Pages that link to "Q29614836"
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The following pages link to Mutations of optineurin in amyotrophic lateral sclerosis (Q29614836):
Displaying 50 items.
- amyotrophic lateral sclerosis (Q206901) (← links)
- Genetic counseling for FTD/ALS caused by the C9ORF72 hexanucleotide expansion (Q21195686) (← links)
- Dysregulation of the autophagy-endolysosomal system in amyotrophic lateral sclerosis and related motor neuron diseases (Q21285051) (← links)
- The heritability of amyotrophic lateral sclerosis in a clinically ascertained United States research registry (Q22255529) (← links)
- Towards a unifying, systems biology understanding of large-scale cellular death and destruction caused by poorly liganded iron: Parkinson’s, Huntington’s, Alzheimer’s, prions, bactericides, chemical toxicology and others as examples (Q24289511) (← links)
- Ubiquitylation of autophagy receptor Optineurin by HACE1 activates selective autophagy for tumor suppression (Q24300797) (← links)
- Characterization of the Properties of a Novel Mutation in VAPB in Familial Amyotrophic Lateral Sclerosis (Q24302479) (← links)
- Interaction between optineurin and the bZIP transcription factor NRL (Q24318552) (← links)
- Haploinsufficiency of TBK1 causes familial ALS and fronto-temporal dementia (Q24323876) (← links)
- Mutations in UBQLN2 cause dominant X-linked juvenile and adult-onset ALS and ALS/dementia (Q24600027) (← links)
- Whole-genome sequencing reveals a coding non-pathogenic variant tagging a non-coding pathogenic hexanucleotide repeat expansion in C9orf72 as cause of amyotrophic lateral sclerosis (Q24623830) (← links)
- A hexanucleotide repeat expansion in C9ORF72 is the cause of chromosome 9p21-linked ALS-FTD (Q24634583) (← links)
- Conjoint pathologic cascades mediated by ALS/FTLD-U linked RNA-binding proteins TDP-43 and FUS (Q24634807) (← links)
- From animal models to human disease: a genetic approach for personalized medicine in ALS (Q26741250) (← links)
- Recent advances in amyotrophic lateral sclerosis (Q26749521) (← links)
- Toward precision medicine in amyotrophic lateral sclerosis (Q26764950) (← links)
- Impaired Autophagy and Defective Mitochondrial Function: Converging Paths on the Road to Motor Neuron Degeneration (Q26766040) (← links)
- Genotype-phenotype correlations of amyotrophic lateral sclerosis (Q26769063) (← links)
- Parkin Regulation and Neurodegenerative Disorders (Q26770443) (← links)
- Golgi Fragmentation in ALS Motor Neurons. New Mechanisms Targeting Microtubules, Tethers, and Transport Vesicles (Q26773168) (← links)
- TNF biology, pathogenic mechanisms and emerging therapeutic strategies (Q26776492) (← links)
- Ultrastructural studies of ALS mitochondria connect altered function and permeability with defects of mitophagy and mitochondriogenesis (Q26782995) (← links)
- Clinical and genetic basis of familial amyotrophic lateral sclerosis (Q26783236) (← links)
- Autophagy and Neurodegeneration: Insights from a Cultured Cell Model of ALS (Q26796599) (← links)
- Molecular motor proteins and amyotrophic lateral sclerosis (Q26820831) (← links)
- Transplantation of stem cell-derived astrocytes for the treatment of amyotrophic lateral sclerosis and spinal cord injury (Q26825854) (← links)
- Pathological mechanisms underlying TDP-43 driven neurodegeneration in FTLD-ALS spectrum disorders (Q26828357) (← links)
- Converging mechanisms in ALS and FTD: disrupted RNA and protein homeostasis (Q26863439) (← links)
- State of play in amyotrophic lateral sclerosis genetics (Q26864816) (← links)
- Sumoylation of critical proteins in amyotrophic lateral sclerosis: emerging pathways of pathogenesis (Q26866679) (← links)
- Autophagy and neurodegeneration (Q26991692) (← links)
- Functional analysis of optineurin and some of its disease-associated mutants (Q26996024) (← links)
- Therapeutic targeting of autophagy in neurodegenerative and infectious diseases (Q27021382) (← links)
- Redox regulation in amyotrophic lateral sclerosis (Q27026894) (← links)
- RNA-Seq profiling of spinal cord motor neurons from a presymptomatic SOD1 ALS mouse (Q27321207) (← links)
- Hyperphosphorylation as a defense mechanism to reduce TDP-43 aggregation (Q27325625) (← links)
- Loss of optineurin in vivo results in elevated cell death and alters axonal trafficking dynamics (Q27336244) (← links)
- Mitochondrial pathogenic mechanism and degradation in optineurin E50K mutation-mediated retinal ganglion cell degeneration (Q27345731) (← links)
- Inhibitory Synaptic Regulation of Motoneurons: A New Target of Disease Mechanisms in Amyotrophic Lateral Sclerosis (Q27687333) (← links)
- The GARP complex is required for cellular sphingolipid homeostasis (Q27932843) (← links)
- Sending Out an SOS: Mitochondria as a Signaling Hub (Q28073077) (← links)
- A perspective on stem cell modeling of amyotrophic lateral sclerosis (Q28080614) (← links)
- TDP-43 Proteinopathy and ALS: Insights into Disease Mechanisms and Therapeutic Targets (Q28080628) (← links)
- Systems biology of neurodegenerative diseases (Q28080741) (← links)
- Frontotemporal dementia: a bridge between dementia and neuromuscular disease (Q28081198) (← links)
- Calcium dysregulation links ALS defective proteins and motor neuron selective vulnerability (Q28084373) (← links)
- Autophagosome dynamics in neurodegeneration at a glance (Q28084804) (← links)
- The promise and perils of HDAC inhibitors in neurodegeneration (Q28087539) (← links)
- Optineurin is an autophagy receptor for damaged mitochondria in parkin-mediated mitophagy that is disrupted by an ALS-linked mutation (Q28118966) (← links)
- TDP-43 and FUS in amyotrophic lateral sclerosis and frontotemporal dementia (Q28294001) (← links)