PUBLICACIÓN

Selected peptides targeted to the NMDA receptor channel protect neurons from excitotoxic death

ACCEDER A LA PUBLICACIÓN: Scopus Orcid

Ferrer-Montiel, A.V., Merino, J.M., Blondelle, S.E., Perez-Payà, E., Houghten, R.A., Montal, M.

1998 Nature Biotechnology

CITAS

42

DOI

10.1038/nbt0398-286

EID

2-s2.0-0031934090

ISSN

1087-0156

BIBTEX

@article{Merino1998,title = {Selected peptides targeted to the NMDA receptor channel protect neurons from excitotoxic death},journal = {Nature Biotechnology},year = {1998},volume = {16},number = {3},pages = {286-291},author = {Ferrer-Montiel, A.V. and Merino, J.M. and Blondelle, S.E. and Perez-Pay{\`a}, E. and Houghten, R.A. and Montal, M.}}

AUTORES DE LA UEX

Jaime María Merino Fernández

OTRAS PUBLICACIONES DE INTERÉS

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Involvement Of Β-Catenin Expression In Hepatocellular Carcinoma Prognosis In A Cohort Of Patients Undergoing Curative Treatment
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Involvement Of Β-Catenin Expression In Hepatocellular Carcinoma Prognosis In A Cohort Of Patients Undergoing Curative Treatment
Involvement Of Β-Catenin Expression In Hepatocellular Carcinoma Prognosis In A Cohort Of Patients Undergoing Curative Treatment.
From Nucleus To Organs: Insights Of Aryl Hydrocarbon Receptor Molecular Mechanisms
Involvement Of Β-Catenin Expression In Hepatocellular Carcinoma Prognosis In A Cohort Of Patients Undergoing Curative Treatment.
From Nucleus To Organs: Insights Of Aryl Hydrocarbon Receptor Molecular Mechanisms
Liver Regeneration After Partial Hepatectomy Is Improved In The Absence Of Aryl Hydrocarbon Receptor
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Liver Regeneration After Partial Hepatectomy Is Improved In The Absence Of Aryl Hydrocarbon Receptor
Aryl Hydrocarbon Receptor: From Homeostasis To Tumor Progression
Liver Regeneration After Partial Hepatectomy Is Improved In The Absence Of Aryl Hydrocarbon Receptor
Aryl Hydrocarbon Receptor: From Homeostasis To Tumor Progression
Aryl Hydrocarbon Receptor Blocks Aging-Induced Senescence In The Liver And Fibroblast Cells
Aryl Hydrocarbon Receptor: From Homeostasis To Tumor Progression
Aryl Hydrocarbon Receptor Blocks Aging-Induced Senescence In The Liver And Fibroblast Cells
The Aryl Hydrocarbon Receptor Promotes Differentiation During Mouse Preimplantational Embryo Development
Aryl Hydrocarbon Receptor Blocks Aging-Induced Senescence In The Liver And Fibroblast Cells
The Aryl Hydrocarbon Receptor Promotes Differentiation During Mouse Preimplantational Embryo Development
Loss Of Aryl Hydrocarbon Receptor Favors K-Rasg12d-Driven Non-Small Cell Lung Cancer
The Aryl Hydrocarbon Receptor Promotes Differentiation During Mouse Preimplantational Embryo Development
Loss Of Aryl Hydrocarbon Receptor Favors K-Rasg12d-Driven Non-Small Cell Lung Cancer
Aryl Hydrocarbon Receptor Controls Skin Homeostasis, Regeneration, And Hair Follicle Cycling By Adjusting Epidermal Stem Cell Function
Loss Of Aryl Hydrocarbon Receptor Favors K-Rasg12d-Driven Non-Small Cell Lung Cancer
Aryl Hydrocarbon Receptor Controls Skin Homeostasis, Regeneration, And Hair Follicle Cycling By Adjusting Epidermal Stem Cell Function
Alu Retrotransposons Modulate Nanog Expression Through Dynamic Changes In Regional Chromatin Conformation Via Aryl Hydrocarbon Receptor
Aryl Hydrocarbon Receptor Controls Skin Homeostasis, Regeneration, And Hair Follicle Cycling By Adjusting Epidermal Stem Cell Function
Alu Retrotransposons Modulate Nanog Expression Through Dynamic Changes In Regional Chromatin Conformation Via Aryl Hydrocarbon Receptor
Aryl Hydrocarbon Receptor Promotes Liver Polyploidization And Inhibits Pi3k, Erk, And Wnt/β-Catenin Signaling
