PUBLICACIÓN

Autophagy is required for the activation of NFκB

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ACCEDER A LA PUBLICACIÓN: Scopus Orcid

Criollo, A.; Chereau, F.; Malik, S.A.; Niso-Santano, M.; Mariño, G.; Galluzzi, L.; Maiuri, M.C.; Baud, V.; Kroemer, G.

2012 CELL CYCLE

Cell Biology (Q1), Developmental Biology (Q1), Medicine (miscellaneous) (Q1), Molecular Biology (Q1)

JCR: 5.321

SJR: 2.43

CITAS

96

DOI

10.4161/cc.11.1.18669

EID

2-s2.0-84855698457

ISSN

1538-4101

EISSN

1551-4005

BIBTEX

@article{Niso-Santano2012,title = {Autophagy is required for the activation of NF?B},journal = {Cell Cycle},year = {2012},volume = {11},number = {1},pages = {194-199},author = {Criollo, A. and Chereau, F. and Malik, S.A. and Niso-Santano, M. and Mari{\~n}o, G. and Galluzzi, L. and Maiuri, M.C. and Baud, V. and Kroemer, G.}}

AUTORES DE LA UEX

Mireia Niso Santano

OTRAS PUBLICACIONES DE INTERÉS

Paraquat-Induced Apoptotic Cell Death In Cerebellar Granule Cells
Immunological Aspects Of Central Neurodegeneration
Role Of Tfeb In Huntington’s Disease
Immunological Aspects Of Central Neurodegeneration
Role Of Tfeb In Huntington’s Disease
Links Between Paraquat And Parkinson’s Disease
Role Of Tfeb In Huntington’s Disease
Links Between Paraquat And Parkinson’s Disease
Neuroprotective Properties Of Queen Bee Acid By Autophagy Induction
Links Between Paraquat And Parkinson’s Disease
Neuroprotective Properties Of Queen Bee Acid By Autophagy Induction
Changes In Liver Lipidomic Profile In G2019s-Lrrk2 Mouse Model Of Parkinson’s Disease
Neuroprotective Properties Of Queen Bee Acid By Autophagy Induction
Changes In Liver Lipidomic Profile In G2019s-Lrrk2 Mouse Model Of Parkinson’s Disease
The Parkinsonian Lrrk2 R1441g Mutation Shows Macroautophagy-Mitophagy Dysregulation Concomitant With Endoplasmic Reticulum Stress
Changes In Liver Lipidomic Profile In G2019s-Lrrk2 Mouse Model Of Parkinson’s Disease
The Parkinsonian Lrrk2 R1441g Mutation Shows Macroautophagy-Mitophagy Dysregulation Concomitant With Endoplasmic Reticulum Stress
Loss Of Keap1 Causes An Accumulation Of Nondegradative Organelles
The Parkinsonian Lrrk2 R1441g Mutation Shows Macroautophagy-Mitophagy Dysregulation Concomitant With Endoplasmic Reticulum Stress
Loss Of Keap1 Causes An Accumulation Of Nondegradative Organelles
In Vitro And In Vivo Models To Study The Biological And Pharmacological Properties Of Queen Bee Acid (Qba, 10-Hydroxy-2-Decenoic Acid): A Systematic Review
Loss Of Keap1 Causes An Accumulation Of Nondegradative Organelles
In Vitro And In Vivo Models To Study The Biological And Pharmacological Properties Of Queen Bee Acid (Qba, 10-Hydroxy-2-Decenoic Acid): A Systematic Review
Biological Effects Of Olive Oil Phenolic Compounds On Mitochondria
In Vitro And In Vivo Models To Study The Biological And Pharmacological Properties Of Queen Bee Acid (Qba, 10-Hydroxy-2-Decenoic Acid): A Systematic Review
Biological Effects Of Olive Oil Phenolic Compounds On Mitochondria
Neuroprotective And Anti-Inflammatory Effects Of Linoleic Acid In Models Of Parkinson’s Disease: The Implication Of Lipid Droplets And Lipophagy
Biological Effects Of Olive Oil Phenolic Compounds On Mitochondria
Neuroprotective And Anti-Inflammatory Effects Of Linoleic Acid In Models Of Parkinson’s Disease: The Implication Of Lipid Droplets And Lipophagy
Delay Of Egf-Stimulated Egfr Degradation In Myotonic Dystrophy Type 1 (Dm1)
