals A Key Role For Reactive Oxygen Species Production At The Plasma Membrane In The Commitment To Apoptosis
Fluorescence Measurements Of Steady State Peroxynitrite Production Upon Sin-1 Decomposition: Nadh Versus Dihydrodichlorofluorescein And Dihydrorhodamine 123
Inhibition Of Mouth Skeletal Muscle Relaxation By Flavonoids Of Cistus Ladanifer L.: A Plant Defense Mechanism Against Herbivores
Fluorescence Measurements Of Steady State Peroxynitrite Production Upon Sin-1 Decomposition: Nadh Versus Dihydrodichlorofluorescein And Dihydrorhodamine 123
Inhibition Of Mouth Skeletal Muscle Relaxation By Flavonoids Of Cistus Ladanifer L.: A Plant Defense Mechanism Against Herbivores
The Drosophila Selenoprotein Bthd Is Required For Survival And Has A Role In Salivary Gland Development
Inhibition Of Mouth Skeletal Muscle Relaxation By Flavonoids Of Cistus Ladanifer L.: A Plant Defense Mechanism Against Herbivores
The Drosophila Selenoprotein Bthd Is Required For Survival And Has A Role In Salivary Gland Development
Projection Map Of Covalently Phosphorylated Ca-Atpase From Tubular Crystals
The Drosophila Selenoprotein Bthd Is Required For Survival And Has A Role In Salivary Gland Development
Projection Map Of Covalently Phosphorylated Ca-Atpase From Tubular Crystals
Inhibition Of Oxidative Stress Produced By Plasma Membrane Nadh Oxidase Delays Low-Potassium-Induced Apoptosis Of Cerebellar Granule Cells
Projection Map Of Covalently Phosphorylated Ca-Atpase From Tubular Crystals
Inhibition Of Oxidative Stress Produced By Plasma Membrane Nadh Oxidase Delays Low-Potassium-Induced Apoptosis Of Cerebellar Granule Cells
The Nadh Oxidase Activity Of The Plasma Membrane Of Synaptosomes Is A Major Source Of Superoxide Anion And Is Inhibited By Peroxynitrite
Inhibition Of Oxidative Stress Produced By Plasma Membrane Nadh Oxidase Delays Low-Potassium-Induced Apoptosis Of Cerebellar Granule Cells
The Nadh Oxidase Activity Of The Plasma Membrane Of Synaptosomes Is A Major Source Of Superoxide Anion And Is Inhibited By Peroxynitrite
Synaptosomal Plasma Membrane Ca2+ Pump Activity Inhibition By Repetitive Micromolar Onoo- Pulses
The Nadh Oxidase Activity Of The Plasma Membrane Of Synaptosomes Is A Major Source Of Superoxide Anion And Is Inhibited By Peroxynitrite
Synaptosomal Plasma Membrane Ca2+ Pump Activity Inhibition By Repetitive Micromolar Onoo- Pulses
Selenium Metabolism In Drosophila. Selenoproteins, Selenoprotein Mrna Expression, Fertility, And Mortality
Synaptosomal Plasma Membrane Ca2+ Pump Activity Inhibition By Repetitive Micromolar Onoo- Pulses
Selenium Metabolism In Drosophila. Selenoproteins, Selenoprotein Mrna Expression, Fertility, And Mortality
The Content Of Glycogen Phosphorylase And Glycogen In Preparations Of Sarcoplasmic Reticulum - Glycogenolytic Complex Is Enhanced In Diabetic Rat Skeletal Muscle
Selenium Metabolism In Drosophila. Selenoproteins, Selenoprotein Mrna Expression, Fertility, And Mortality
The Content Of Glycogen Phosphorylase And Glycogen In Preparations Of Sarcoplasmic Reticulum - Glycogenolytic Complex Is Enhanced In Diabetic Rat Skeletal Muscle
Phosphorylated Ca2+-Atpase Stable Enough For Structural Studies
The Content Of Glycogen Phosphorylase And Glycogen In Preparations Of Sarcoplasmic Reticulum - Glycogenolytic Complex Is Enhanced In Diabetic Rat Skeletal Muscle
Phosphorylated Ca2+-Atpase Stable Enough For Structural Studies
