| scholarly article | Q13442814 |
| P50 | author | Jan H Veldink | Q76753542 |
| Leonard H van den Berg | Q56999697 | ||
| P2093 | author name string | R Jeroen Pasterkamp | |
| Alain de Bruin | |||
| Henk-Jan Westeneng | |||
| Sameh A Youssef | |||
| Liesbeth Harkema | |||
| Marina de Wit | |||
| Caroline A C Zundel | |||
| Emma Sudria-Lopez | |||
| Max Koppers | |||
| Christiaan van der Meer | |||
| P2860 | cites work | C9orf72 ablation in mice does not cause motor neuron degeneration or motor deficits | Q36555249 |
| C9orf72 ablation causes immune dysregulation characterized by leukocyte expansion, autoantibody production, and glomerulonephropathy in mice. | Q36691051 | ||
| Reduced C9orf72 protein levels in frontal cortex of amyotrophic lateral sclerosis and frontotemporal degeneration brain with the C9ORF72 hexanucleotide repeat expansion | Q37706316 | ||
| C9orf72 is required for proper macrophage and microglial function in mice | Q42364302 | ||
| P275 | copyright license | Creative Commons Attribution 4.0 International | Q20007257 |
| P6216 | copyright status | copyrighted | Q50423863 |
| P433 | issue | 1 | |
| P407 | language of work or name | English | Q1860 |
| P921 | main subject | pathology | Q7208 |
| P304 | page(s) | 145-147 | |
| P577 | publication date | 2016-05-20 | |
| P1433 | published in | Acta Neuropathologica | Q343168 |
| P1476 | title | Full ablation of C9orf72 in mice causes immune system-related pathology and neoplastic events but no motor neuron defects | |
| P478 | volume | 132 |
| Q47344945 | A proteomic network approach across the ALS-FTD disease spectrum resolves clinical phenotypes and genetic vulnerability in human brain. |
| Q47230701 | A zebrafish model for C9orf72 ALS reveals RNA toxicity as a pathogenic mechanism. |
| Q99547009 | ALS Genetics: Gains, Losses, and Implications for Future Therapies |
| Q56531746 | Amyotrophic lateral sclerosis |
| Q33614811 | C9ORF72 hexanucleotide repeat exerts toxicity in a stable, inducible motor neuronal cell model, which is rescued by partial depletion of Pten |
| Q42425843 | C9ORF72 interaction with cofilin modulates actin dynamics in motor neurons |
| Q92794366 | C9ORF72-related cellular pathology in skeletal myocytes derived from ALS-patient induced pluripotent stem cells |
| Q51371013 | C9orf72 plays a central role in Rab GTPase-dependent regulation of autophagy. |
| Q64948055 | C9orf72-mediated ALS and FTD: multiple pathways to disease. |
| Q39165154 | C9orf72: At the intersection of lysosome cell biology and neurodegenerative disease |
| Q38782125 | Gene discovery in amyotrophic lateral sclerosis: implications for clinical management |
| Q37380290 | Increased prevalence of autoimmune disease within C9 and FTD/MND cohorts: Completing the picture |
| Q93346244 | Inflammation in ALS/FTD pathogenesis |
| Q29465544 | Loss of C9orf72 Enhances Autophagic Activity via Deregulated mTOR and TFEB Signaling |
| Q90333276 | Low Serum High-Density Lipoprotein Cholesterol Levels Associate with the C9orf72 Repeat Expansion in Frontotemporal Lobar Degeneration Patients |
| Q39454075 | Microglia and C9orf72 in neuroinflammation and ALS and frontotemporal dementia |
| Q38741408 | Modeling the C9ORF72 repeat expansion mutation using human induced pluripotent stem cells |
| Q61816243 | Molecular Mechanisms of Neurodegeneration Related to Hexanucleotide Repeat Expansion |
| Q91564585 | Motor dysfunction and neurodegeneration in a C9orf72 mouse line expressing poly-PR |
| Q33665800 | Motor neuron vulnerability and resistance in amyotrophic lateral sclerosis |
| Q98177370 | Multifaceted Genes in Amyotrophic Lateral Sclerosis-Frontotemporal Dementia |
| Q39428501 | Multifaceted role of SMCR8 as autophagy regulator. |
| Q92035807 | Neuroinflammation in frontotemporal dementia |
| Q90263593 | Neurons Induced From Fibroblasts of c9ALS/FTD Patients Reproduce the Pathology Seen in the Central Nervous System |
| Q58801329 | Novel antibodies reveal presynaptic localization of C9orf72 protein and reduced protein levels in C9orf72 mutation carriers |
| Q38952327 | Pathogenic determinants and mechanisms of ALS/FTD linked to hexanucleotide repeat expansions in the C9orf72 gene |
| Q92597079 | Reduced autophagy upon C9ORF72 loss synergizes with dipeptide repeat protein toxicity in G4C2 repeat expansion disorders |
| Q48145508 | Sense and antisense RNA are not toxic in Drosophila models of C9orf72-associated ALS/FTD. |
| Q46799396 | Sense-encoded poly-GR dipeptide repeat proteins correlate to neurodegeneration and uniquely co-localize with TDP-43 in dendrites of repeat-expanded C9orf72 amyotrophic lateral sclerosis. |
| Q59339808 | Stable transgenic C9orf72 zebrafish model key aspects of the ALS/FTD phenotype and reveal novel pathological features |
| Q64231298 | Targeting RNA-Mediated Toxicity in C9orf72 ALS and/or FTD by RNAi-Based Gene Therapy |
| Q64267537 | The ALS-FTD-linked gene product, C9orf72, regulates neuronal morphogenesis via autophagy |
| Q39662062 | The C9orf72 protein interacts with Rab1a and the ULK1 complex to regulate initiation of autophagy |
| Q89794612 | [Gene-specific treatment approaches in amyotrophic lateral sclerosis in the present and future] |
Search more.