Cu/Zn superoxide dismutase typical for familial amyotrophic lateral sclerosis increases the vulnerability of mitochondria and perturbs Ca2+ homeostasis in SOD1G93A mice.
about
Impairment of mitochondrial calcium handling in a mtSOD1 cell culture model of motoneuron diseaseImpaired Autophagy and Defective Mitochondrial Function: Converging Paths on the Road to Motor Neuron DegenerationAdducin at the Neuromuscular Junction in Amyotrophic Lateral Sclerosis: Hanging on for Dear LifeALS Patient Stem Cells for Unveiling Disease Signatures of Motoneuron Susceptibility: Perspectives on the Deadly Mitochondria, ER Stress and Calcium TriadUltrastructural studies of ALS mitochondria connect altered function and permeability with defects of mitophagy and mitochondriogenesisSOD1 misplacing and mitochondrial dysfunction in amyotrophic lateral sclerosis pathogenesisMechanisms of mutant SOD1 induced mitochondrial toxicity in amyotrophic lateral sclerosisOxidative stress and mitochondrial damage: importance in non-SOD1 ALSCalcium dysregulation links ALS defective proteins and motor neuron selective vulnerabilityThe role of oxidative stress in degeneration of the neuromuscular junction in amyotrophic lateral sclerosisEffects of natural antioxidants in neurodegenerative disease.Mitochondrial pathobiology in ALS.Mitochondrial dysfunction and intracellular calcium dysregulation in ALSDNA repair deficiency in neurodegeneration.Mitochondrial and Cell Death Mechanisms in Neurodegenerative Diseases.Riluzole But Not Melatonin Ameliorates Acute Motor Neuron Degeneration and Moderately Inhibits SOD1-Mediated Excitotoxicity Induced Disrupted Mitochondrial Ca2+ Signaling in Amyotrophic Lateral SclerosisTherapeutic opportunities and challenges of induced pluripotent stem cells-derived motor neurons for treatment of amyotrophic lateral sclerosis and motor neuron disease.GNX-4728, a novel small molecule drug inhibitor of mitochondrial permeability transition, is therapeutic in a mouse model of amyotrophic lateral sclerosis.Human iPSC-derived motoneurons harbouring TARDBP or C9ORF72 ALS mutations are dysfunctional despite maintaining viabilityElevated mRNA-levels of distinct mitochondrial and plasma membrane Ca(2+) transporters in individual hypoglossal motor neurons of endstage SOD1 transgenic mice.Activation of the endoplasmic reticulum stress response in skeletal muscle of G93A*SOD1 amyotrophic lateral sclerosis mice.Seeking homeostasis: temporal trends in respiration, oxidation, and calcium in SOD1 G93A Amyotrophic Lateral Sclerosis mice.Dysregulated expression of death, stress and mitochondrion related genes in the sciatic nerve of presymptomatic SOD1(G93A) mouse model of Amyotrophic Lateral Sclerosis.Biology of mitochondria in neurodegenerative diseases.State of the field: An informatics-based systematic review of the SOD1-G93A amyotrophic lateral sclerosis transgenic mouse model.Promise and Pitfalls of Mitochondrial Replacement for Prevention and Cure of Heritable Neurodegenerative Diseases Caused by Deleterious Mutations in Mitochondrial DNAMitochondria: a therapeutic target in neurodegenerationThe mitochondrial permeability transition pore: a molecular target for amyotrophic lateral sclerosis therapy.SOD1 and TDP-43 animal models of amyotrophic lateral sclerosis: recent advances in understanding disease toward the development of clinical treatments.Mitochondrial dysfunction in familial amyotrophic lateral sclerosis.SOD1 and mitochondria in ALS: a dangerous liaison.Endoplasmic reticulum stress and the ER mitochondrial calcium cycle in amyotrophic lateral sclerosis.Neuronal calcium signaling: function and dysfunction.The ER mitochondria calcium cycle and ER stress response as therapeutic targets in amyotrophic lateral sclerosis.ER stress and unfolded protein response in amyotrophic lateral sclerosis-a controversial role of protein disulphide isomerase.Selective vulnerability of