Pages that link to "Q44495460"
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The following pages link to Calpain is a major cell death effector in selective striatal degeneration induced in vivo by 3-nitropropionate: implications for Huntington's disease. (Q44495460):
Displaying 43 items.
- Calpain 10 is required for cell viability and is decreased in the aging kidney (Q28567446) (← links)
- S-glutathionylation: from molecular mechanisms to health outcomes (Q30398587) (← links)
- Genetic and pharmacological inhibition of calcineurin corrects the BDNF transport defect in Huntington's disease (Q30491641) (← links)
- Normal aging modulates the neurotoxicity of mutant huntingtin (Q33413070) (← links)
- Protection from mitochondrial complex II inhibition in vitro and in vivo by Nrf2-mediated transcription (Q33551416) (← links)
- Growth Hormone Deteriorates the Functional Outcome in an Experimental Model of Huntington's Disease Induced by 3-Nitropionic Acid (Q33636220) (← links)
- The mitochondrial inhibitor oligomycin induces an inflammatory response in the rat knee joint (Q33792205) (← links)
- Altered microRNA regulation in Huntington's disease models (Q34146968) (← links)
- Involvement of mitochondrial complex II defects in neuronal death produced by N-terminus fragment of mutated huntingtin (Q34483577) (← links)
- Developmental changes in NMDA neurotoxicity reflect developmental changes in subunit composition of NMDA receptors. (Q34502494) (← links)
- Cysteine proteases bleomycin hydrolase and cathepsin Z mediate N-terminal proteolysis and toxicity of mutant huntingtin (Q34752467) (← links)
- Deleterious effects of minocycline after in vivo target deprivation of thalamocortical neurons in the immature, metallothionein-deficient mouse brain (Q35097284) (← links)
- Glycogen accumulation in cardiomyocytes and cardiotoxic effects after 3NPA treatment (Q35184309) (← links)
- Experimental therapeutics in transgenic mouse models of Huntington's disease (Q35752429) (← links)
- pH as a biomarker of neurodegeneration in Huntington's disease: a translational rodent-human MRS study. (Q35939218) (← links)
- Calpain activation impairs neuromuscular transmission in a mouse model of the slow-channel myasthenic syndrome (Q35987568) (← links)
- Brief mitochondrial inhibition causes lasting changes in motor behavior and corticostriatal synaptic physiology in the Fischer 344 rat. (Q36019780) (← links)
- Promethazine protects against 3-nitropropionic acid-induced neurotoxicity. (Q36253348) (← links)
- Calpain and synaptic function (Q36586276) (← links)
- Involvement of calpain activation in neurodegenerative processes. (Q36588397) (← links)
- Ginsenosides: are any of them candidates for drugs acting on the central nervous system? (Q37031566) (← links)
- A role of mitochondrial complex II defects in genetic models of Huntington's disease expressing N-terminal fragments of mutant huntingtin (Q37153804) (← links)
- Calpain-mediated signaling mechanisms in neuronal injury and neurodegeneration (Q37237452) (← links)
- Mitochondrial functional alterations in relation to pathophysiology of Huntington's disease (Q37750542) (← links)
- Molecular Mechanisms and Potential Therapeutical Targets in Huntington's Disease (Q37776087) (← links)
- PARP-1 cleavage fragments: signatures of cell-death proteases in neurodegeneration (Q37822920) (← links)
- Oxidative stress in transgenic mice with oligodendroglial alpha-synuclein overexpression replicates the characteristic neuropathology of multiple system atrophy (Q38585651) (← links)
- Imaging and spectroscopic approaches to probe brain energy metabolism dysregulation in neurodegenerative diseases (Q38918493) (← links)
- Huntington's Disease: Mechanisms of Pathogenesis and Therapeutic Strategies (Q39035495) (← links)
- Mutant huntingtin N-terminal fragments of specific size mediate aggregation and toxicity in neuronal cells (Q39885698) (← links)
- Uncoupling oxidative/energy metabolism with low sub chronic doses of 3-nitropropionic acid or iodoacetate in vivo produces striatal cell damage (Q40290500) (← links)
- Inhibition of the cdk5/MEF2 pathway is involved in the antiapoptotic properties of calpain inhibitors in cerebellar neurons. (Q41863662) (← links)
- Apoptosis signal-regulating kinase 1 mediates striatal degeneration via the regulation of C1q. (Q43106342) (← links)
- Regulation of GSK-3beta by calpain in the 3-nitropropionic acid model (Q43284375) (← links)
- Region-specific changes in activities of cell death-related proteases and nitric oxide metabolism in rat brain in a chronic unpredictable stress model. (Q43349783) (← links)
- Curcumin nanoparticles attenuate neurochemical and neurobehavioral deficits in experimental model of Huntington's disease (Q43687507) (← links)
- The biology of Huntington's disease. (Q45290121) (← links)
- Sequential activation of individual caspases, and of alterations in Bcl‐2 proapoptotic signals in a mouse model of Huntington's disease (Q45291644) (← links)
- Polyglutamine-modulated striatal calpain activity in YAC transgenic huntington disease mouse model: impact on NMDA receptor function and toxicity (Q45291700) (← links)
- Inhibition of calcineurin by FK506 protects against polyglutamine-huntingtin toxicity through an increase of huntingtin phosphorylation at S421. (Q45299979) (← links)
- Targeting neuro-inflammatory cytokines and oxidative stress by minocycline attenuates quinolinic-acid-induced Huntington's disease-like symptoms in rats (Q45306608) (← links)
- Contribution of NMDA and non-NMDA receptors to in vivo glutamate-induced calpain activation in the rat striatum. Relation to neuronal damage (Q46757093) (← links)
- 3-Nitropropionic acid toxicity in hippocampus: protection through N-methyl-D-aspartate receptor antagonism (Q48451450) (← links)