Alu Retrotransposons Modulate Nanog Expression Through Dynamic Changes In Regional Chromatin Conformation Via Aryl Hydrocarbon Receptor
Aryl Hydrocarbon Receptor Promotes Liver Polyploidization And Inhibits Pi3k, Erk, And Wnt/β-Catenin Signaling
The Aryl Hydrocarbon Receptor In The Crossroad Of Signalling Networks With Therapeutic Value
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The Aryl Hydrocarbon Receptor In The Crossroad Of Signalling Networks With Therapeutic Value
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The Aryl Hydrocarbon Receptor In The Crossroad Of Signalling Networks With Therapeutic Value
The Aryl Hydrocarbon Receptor In The Crossroad Of Signalling Networks With Therapeutic Value.
Lung Regeneration After Toxic Injury Is Improved In Absence Of Dioxin Receptor
The Aryl Hydrocarbon Receptor In The Crossroad Of Signalling Networks With Therapeutic Value.
Lung Regeneration After Toxic Injury Is Improved In Absence Of Dioxin Receptor
Dioxin Receptor Adjusts Liver Regeneration After Acute Toxic Injury And Protects Against Liver Carcinogenesis
Lung Regeneration After Toxic Injury Is Improved In Absence Of Dioxin Receptor
Dioxin Receptor Adjusts Liver Regeneration After Acute Toxic Injury And Protects Against Liver Carcinogenesis
Pirna-Associated Proteins And Retrotransposons Are Differentially Expressed In Murine Testis And Ovary Of Aryl Hydrocarbon Receptor Deficient Mice
Dioxin Receptor Adjusts Liver Regeneration After Acute Toxic Injury And Protects Against Liver Carcinogenesis
Pirna-Associated Proteins And Retrotransposons Are Differentially Expressed In Murine Testis And Ovary Of Aryl Hydrocarbon Receptor Deficient Mice
Ahr-Dependent 2,3,7,8-Tetrachlorodibenzo-P-Dioxin Toxicity In Human Neuronal Cell Line Shsy5y
Pirna-Associated Proteins And Retrotransposons Are Differentially Expressed In Murine Testis And Ovary Of Aryl Hydrocarbon Receptor Deficient Mice
Ahr-Dependent 2,3,7,8-Tetrachlorodibenzo-P-Dioxin Toxicity In Human Neuronal Cell Line Shsy5y
Alu Retrotransposons Promote Differentiation Of Human Carcinoma Cells Through The Aryl Hydrocarbon Receptor
Ahr-Dependent 2,3,7,8-Tetrachlorodibenzo-P-Dioxin Toxicity In Human Neuronal Cell Line Shsy5y
Alu Retrotransposons Promote Differentiation Of Human Carcinoma Cells Through The Aryl Hydrocarbon Receptor
Dioxin Receptor Regulates Aldehyde Dehydrogenase To Block Melanoma Tumorigenesis And Metastasis
Alu Retrotransposons Promote Differentiation Of Human Carcinoma Cells Through The Aryl Hydrocarbon Receptor
Dioxin Receptor Regulates Aldehyde Dehydrogenase To Block Melanoma Tumorigenesis And Metastasis
2,3,7,8-Tetrachlorodibenzo-P-Dioxin Induces Apoptosis By Disruption Of Intracellular Calcium Homeostasis In Human Neuronal Cell Line Shsy5y
Dioxin Receptor Regulates Aldehyde Dehydrogenase To Block Melanoma Tumorigenesis And Metastasis
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The Ahr Regulates Cell Adhesion And Migration By Interacting With Oncogene And Growth Factor-Dependent Signaling
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The Ahr Regulates Cell Adhesion And Migration By Interacting With Oncogene And Growth Factor-Dependent Signaling
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The Ahr Regulates Cell Adhesion And Migration By Interacting With Oncogene And Growth Factor-Dependent Signaling
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Small Peptides Patterned After The N-Terminus Domain Of Snap25 Inhibit Snare Complex Assembly And Regulated Exocytosis
Down-Regulation Of Cyp1a2 Induction During The Maturation Of Mouse Cerebellar Granule Cells In Culture: Role Of Nitric Oxide Accumulation
