| Publication |
Sentence |
Publish Date |
Extraction Date |
Species |
| Mariusz Berdyński, Przemysław Miszta, Krzysztof Safranow, Peter M Andersen, Mitsuya Morita, Sławomir Filipek, Cezary Żekanowski, Magdalena Kuźma-Kozakiewic. SOD1 mutations associated with amyotrophic lateral sclerosis analysis of variant severity. Scientific reports. vol 12. issue 1. 2022-01-08. PMID:34996976. |
mutations in superoxide dismutase 1 gene (sod1) are linked to amyotrophic lateral sclerosis (als), a neurodegenerative disorder predominantly affecting upper and lower motor neurons. |
2022-01-08 |
2023-08-13 |
Not clear |
| Bing Zhao, Xinyu Bian, Xiaoyu Zhuang, Shu Liu, Zhiqiang Liu, Fengrui Son. Screening apo-SOD1 conformation stabilizers from natural flavanones by using Native ion mobility mass spectrometry and fluorescence spectroscopy methods. Rapid communications in mass spectrometry : RCM. 2022-01-03. PMID:34978114. |
a large number of studies have shown that the production of aberrant and deleterious copper zinc superoxide dismutase (sod1) species are closely related to amyotrophic lateral sclerosis (als). |
2022-01-03 |
2023-08-13 |
Not clear |
| Cylia Rochat, Nathalie Bernard-Marissal, Emma Källstig, Sylvain Pradervand, Florence E Perrin, Patrick Aebischer, Cédric Raoul, Bernard L Schneide. Astrocyte-targeting RNA interference against mutated superoxide dismutase 1 induces motoneuron plasticity and protects fast-fatigable motor units in a mouse model of amyotrophic lateral sclerosis. Glia. 2022-01-03. PMID:34978340. |
in amyotrophic lateral sclerosis (als) caused by sod1 gene mutations, both cell-autonomous and noncell-autonomous mechanisms lead to the selective degeneration of motoneurons (mn). |
2022-01-03 |
2023-08-13 |
mouse |
| Núria Gaja-Capdevila, Neus Hernández, Xavier Navarro, Mireia Herrando-Grabulos. Sigma-1 Receptor is a Pharmacological Target to Promote Neuroprotection in the SOD1 Frontiers in pharmacology. vol 12. 2021-12-27. PMID:34955848. |
sigma-1 receptor is a pharmacological target to promote neuroprotection in the sod1 amyotrophic lateral sclerosis (als) is a neurodegenerative disorder characterized by the death of motoneurons (mns) with a poor prognosis. |
2021-12-27 |
2023-08-13 |
Not clear |
| Stepan Timr, Fabio Sterpon. Computational Insights into the Unfolding of a Destabilized Superoxide Dismutase 1 Mutant. Biology. vol 10. issue 12. 2021-12-24. PMID:34943155. |
in this work, we investigate the β-barrel of superoxide dismutase 1 (sod1) in a mutated form, the isoleucine 35 to alanine (i35a) mutant, commonly used as a model system to decipher the role of the full-length aposod1 protein in amyotrophic lateral sclerosis (als). |
2021-12-24 |
2023-08-13 |
Not clear |
| Yeong Jin Tak, Seongman Kan. The E2 ubiquitin-conjugating enzyme HIP2 is a crucial regulator of quality control against mutant SOD1 proteotoxicity. Biochimica et biophysica acta. Molecular basis of disease. vol 1868. issue 2. 2021-12-11. PMID:34856358. |
mutations in superoxide dismutase 1 (sod1) leading to the formation of intracellular protein aggregates cause amyotrophic lateral sclerosis (als), a fatal neurodegenerative disorder characterized by a selective degeneration of motor neurons. |
2021-12-11 |
2023-08-13 |
mouse |
| Jeremy S Lum, Mikayla L Brown, Natalie E Farrawell, Luke McAlary, Diane Ly, Christen G Chisholm, Josh Snow, Kara L Vine, Tim Karl, Fabian Kreilaus, Lachlan E McInnes, Sara Nikseresht, Paul S Donnelly, Peter J Crouch, Justin J Yerbur. CuATSM improves motor function and extends survival but is not tolerated at a high dose in SOD1 Scientific reports. vol 11. issue 1. 2021-12-07. PMID:34588483. |
cuatsm improves motor function and extends survival but is not tolerated at a high dose in sod1 the synthetic copper-containing compound, cuatsm, has emerged as one of the most promising drug candidates developed for the treatment of amyotrophic lateral sclerosis (als). |
2021-12-07 |
2023-08-13 |
mouse |
| Chisako Funada, Nanami Tanino, Miina Fukaya, Yu Mikajiri, Masayoshi Nishiguchi, Masato Otake, Hiroko Nakasuji, Reika Kawahito, Fumiyoshi Ab. SOD1 mutations cause hypersensitivity to high-pressure-induced oxidative stress in Saccharomyces cerevisiae. Biochimica et biophysica acta. General subjects. vol 1866. issue 2. 2021-12-05. PMID:34728328. |
of the various sod1 mutations associated with familial amyotrophic lateral sclerosis, h46q and s134n substitutions diminished sod activity to levels comparable to those of catalytically deficient h63a and null mutants. |
2021-12-05 |
2023-08-13 |
human |
| Nikolay A Alemasov, Vladimir S Timofeev, Nikita V Ivanisenko, Nikolay A Kolchanov, Vladimir A Ivanisenk. Computer analysis of the relation between hydrogen bond stability in SOD1 mutants and the survival time of amyotrophic lateral sclerosis patients. Journal of molecular graphics & modelling. vol 110. 2021-11-30. PMID:34653813. |