A Remarkably Stable Phosphorylated Form Of Ca2+-Atpase Prepared From Ca2+-Loaded And Fluorescein Isothiocyanate-Labeled Sarcoplasmic Reticulum Vesicles
Phosphorylated Ca2+-Atpase Stable Enough For Structural Studies
A Remarkably Stable Phosphorylated Form Of Ca2+-Atpase Prepared From Ca2+-Loaded And Fluorescein Isothiocyanate-Labeled Sarcoplasmic Reticulum Vesicles
Potassium-Induced Apoptosis In Rat Cerebellar Granule Cells Involves Cell-Cycle Blockade At The G1/s Transition
A Remarkably Stable Phosphorylated Form Of Ca2+-Atpase Prepared From Ca2+-Loaded And Fluorescein Isothiocyanate-Labeled Sarcoplasmic Reticulum Vesicles
Potassium-Induced Apoptosis In Rat Cerebellar Granule Cells Involves Cell-Cycle Blockade At The G1/s Transition
Plausible Stoichiometry Of The Interacting Nucleotide-Binding Sites In The Ca2+-Atpase From Sarcoplasmic Reticulum Membranes
Potassium-Induced Apoptosis In Rat Cerebellar Granule Cells Involves Cell-Cycle Blockade At The G1/s Transition
Plausible Stoichiometry Of The Interacting Nucleotide-Binding Sites In The Ca2+-Atpase From Sarcoplasmic Reticulum Membranes
Characterization Of A Protease-Resistant Domain Of The Cytosolic Portion Of Sarcoplasmic Reticulum Ca2+-Atpase. Nucleotide- And Metal-Binding Sites
Plausible Stoichiometry Of The Interacting Nucleotide-Binding Sites In The Ca2+-Atpase From Sarcoplasmic Reticulum Membranes
Characterization Of A Protease-Resistant Domain Of The Cytosolic Portion Of Sarcoplasmic Reticulum Ca2+-Atpase. Nucleotide- And Metal-Binding Sites
Dissociation Of Ca2+ From Sarcoplasmic Reticulum Ca2+-Atpase And Changes In Fluorescence Of Optically Selected Trp Residues. Effects Of Kcl And Nacl And Implications For Substeps In Ca2+ Dissociation
Characterization Of A Protease-Resistant Domain Of The Cytosolic Portion Of Sarcoplasmic Reticulum Ca2+-Atpase. Nucleotide- And Metal-Binding Sites
Dissociation Of Ca2+ From Sarcoplasmic Reticulum Ca2+-Atpase And Changes In Fluorescence Of Optically Selected Trp Residues. Effects Of Kcl And Nacl And Implications For Substeps In Ca2+ Dissociation
Structural Changes Of The Sarcoplasmic Reticulum Ca(Ii)-Atpase Nucleotide Binding Domain By Ph And La(Iii)
Dissociation Of Ca2+ From Sarcoplasmic Reticulum Ca2+-Atpase And Changes In Fluorescence Of Optically Selected Trp Residues. Effects Of Kcl And Nacl And Implications For Substeps In Ca2+ Dissociation
Structural Changes Of The Sarcoplasmic Reticulum Ca(Ii)-Atpase Nucleotide Binding Domain By Ph And La(Iii)
Ca2+ Uptake Coupled To Glycogen Phosphorolysis In The Glycogenolytic-Sarcoplasmic Reticulum Complex From Rat Skeletal Muscle
Structural Changes Of The Sarcoplasmic Reticulum Ca(Ii)-Atpase Nucleotide Binding Domain By Ph And La(Iii)
Ca2+ Uptake Coupled To Glycogen Phosphorolysis In The Glycogenolytic-Sarcoplasmic Reticulum Complex From Rat Skeletal Muscle
Involvement Of Free Radicals In Signalling Of Low-Potassium Induced Apoptosis In Cultured Cerebellar Granule Cells.
Ca2+ Uptake Coupled To Glycogen Phosphorolysis In The Glycogenolytic-Sarcoplasmic Reticulum Complex From Rat Skeletal Muscle
Involvement Of Free Radicals In Signalling Of Low-Potassium Induced Apoptosis In Cultured Cerebellar Granule Cells.
Inactivation Of Ecto-Atpase Activity Of Rat Brain Synaptosomes
Involvement Of Free Radicals In Signalling Of Low-Potassium Induced Apoptosis In Cultured Cerebellar Granule Cells.