Neuroprotective And Anti-Inflammatory Effects Of Linoleic Acid In Models Of Parkinson’s Disease: The Implication Of Lipid Droplets And Lipophagy
Delay Of Egf-Stimulated Egfr Degradation In Myotonic Dystrophy Type 1 (Dm1)
Guidelines For The Use And Interpretation Of Assays For Monitoring Autophagy (4th Edition)1
Delay Of Egf-Stimulated Egfr Degradation In Myotonic Dystrophy Type 1 (Dm1)
Guidelines For The Use And Interpretation Of Assays For Monitoring Autophagy (4th Edition)1
Metabolic Alterations In Plasma From Patients With Familial And Idiopathic Parkinson's Disease
Guidelines For The Use And Interpretation Of Assays For Monitoring Autophagy (4th Edition)1
Metabolic Alterations In Plasma From Patients With Familial And Idiopathic Parkinson's Disease
Toxicity Of Necrostatin-1 In Parkinson’s Disease Models
Metabolic Alterations In Plasma From Patients With Familial And Idiopathic Parkinson's Disease
Toxicity Of Necrostatin-1 In Parkinson’s Disease Models
The Paradigm Of Protein Acetylation In Parkinson's Disease
Toxicity Of Necrostatin-1 In Parkinson’s Disease Models
The Paradigm Of Protein Acetylation In Parkinson's Disease
Impaired Mitophagy And Protein Acetylation Levels In Fibroblasts From Parkinson’s Disease Patients
The Paradigm Of Protein Acetylation In Parkinson's Disease
Impaired Mitophagy And Protein Acetylation Levels In Fibroblasts From Parkinson’s Disease Patients
Erratum: Acyl-Coa-Binding Protein Is A Lipogenic Factor That Triggers Food Intake And Obesity (Cell Metabolism (2019) 30(4) (754–767.e9), (S1550413119303833), (10.1016/j.cmet.2019.07.010))
Impaired Mitophagy And Protein Acetylation Levels In Fibroblasts From Parkinson’s Disease Patients
Erratum: Acyl-Coa-Binding Protein Is A Lipogenic Factor That Triggers Food Intake And Obesity (Cell Metabolism (2019) 30(4) (754–767.e9), (S1550413119303833), (10.1016/j.cmet.2019.07.010))
Acyl-Coa-Binding Protein Is A Lipogenic Factor That Triggers Food Intake And Obesity
Erratum: Acyl-Coa-Binding Protein Is A Lipogenic Factor That Triggers Food Intake And Obesity (Cell Metabolism (2019) 30(4) (754–767.e9), (S1550413119303833), (10.1016/j.cmet.2019.07.010))
Acyl-Coa-Binding Protein Is A Lipogenic Factor That Triggers Food Intake And Obesity
Acetylome In Human Fibroblasts From Parkinson’s Disease Patients
Acyl-Coa-Binding Protein Is A Lipogenic Factor That Triggers Food Intake And Obesity
Acetylome In Human Fibroblasts From Parkinson’s Disease Patients
Er-Mitochondria Signaling In Parkinson's Disease Review-Article
Acetylome In Human Fibroblasts From Parkinson’s Disease Patients
Er-Mitochondria Signaling In Parkinson's Disease Review-Article
Mitochondria-Associated Membranes (Mams): Overview And Its Role In Parkinson’s Disease
Er-Mitochondria Signaling In Parkinson's Disease Review-Article
Mitochondria-Associated Membranes (Mams): Overview And Its Role In Parkinson’s Disease
Turnover Of Lipidated Lc3 And Autophagic Cargoes In Mammalian Cells
Mitochondria-Associated Membranes (Mams): Overview And Its Role In Parkinson’s Disease
Turnover Of Lipidated Lc3 And Autophagic Cargoes In Mammalian Cells
Fluorescent Fyve Chimeras To Quantify Ptdins3p Synthesis During Autophagy
Turnover Of Lipidated Lc3 And Autophagic Cargoes In Mammalian Cells
Fluorescent Fyve Chimeras To Quantify Ptdins3p Synthesis During Autophagy
Inhibitor Of Growth Protein 4 Interacts With Beclin 1 And Represses Autophagy
Fluorescent Fyve Chimeras To Quantify Ptdins3p Synthesis During Autophagy