Identification Of Snare Complex Modulators That Inhibit Exocytosis From An Α-Helix-Constrained Combinatorial Library
Down-Regulation Of Cyp1a2 Induction During The Maturation Of Mouse Cerebellar Granule Cells In Culture: Role Of Nitric Oxide Accumulation
Identification Of Snare Complex Modulators That Inhibit Exocytosis From An Α-Helix-Constrained Combinatorial Library
Neuroprotection Against Excitotoxicity By N-Alkylglycines In Rat Hippocampal Neurons
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A Novel N-Methyl-D-Aspartate Receptor Open Channel Blocker With In Vivo Neuroprotectant Activity
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Identification Of An Aspartic Residue In The P-Loop Of The Vanilloid Receptor That Modulates Pore Properties
Arginine-Rich Peptides Are Blockers Of Vr-1 Channels With Analgesic Activity
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Arginine-Rich Peptides Are Blockers Of Vr-1 Channels With Analgesic Activity
Ph And Ligand Binding Modulate The Strength Of Protein-Protein Interactions In The Ca2+-Atpase From Sarcoplasmic Reticulum Membranes
Arginine-Rich Peptides Are Blockers Of Vr-1 Channels With Analgesic Activity
Ph And Ligand Binding Modulate The Strength Of Protein-Protein Interactions In The Ca2+-Atpase From Sarcoplasmic Reticulum Membranes
Plausible Stoichiometry Of The Interacting Nucleotide-Binding Sites In The Ca2+-Atpase From Sarcoplasmic Reticulum Membranes
Ph And Ligand Binding Modulate The Strength Of Protein-Protein Interactions In The Ca2+-Atpase From Sarcoplasmic Reticulum Membranes
Plausible Stoichiometry Of The Interacting Nucleotide-Binding Sites In The Ca2+-Atpase From Sarcoplasmic Reticulum Membranes
Selected Peptides Targeted To The Nmda Receptor Channel Protect Neurons From Excitotoxic Death
Plausible Stoichiometry Of The Interacting Nucleotide-Binding Sites In The Ca2+-Atpase From Sarcoplasmic Reticulum Membranes
Selected Peptides Targeted To The Nmda Receptor Channel Protect Neurons From Excitotoxic Death
Structural Determinants Of The Blocker Binding Site In Glutamate And Nmda Receptor Channels
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Structural Determinants Of The Blocker Binding Site In Glutamate And Nmda Receptor Channels
Structural Changes Of The Sarcoplasmic Reticulum Ca(Ii)-Atpase Nucleotide Binding Domain By Ph And La(Iii)
Structural Determinants Of The Blocker Binding Site In Glutamate And Nmda Receptor Channels
Structural Changes Of The Sarcoplasmic Reticulum Ca(Ii)-Atpase Nucleotide Binding Domain By Ph And La(Iii)
Estudio Sobre Relaciones Estructura-Función En La Ca2+,mg2+-Atpasa Del Retículo Sarcoplásmico Del Músculo Esquelético
Structural Changes Of The Sarcoplasmic Reticulum Ca(Ii)-Atpase Nucleotide Binding Domain By Ph And La(Iii)
Estudio Sobre Relaciones Estructura-Función En La Ca2+,mg2+-Atpasa Del Retículo Sarcoplásmico Del Músculo Esquelético
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Estudio Sobre Relaciones Estructura-Función En La Ca2+,mg2+-Atpasa Del Retículo Sarcoplásmico Del Músculo Esquelético
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Thermal Unfolding Of Monomeric Ca(Ii),mg(Ii)-Atpase From Sarcoplasmic Reticulum Of Rabbit Skeletal Muscle
Mg2+-Adp Protects Against Inactivation Of Sarcoplasmic Reticulum Ca2+, Mg2+-Atpase By N-Cyclohexyl-N′-(4-Dimethylamino-Α-Naphthyl) Carbodiimide
Thermal Unfolding Of Monomeric Ca(Ii),mg(Ii)-Atpase From Sarcoplasmic Reticulum Of Rabbit Skeletal Muscle
Fluorescence Energy Transfer As A Tool To Locate Functional Sites In Membrane Proteins
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Fluorescence Energy Transfer As A Tool To Locate Functional Sites In Membrane Proteins
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