motoneuron and perturbed mitochondrial calcium homeostasis in amyotrophic lateral sclerosis: implications for motoneurons specific calcium dysregulation.Selective mitochondrial Ca2+ uptake deficit in disease endstage vulnerable motoneurons of the SOD1G93A mouse model of amyotrophic lateral sclerosis.Mutant SOD1 and mitochondrial damage alter expression and splicing of genes controlling neuritogenesis in models of neurodegeneration.4-Aminopyridine Induced Activity Rescues Hypoexcitable Motor Neurons from Amyotrophic Lateral Sclerosis Patient-Derived Induced Pluripotent Stem Cells.Enhancing mitochondrial calcium buffering capacity reduces aggregation of misfolded SOD1 and motor neuron cell death without extending survival in mouse models of inherited amyotrophic lateral sclerosis
P2860
Q21262978-DC8407EE-6BAC-485B-9C22-61A522F2882DQ26766040-BABF78CF-510C-4DF3-AFF2-6EA41267A6D6Q26767792-636849AA-DB04-4142-B6DF-E9C68E182F0CQ26774824-448F32AA-CB17-4860-B9CA-CE4F602151DAQ26782995-94924B0B-BCE2-4ADB-971C-A01968B24CA1Q26785352-8777B4A9-52AB-4D38-9EB6-73578A18A5EDQ26998585-C332400D-E97E-49B5-A4EC-6A851F27AB45Q27023941-19CA39BA-EE0F-48C5-864B-E95D1F1D571AQ28084373-14699355-055D-4E1F-9DC0-DD50AD0CB8FCQ33633778-A8D4B1B9-2A9E-49A7-AD36-0AD17E2B7CBAQ34030539-0354A7BD-1943-4262-8AED-4001AA8160E0Q34038775-B1F3A053-B82D-493E-BF52-0C32CF083900Q34103782-EBEF6CFE-995D-4922-A7E7-240657B3F953Q34183328-0FEBE69F-2765-4FB7-BF1B-58841301C657Q34502221-7E367E3C-F5D3-4875-B7A9-2C9438BB1C19Q34549829-25BABBEC-41C0-4780-8549-C7CFE522B39FQ34557892-0CCDD2C7-A42B-45B2-A85B-B830ADAC1845Q34741619-8F1D7008-EFD1-46F8-B2DB-D0AA7647DFABQ35114316-1C58A035-75CA-4DBB-8C36-EEBBAB96AA17Q35469175-66ADACA0-8192-4B1F-A453-A0DE37E8CBD9Q35617613-111A8EC9-B6BF-4B0D-92D9-CC342E25A527Q35802837-155769F4-5955-4725-98B6-84F274AA034BQ36012034-44518D38-D2B3-4CDA-873B-323DE6C3B47CQ36488715-4B1CDC3D-7E30-412A-886A-2DB86FF06E92Q36494315-90C25938-0432-4E18-ACA8-4DCBE13CBA40Q37277363-F796DBCA-66F8-43EC-B029-66DE0836153DQ37466059-1AB2A74F-88A6-44BD-8B0F-A3A185A60AEDQ37466115-DB4DA752-6D81-449F-A9B7-B335F7A58A51Q37894600-A89C6EF9-C7CE-45C6-934F-7F6B37B8609FQ37954547-D6132654-5749-4143-8D62-3889B7737B7DQ37955818-1668941C-A6C3-43EA-944D-FF09A1567032Q37980249-5E4778BA-12C5-43D8-A82C-ED85518DFFB8Q38179996-56AB6003-E960-427E-89DF-1C3408BFC220Q38218666-BABEA6A8-798D-4820-A26B-ED16350C29BAQ38292610-B2BEA0D6-606C-40D4-B2DD-63B444C67238Q38521756-65C89728-EB18-4F6D-9D81-08B9A99A5E47Q39468775-1DAB3B2A-91EB-4D5C-8CE1-B26080D84039Q39625408-6DC40FB2-FA68-4410-A3B5-ED9951A2EF29Q39945217-69835313-E3B9-4CAD-A5D6-91729E808679Q41842786-E404346D-52C1-40A7-88D2-A0217F4A869E
P2860
Cu/Zn superoxide dismutase typical for familial amyotrophic lateral sclerosis increases the vulnerability of mitochondria and perturbs Ca2+ homeostasis in SOD1G93A mice.
description
2008 nî lūn-bûn
@nan
2008 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած
@hyw
2008 թվականի դեկտեմբերին հրատարակված գիտական հոդված
@hy
2008年の論文
@ja
2008年論文
@yue
2008年論文
@zh-hant
2008年論文
@zh-hk
2008年論文
@zh-mo
2008年論文
@zh-tw
2008年论文
@wuu
name
Cu/Zn superoxide dismutase typ ...... homeostasis in SOD1G93A mice.
@ast
Cu/Zn superoxide dismutase typ ...... homeostasis in SOD1G93A mice.
@en
Cu/Zn superoxide dismutase typ ...... homeostasis in SOD1G93A mice.
@nl
type
label
Cu/Zn superoxide dismutase typ ...... homeostasis in SOD1G93A mice.
@ast
Cu/Zn superoxide dismutase typ ...... homeostasis in SOD1G93A mice.
@en
Cu/Zn superoxide dismutase typ ...... homeostasis in SOD1G93A mice.
@nl
prefLabel
Cu/Zn superoxide dismutase typ ...... homeostasis in SOD1G93A mice.
@ast
Cu/Zn superoxide dismutase typ ...... homeostasis in SOD1G93A mice.
@en
Cu/Zn superoxide dismutase typ ...... homeostasis in SOD1G93A mice.
@nl
P356
P1476
Cu/Zn superoxide dismutase typ ...... homeostasis in SOD1G93A mice.
@en
P2093
Bernhard U Keller
Manoj Kumar Jaiswal
P304
P356
10.1124/MOL.108.050831
P577
2008-12-05T00:00:00Z