Inhibitor Of Growth Protein 4 Interacts With Beclin 1 And Represses Autophagy
Guidelines For The Use And Interpretation Of Assays For Monitoring Autophagy (3rd Edition)
Inhibitor Of Growth Protein 4 Interacts With Beclin 1 And Represses Autophagy
Guidelines For The Use And Interpretation Of Assays For Monitoring Autophagy (3rd Edition)
Erratum To: Guidelines For The Use And Interpretation Of Assays For Monitoring Autophagy (3rd Edition) (Autophagy, 12, 1, 1-222, 10.1080/15548627.2015.1100356
Guidelines For The Use And Interpretation Of Assays For Monitoring Autophagy (3rd Edition)
Erratum To: Guidelines For The Use And Interpretation Of Assays For Monitoring Autophagy (3rd Edition) (Autophagy, 12, 1, 1-222, 10.1080/15548627.2015.1100356
Pompe Disease And Autophagy: Partners In Crime, Or Cause And Consequence?
Erratum To: Guidelines For The Use And Interpretation Of Assays For Monitoring Autophagy (3rd Edition) (Autophagy, 12, 1, 1-222, 10.1080/15548627.2015.1100356
Pompe Disease And Autophagy: Partners In Crime, Or Cause And Consequence?
G2019s Mutation Of Lrrk2 Increases Autophagy Via Mek/erk Pathway
Pompe Disease And Autophagy: Partners In Crime, Or Cause And Consequence?
G2019s Mutation Of Lrrk2 Increases Autophagy Via Mek/erk Pathway
Pharmacological Inhibition Of Fatty-Acid Oxidation Synergistically Enhances The Effect Of L-Asparaginase In Childhood All Cells
G2019s Mutation Of Lrrk2 Increases Autophagy Via Mek/erk Pathway
Pharmacological Inhibition Of Fatty-Acid Oxidation Synergistically Enhances The Effect Of L-Asparaginase In Childhood All Cells
Unsaturated Fatty Acids Induce Non-Canonical Autophagy
Pharmacological Inhibition Of Fatty-Acid Oxidation Synergistically Enhances The Effect Of L-Asparaginase In Childhood All Cells
Unsaturated Fatty Acids Induce Non-Canonical Autophagy
Metabolomic Analyses Reveal That Anti-Aging Metabolites Are Depleted By Palmitate But Increased By Oleate In Vivo
Unsaturated Fatty Acids Induce Non-Canonical Autophagy
Metabolomic Analyses Reveal That Anti-Aging Metabolites Are Depleted By Palmitate But Increased By Oleate In Vivo
Novel Inducers Of Becn1-Independent Autophagy: Cis-Unsaturated Fatty Acids
Metabolomic Analyses Reveal That Anti-Aging Metabolites Are Depleted By Palmitate But Increased By Oleate In Vivo
Novel Inducers Of Becn1-Independent Autophagy: Cis-Unsaturated Fatty Acids
Spermidine Induces Autophagy By Inhibiting The Acetyltransferase Ep300
Novel Inducers Of Becn1-Independent Autophagy: Cis-Unsaturated Fatty Acids
Spermidine Induces Autophagy By Inhibiting The Acetyltransferase Ep300
Mitochondrial Impairment Increases Fl-Pink1 Levels By Calcium-Dependent Gene Expression
Spermidine Induces Autophagy By Inhibiting The Acetyltransferase Ep300
Mitochondrial Impairment Increases Fl-Pink1 Levels By Calcium-Dependent Gene Expression
Links Between Paraquat And Parkinson's Disease
Mitochondrial Impairment Increases Fl-Pink1 Levels By Calcium-Dependent Gene Expression
Links Between Paraquat And Parkinson's Disease
Cancer Cell–autonomous Contribution Of Type I Interferon Signaling To The Efficacy Of Chemotherapy
Links Between Paraquat And Parkinson's Disease
Cancer Cell–autonomous Contribution Of Type I Interferon Signaling To The Efficacy Of Chemotherapy
Coffee Induces Autophagy In Vivo
Cancer Cell–autonomous Contribution Of Type I Interferon Signaling To The Efficacy Of Chemotherapy
Coffee Induces Autophagy In Vivo
