Pages that link to "Q37100955"

The following pages link to The Psi(m) depolarization that accompanies mitochondrial Ca2+ uptake is greater in mutant SOD1 than in wild-type mouse motor terminals. (Q37100955):

Displaying 36 items.

• The mitochondrial Ca2+ uniporter MCU is essential for glucose-induced ATP increases in pancreatic β-cells (Q24294221) (← links)
• Impaired Autophagy and Defective Mitochondrial Function: Converging Paths on the Road to Motor Neuron Degeneration (Q26766040) (← links)
• ALS Patient Stem Cells for Unveiling Disease Signatures of Motoneuron Susceptibility: Perspectives on the Deadly Mitochondria, ER Stress and Calcium Triad (Q26774824) (← links)
• Mitochondria in motor nerve terminals: function in health and in mutant superoxide dismutase 1 mouse models of familial ALS (Q26850686) (← links)
• Mitochondrial calcium uptake underlies ROS generation during aminoglycoside-induced hair cell death (Q30805331) (← links)
• Hyperactive intracellular calcium signaling associated with localized mitochondrial defects in skeletal muscle of an animal model of amyotrophic lateral sclerosis (Q33581470) (← links)
• ER-mitochondrial calcium flow underlies vulnerability of mechanosensory hair cells to damage (Q33906624) (← links)
• ALS-linked mutant SOD1 damages mitochondria by promoting conformational changes in Bcl-2. (Q33980322) (← links)
• Mitochondrial pathobiology in ALS. (Q34038775) (← links)
• Mitochondrial dysfunction and intracellular calcium dysregulation in ALS (Q34103782) (← links)
• Misfolded mutant SOD1 directly inhibits VDAC1 conductance in a mouse model of inherited ALS (Q34139970) (← links)
• Mitochondrial and Cell Death Mechanisms in Neurodegenerative Diseases (Q34502221) (← links)
• Repetitive nerve stimulation transiently opens the mitochondrial permeability transition pore in motor nerve terminals of symptomatic mutant SOD1 mice (Q34819311) (← links)
• Early changes of neuromuscular transmission in the SOD1(G93A) mice model of ALS start long before motor symptoms onset (Q34989403) (← links)
• Increased axonal mitochondrial mobility does not slow amyotrophic lateral sclerosis (ALS)-like disease in mutant SOD1 mice (Q35067857) (← links)
• Activity-dependent degeneration of axotomized neuromuscular synapses in Wld S mice (Q35185311) (← links)
• Comparison of dendritic calcium transients in juvenile wild type and SOD1(G93A) mouse lumbar motoneurons (Q35357235) (← links)
• Elevated mRNA-levels of distinct mitochondrial and plasma membrane Ca(2+) transporters in individual hypoglossal motor neurons of endstage SOD1 transgenic mice (Q35469175) (← links)
• Gender-Specific Mechanism of Synaptic Impairment and Its Prevention by GCSF in a Mouse Model of ALS. (Q35613992) (← links)
• An approach to experimental synaptic pathology using green fluorescent protein-transgenic mice and gene knockout mice to show mitochondrial permeability transition pore-driven excitotoxicity in interneurons and motoneurons (Q36455346) (← links)
• Biology of mitochondria in neurodegenerative diseases (Q36488715) (← links)
• Mitochondrial dynamics and bioenergetic dysfunction is associated with synaptic alterations in mutant SOD1 motor neurons (Q36593996) (← links)
• Pre-symptomatic detection of chronic motor deficits and genotype prediction in congenic B6.SOD1(G93A) ALS mouse model. (Q37440150) (← links)
• The mitochondrial permeability transition pore: a molecular target for amyotrophic lateral sclerosis therapy (Q37466115) (← links)
• Insulin and Insulin-Sensitizing Drugs in Neurodegeneration: Mitochondria as Therapeutic Targets (Q37689883) (← links)
• Review: The role of mitochondria in the pathogenesis of amyotrophic lateral sclerosis. (Q37836981) (← links)
• Mitochondrial dysfunction in familial amyotrophic lateral sclerosis (Q37954547) (← links)
• Selective mitochondrial Ca2+ uptake deficit in disease endstage vulnerable motoneurons of the SOD1G93A mouse model of amyotrophic lateral sclerosis (Q39468775) (← links)
• Mutant SOD1 and mitochondrial damage alter expression and splicing of genes controlling neuritogenesis in models of neurodegeneration. (Q39625408) (← links)
• Dysfunctional mitochondrial Ca(2+) handling in mutant SOD1 mouse models of fALS: integration of findings from motor neuron somata and motor terminals (Q41849171) (← links)
• SOD1 and MitoTEMPO partially prevent mitochondrial permeability transition pore opening, necrosis, and mitochondrial apoptosis after ATP depletion recovery (Q41945438) (← links)
• Vesicular ATPase inserted into the plasma membrane of motor terminals by exocytosis alkalinizes cytosolic pH and facilitates endocytosis (Q41957038) (← links)
• Links between electrophysiological and molecular pathology of amyotrophic lateral sclerosis (Q43577107) (← links)
• Platform Communications (Q58286741) (← links)
• Excitatory Dendritic Mitochondrial Calcium Toxicity: Implications for Parkinson's and Other Neurodegenerative Diseases (Q58803405) (← links)
• A VDAC1-Derived N-Terminal Peptide Inhibits Mutant SOD1-VDAC1 Interactions and Toxicity in the SOD1 Model of ALS (Q93046785) (← links)