Inactivation Of Ecto-Atpase Activity Of Rat Brain Synaptosomes
Fluorescnece Anisotropy Of Fluorescein Phosphatidylethanolthiocarbamide In Lipid Bilayers And In Ca2+-Atpase/lipid Reconstituted Systems
Inactivation Of Ecto-Atpase Activity Of Rat Brain Synaptosomes
Fluorescnece Anisotropy Of Fluorescein Phosphatidylethanolthiocarbamide In Lipid Bilayers And In Ca2+-Atpase/lipid Reconstituted Systems
Interaction Between Glycogen Phosphorylase And Sarcoplasmic Reticulum Membranes And Its Functional Implications
Fluorescnece Anisotropy Of Fluorescein Phosphatidylethanolthiocarbamide In Lipid Bilayers And In Ca2+-Atpase/lipid Reconstituted Systems
Interaction Between Glycogen Phosphorylase And Sarcoplasmic Reticulum Membranes And Its Functional Implications
Intrasynaptosomal Free Mg2+ Concentration Measured With The Fluorescent Indicator Mag-Fura-2: Modulation By Na+ Gradient And By Extrasynaptosomal Atp
Interaction Between Glycogen Phosphorylase And Sarcoplasmic Reticulum Membranes And Its Functional Implications
Intrasynaptosomal Free Mg2+ Concentration Measured With The Fluorescent Indicator Mag-Fura-2: Modulation By Na+ Gradient And By Extrasynaptosomal Atp
Quantification And Removal Of Glycogen Phosphorylase And Other Enzymes Associated With Sarcoplasmic Reticulum Membrane Preparations
Intrasynaptosomal Free Mg2+ Concentration Measured With The Fluorescent Indicator Mag-Fura-2: Modulation By Na+ Gradient And By Extrasynaptosomal Atp
Quantification And Removal Of Glycogen Phosphorylase And Other Enzymes Associated With Sarcoplasmic Reticulum Membrane Preparations
Cancellation Of The Cooperativity Of Ca2+ Binding To Sarcoplasmic Reticulum Ca2+‐atpase By The Non‐ionic Detergent Dodecylmaltoside
Quantification And Removal Of Glycogen Phosphorylase And Other Enzymes Associated With Sarcoplasmic Reticulum Membrane Preparations
Cancellation Of The Cooperativity Of Ca2+ Binding To Sarcoplasmic Reticulum Ca2+‐atpase By The Non‐ionic Detergent Dodecylmaltoside
The Metal Sites On Sarcoplasmic Reticulum Membranes That Bind Lanthanide Ions With The Highest Affinity Are Not The Atpase Ca2+ Transport Sites
Cancellation Of The Cooperativity Of Ca2+ Binding To Sarcoplasmic Reticulum Ca2+‐atpase By The Non‐ionic Detergent Dodecylmaltoside
The Metal Sites On Sarcoplasmic Reticulum Membranes That Bind Lanthanide Ions With The Highest Affinity Are Not The Atpase Ca2+ Transport Sites
Binding Of Gadolinium Ions To Sarcoplasmic Reticulum Membranes
The Metal Sites On Sarcoplasmic Reticulum Membranes That Bind Lanthanide Ions With The Highest Affinity Are Not The Atpase Ca2+ Transport Sites
Binding Of Gadolinium Ions To Sarcoplasmic Reticulum Membranes
Kinetic Characterization Of The Perturbation By Dodecylmaltoside Of Sarcoplasmic Reticulum Ca2+ ‐atpase
Binding Of Gadolinium Ions To Sarcoplasmic Reticulum Membranes
Kinetic Characterization Of The Perturbation By Dodecylmaltoside Of Sarcoplasmic Reticulum Ca2+ ‐atpase
Kinetic Characterization Of The Normal And Procaine‐perturbed Reaction Cycles Of The Sarcoplasmic Reticulum Calcium Pump
Kinetic Characterization Of The Perturbation By Dodecylmaltoside Of Sarcoplasmic Reticulum Ca2+ ‐atpase
Kinetic Characterization Of The Normal And Procaine‐perturbed Reaction Cycles Of The Sarcoplasmic Reticulum Calcium Pump
Modulation Of The Sarcoplasmic Reticulum (Ca2+ + Mg2+)-Atpase By Pentobarbital
Kinetic Characterization Of The Normal And Procaine‐perturbed Reaction Cycles Of The Sarcoplasmic Reticulum Calcium Pump
Modulation Of The Sarcoplasmic Reticulum (Ca2+ + Mg2+)-Atpase By Pentobarbital
Distances Between Functional Sites Of The Ca2++ Mg2+‐atpase From Sarcoplasmic Reticulum Using Co2+ As A Spectroscopic Ruler
Modulation Of The Sarcoplasmic Reticulum (Ca2+ + Mg2+)-Atpase By Pentobarbital
Distances Between Functional Sites Of The Ca2++ Mg2+‐atpase From Sarcoplasmic Reticulum Using Co2+ As A Spectroscopic Ruler
Inhibition Of The Sarcoplasmic Reticulum (Ca2+ + Mg2+-Atpase By Zn(Ii)
Distances Between Functional Sites Of The Ca2++ Mg2+‐atpase From Sarcoplasmic Reticulum Using Co2+ As A Spectroscopic Ruler
Inhibition Of The Sarcoplasmic Reticulum (Ca2+ + Mg2+-Atpase By Zn(Ii)
A Subset Of Orai1α And Orai1β Subunits Heteromerizes To Form Crac Channels
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