Regulation Of Autophagy By Cytosolic Acetyl-Coenzyme A
Coffee Induces Autophagy In Vivo
Regulation Of Autophagy By Cytosolic Acetyl-Coenzyme A
Self-Consumption: The Interplay Of Autophagy And Apoptosis
Regulation Of Autophagy By Cytosolic Acetyl-Coenzyme A
Self-Consumption: The Interplay Of Autophagy And Apoptosis
Implication Of Autophagy In Parkinson's Disease
Self-Consumption: The Interplay Of Autophagy And Apoptosis
Implication Of Autophagy In Parkinson's Disease
Autophagy, Mitochondria And 3-Nitropropionic Acid Joined In The Same Model
Implication Of Autophagy In Parkinson's Disease
Autophagy, Mitochondria And 3-Nitropropionic Acid Joined In The Same Model
The Lrrk2 G2019s Mutant Exacerbates Basal Autophagy Through Activation Of The Mek/erk Pathway
Autophagy, Mitochondria And 3-Nitropropionic Acid Joined In The Same Model
The Lrrk2 G2019s Mutant Exacerbates Basal Autophagy Through Activation Of The Mek/erk Pathway
Regulation Of Autophagy By Stress-Responsive Transcription Factors
The Lrrk2 G2019s Mutant Exacerbates Basal Autophagy Through Activation Of The Mek/erk Pathway
Regulation Of Autophagy By Stress-Responsive Transcription Factors
Direct Interaction Between Stat3 And Eif2ak2 Controls Fatty Acid-Induced Autophagy
Regulation Of Autophagy By Stress-Responsive Transcription Factors
Direct Interaction Between Stat3 And Eif2ak2 Controls Fatty Acid-Induced Autophagy
Autophagy And Parkinson's Disease: A Love-Hate Relationship
Direct Interaction Between Stat3 And Eif2ak2 Controls Fatty Acid-Induced Autophagy
Autophagy And Parkinson's Disease: A Love-Hate Relationship
Direct Molecular Interactions Between Beclin 1 And The Canonical Nfκb Activation Pathway.
Autophagy And Parkinson's Disease: A Love-Hate Relationship
Direct Molecular Interactions Between Beclin 1 And The Canonical Nfκb Activation Pathway.
Prognostic Impact Of Vitamin B6 Metabolism In Lung Cancer
Direct Molecular Interactions Between Beclin 1 And The Canonical Nfκb Activation Pathway.
Prognostic Impact Of Vitamin B6 Metabolism In Lung Cancer
Parkinsons Disease: Leucine-Rich Repeat Kinase 2 And Autophagy, Intimate Enemies
Prognostic Impact Of Vitamin B6 Metabolism In Lung Cancer
Parkinsons Disease: Leucine-Rich Repeat Kinase 2 And Autophagy, Intimate Enemies
Possible Involvement Of The Relationship Of Lrrk2 And Autophagy In Parkinson's Disease
Parkinsons Disease: Leucine-Rich Repeat Kinase 2 And Autophagy, Intimate Enemies
Possible Involvement Of The Relationship Of Lrrk2 And Autophagy In Parkinson's Disease
The Mapk1/3 Pathway Is Essential For The Deregulation Of Autophagy Observed In G2019s Lrrk2 Mutant Fibroblasts
Possible Involvement Of The Relationship Of Lrrk2 And Autophagy In Parkinson's Disease
The Mapk1/3 Pathway Is Essential For The Deregulation Of Autophagy Observed In G2019s Lrrk2 Mutant Fibroblasts
Direct Molecular Interactions Between Beclin 1 And The Canonical Nfκb Activation Pathway
The Mapk1/3 Pathway Is Essential For The Deregulation Of Autophagy Observed In G2019s Lrrk2 Mutant Fibroblasts
Direct Molecular Interactions Between Beclin 1 And The Canonical Nfκb Activation Pathway
Autophagic Removal Of Micronuclei
Direct Molecular Interactions Between Beclin 1 And The Canonical Nfκb Activation Pathway
Autophagic Removal Of Micronuclei
Autophagy Is Required For The Activation Of Nfκb
Autophagic Removal Of Micronuclei
Autophagy Is Required For The Activation Of Nfκb
Autophagy Is Required For The Activation Of Nfkb (Cell Cycle 11, 1 (194-199))
Autophagy Is Required For The Activation Of Nfκb
Autophagy Is Required For The Activation Of Nfkb (Cell Cycle 11, 1 (194-199))
Cytoplasmic Stat3 Represses Autophagy By Inhibiting Pkr Activity
Autophagy Is Required For The Activation Of Nfkb (Cell Cycle 11, 1 (194-199))
Cytoplasmic Stat3 Represses Autophagy By Inhibiting Pkr Activity
Prognostic Impact Of Vitamin B6 Metabolism In Lung Cancer
Cytoplasmic Stat3 Represses Autophagy By Inhibiting Pkr Activity
Prognostic Impact Of Vitamin B6 Metabolism In Lung Cancer
Pro-Autophagic Polyphenols Reduce The Acetylation Of Cytoplasmic Proteins
Prognostic Impact Of Vitamin B6 Metabolism In Lung Cancer
Pro-Autophagic Polyphenols Reduce The Acetylation Of Cytoplasmic Proteins
An Immunosurveillance Mechanism Controls Cancer Cell Ploidy
Pro-Autophagic Polyphenols Reduce The Acetylation Of Cytoplasmic Proteins
An Immunosurveillance Mechanism Controls Cancer Cell Ploidy
Ask1 Overexpression Accelerates Paraquat-Induced Autophagy Via Endoplasmic Reticulum Stress
An Immunosurveillance Mechanism Controls Cancer Cell Ploidy
Ask1 Overexpression Accelerates Paraquat-Induced Autophagy Via Endoplasmic Reticulum Stress
Inhibition Of Autophagy By Tab2 And Tab3
Ask1 Overexpression Accelerates Paraquat-Induced Autophagy Via Endoplasmic Reticulum Stress
Inhibition Of Autophagy By Tab2 And Tab3
Fipronil Is A Powerful Uncoupler Of Oxidative Phosphorylation That Triggers Apoptosis In Human Neuronal Cell Line Shsy5y
Inhibition Of Autophagy By Tab2 And Tab3
Fipronil Is A Powerful Uncoupler Of Oxidative Phosphorylation That Triggers Apoptosis In Human Neuronal Cell Line Shsy5y
Genetic Screening For The Lrrk2, G2019s And R1441 Codon Mutations In Parkinson's Disease Patients From Extremadura, Spain
Fipronil Is A Powerful Uncoupler Of Oxidative Phosphorylation That Triggers Apoptosis In Human Neuronal Cell Line Shsy5y
Genetic Screening For The Lrrk2, G2019s And R1441 Codon Mutations In Parkinson's Disease Patients From Extremadura, Spain
The Neuroprotective Effect Of Talipexole From Paraquat-Induced Cell Death In Dopaminergic Neuronal Cells
Genetic Screening For The Lrrk2, G2019s And R1441 Codon Mutations In Parkinson's Disease Patients From Extremadura, Spain
The Neuroprotective Effect Of Talipexole From Paraquat-Induced Cell Death In Dopaminergic Neuronal Cells
Activation Of Apoptosis Signal-Regulating Kinase 1 Is A Key Factor In Paraquat-Induced Cell Death: Modulation By The Nrf2/trx Axis
The Neuroprotective Effect Of Talipexole From Paraquat-Induced Cell Death In Dopaminergic Neuronal Cells
Activation Of Apoptosis Signal-Regulating Kinase 1 Is A Key Factor In Paraquat-Induced Cell Death: Modulation By The Nrf2/trx Axis
Dj-1 As A Modulator Of Autophagy: An Hypothesis
Activation Of Apoptosis Signal-Regulating Kinase 1 Is A Key Factor In Paraquat-Induced Cell Death: Modulation By The Nrf2/trx Axis
Dj-1 As A Modulator Of Autophagy: An Hypothesis
Effect Of Paraquat Exposure On Nitric Oxide-Responsive Genes In Rat Mesencephalic Cells
Dj-1 As A Modulator Of Autophagy: An Hypothesis
Effect Of Paraquat Exposure On Nitric Oxide-Responsive Genes In Rat Mesencephalic Cells
Curcumin Exposure Induces Expression Of The Parkinson's Disease-Associated Leucine-Rich Repeat Kinase 2 (Lrrk2) In Rat Mesencephalic Cells
Effect Of Paraquat Exposure On Nitric Oxide-Responsive Genes In Rat Mesencephalic Cells
Curcumin Exposure Induces Expression Of The Parkinson's Disease-Associated Leucine-Rich Repeat Kinase 2 (Lrrk2) In Rat Mesencephalic Cells
Curcumin Enhances Paraquat-Induced Apoptosis Of N27 Mesencephalic Cells Via The Generation Of Reactive Oxygen Species
Curcumin Exposure Induces Expression Of The Parkinson's Disease-Associated Leucine-Rich Repeat Kinase 2 (Lrrk2) In Rat Mesencephalic Cells
Curcumin Enhances Paraquat-Induced Apoptosis Of N27 Mesencephalic Cells Via The Generation Of Reactive Oxygen Species
Nitric Oxide-Mediated Toxicity In Paraquat-Exposed Sh-Sy5y Cells: A Protective Role Of 7-Nitroindazole
Curcumin Enhances Paraquat-Induced Apoptosis Of N27 Mesencephalic Cells Via The Generation Of Reactive Oxygen Species
Nitric Oxide-Mediated Toxicity In Paraquat-Exposed Sh-Sy5y Cells: A Protective Role Of 7-Nitroindazole
Silencing Dj-1 Reveals Its Contribution In Paraquat-Induced Autophagy
Nitric Oxide-Mediated Toxicity In Paraquat-Exposed Sh-Sy5y Cells: A Protective Role Of 7-Nitroindazole
Silencing Dj-1 Reveals Its Contribution In Paraquat-Induced Autophagy
Identification Of Genes Associated With Paraquat-Induced Toxicity In Sh-Sy5y Cells By Pcr Array Focused On Apoptotic Pathways
Silencing Dj-1 Reveals Its Contribution In Paraquat-Induced Autophagy
Identification Of Genes Associated With Paraquat-Induced Toxicity In Sh-Sy5y Cells By Pcr Array Focused On Apoptotic Pathways
Relationship Between Autophagy And Apoptotic Cell Death In Human Neuroblastoma Cells Treated With Paraquat: Could Autophagy Be A Brake In Paraquat-Induced Apoptotic Death?
Identification Of Genes Associated With Paraquat-Induced Toxicity In Sh-Sy5y Cells By Pcr Array Focused On Apoptotic Pathways
Relationship Between Autophagy And Apoptotic Cell Death In Human Neuroblastoma Cells Treated With Paraquat: Could Autophagy Be A Brake In Paraquat-Induced Apoptotic Death?
Inhibition Of Paraquat-Induced Autophagy Accelerates The Apoptotic Cell Death In Neuroblastoma Sh-Sy5y Cells
Relationship Between Autophagy And Apoptotic Cell Death In Human Neuroblastoma Cells Treated With Paraquat: Could Autophagy Be A Brake In Paraquat-Induced Apoptotic Death?
Inhibition Of Paraquat-Induced Autophagy Accelerates The Apoptotic Cell Death In Neuroblastoma Sh-Sy5y Cells
Low Concentrations Of Paraquat Induces Early Activation Of Extracellular Signal-Regulated Kinase 1/2, Protein Kinase B, And C-Jun N-Terminal Kinase 1/2 Pathways: Role Of C-Jun N-Terminal Kinase In Paraquat-Induced Cell Death
Inhibition Of Paraquat-Induced Autophagy Accelerates The Apoptotic Cell Death In Neuroblastoma Sh-Sy5y Cells
Low Concentrations Of Paraquat Induces Early Activation Of Extracellular Signal-Regulated Kinase 1/2, Protein Kinase B, And C-Jun N-Terminal Kinase 1/2 Pathways: Role Of C-Jun N-Terminal Kinase In Paraquat-Induced Cell Death
Heat Shock Proteins Protect Both Mpp+ And Paraquat Neurotoxicity
Low Concentrations Of Paraquat Induces Early Activation Of Extracellular Signal-Regulated Kinase 1/2, Protein Kinase B, And C-Jun N-Terminal Kinase 1/2 Pathways: Role Of C-Jun N-Terminal Kinase In Paraquat-Induced Cell Death
Heat Shock Proteins Protect Both Mpp+ And Paraquat Neurotoxicity
Paraquat-Induced Apoptotic Cell Death In Cerebellar Granule Cells
Heat Shock Proteins Protect Both Mpp+ And Paraquat Neurotoxicity
Paraquat-Induced Apoptotic Cell Death In Cerebellar Granule Cells
Immunological Aspects Of Central Neurodegeneration
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