computer analysis of the relation between hydrogen bond stability in sod1 mutants and the survival time of amyotrophic lateral sclerosis patients. |
2021-11-30 |
2023-08-13 |
Not clear |
| Nikolay A Alemasov, Vladimir S Timofeev, Nikita V Ivanisenko, Nikolay A Kolchanov, Vladimir A Ivanisenk. Computer analysis of the relation between hydrogen bond stability in SOD1 mutants and the survival time of amyotrophic lateral sclerosis patients. Journal of molecular graphics & modelling. vol 110. 2021-11-30. PMID:34653813. |
mutations in the sod1 protein can lead to the death of motor neurons, which, in turn, causes an incurable disease called amyotrophic lateral sclerosis (als). |
2021-11-30 |
2023-08-13 |
Not clear |
| Hsiao-Chien Ting, Hui-I Yang, Horng-Jyh Harn, Ing-Ming Chiu, Hong-Lin Su, Xiang Li, Mei-Fang Chen, Tsung-Jung Ho, Ching-Ann Liu, Yung-Jen Tsai, Tzyy-Wen Chiou, Shinn-Zong Lin, Chia-Yu Chan. Coactivation of GSK3β and IGF-1 Attenuates Amyotrophic Lateral Sclerosis Nerve Fiber Cytopathies in SOD1 Mutant Patient-Derived Motor Neurons. Cells. vol 10. issue 10. 2021-11-30. PMID:34685754. |
coactivation of gsk3β and igf-1 attenuates amyotrophic lateral sclerosis nerve fiber cytopathies in sod1 mutant patient-derived motor neurons. |
2021-11-30 |
2023-08-13 |
Not clear |
| Yuan Bai, Yong'an Zhou, Jianwei Li, Junmei Geng, Xingxing Li, Zhe Li, Jianping Cheng, Yaxin Han, Ruirui Re. [Identification of a novel SOD1 variant in a Chinese patient with amyotrophic lateral sclerosis]. Zhonghua yi xue yi chuan xue za zhi = Zhonghua yixue yichuanxue zazhi = Chinese journal of medical genetics. vol 38. issue 12. 2021-11-30. PMID:34839512. |
[identification of a novel sod1 variant in a chinese patient with amyotrophic lateral sclerosis]. |
2021-11-30 |
2023-08-13 |
Not clear |
| Suzanna Edgar, Melina Ellis, Nur Adilah Abdul-Aziz, Khean-Jin Goh, Nortina Shahrizaila, Marina L Kennerson, Azlina Ahmad-Annua. Mutation analysis of SOD1, C9orf72, TARDBP and FUS genes in ethnically-diverse Malaysian patients with amyotrophic lateral sclerosis (ALS). Neurobiology of aging. vol 108. 2021-11-24. PMID:34404558. |
mutation analysis of sod1, c9orf72, tardbp and fus genes in ethnically-diverse malaysian patients with amyotrophic lateral sclerosis (als). |
2021-11-24 |
2023-08-13 |
Not clear |
| Sarbesh R Pandeya, Janice A Nagy, Daniela Riveros, Carson Semple, Rebecca S Taylor, Benjamin Sanchez, Seward B Rutkov. Relationships between in vivo surface and ex vivo electrical impedance myography measurements in three different neuromuscular disorder mouse models. PloS one. vol 16. issue 10. 2021-11-23. PMID:34714853. |
here we studied three groups of diseased and wild-type (wt) animals, including a duchenne muscular dystrophy model (the d2-mdx mouse), an amyotrophic lateral sclerosis (als) model (the sod1 g93a mouse), and a model of fat-related atrophy (the db/db diabetic obese mouse), performing hind limb measurements using a standard surface array and ex vivo measurements on freshly excised gastrocnemius muscle. |
2021-11-23 |
2023-08-13 |
mouse |
| Natalie E Farrawell, Justin J Yerbur. Mutant Cu/Zn Superoxide Dismutase (A4V) Turnover Is Altered in Cells Containing Inclusions. Frontiers in molecular neuroscience. vol 14. 2021-11-23. PMID:34803609. |
sod1 mutations account for ∼20% of familial amyotrophic lateral sclerosis (als) cases in which the hallmark pathological feature is insoluble sod1 aggregates within motor neurons. |
2021-11-23 |
2023-08-13 |
Not clear |
| Shlomit Ezer, Muhannad Daana, Julien H Park, Shira Yanovsky-Dagan, Ulrika Nordström, Adily Basal, Simon Edvardson, Ann Saada, Markus Otto, Vardiella Meiner, Stefan L Marklund, Peter Munch Andersen, Tamar Hare. Infantile SOD1 deficiency syndrome caused by a homozygous SOD1 variant with absence of enzyme activity. Brain : a journal of neurology. 2021-11-17. PMID:34788402. |
pathogenic variants in sod1, encoding superoxide dismutase 1, are responsible for about 20% of all familial amyotrophic lateral sclerosis cases, through a gain-of-function mechanism. |
2021-11-17 |
2023-08-13 |
Not clear |
| Pieter A Leermakers, Martin Skov, Anders Riisager, Ole B Nielsen, Thomas H Pederse. Alterations in fast-twitch muscle membrane conductance regulation do not explain decreased muscle function of SOD1 Muscle & nerve. vol 64. issue 6. 2021-11-16. PMID:34486134. |
alterations in fast-twitch muscle membrane conductance regulation do not explain decreased muscle function of sod1 both neuromuscular junction (nmj) dysfunction and altered electrophysiological properties of muscle fibers have been reported in amyotrophic lateral sclerosis (als) patients. |
2021-11-16 |
2023-08-13 |
Not clear |
| Silvia Scaricamazza, Illari Salvatori, Susanna Amadio, Valentina Nesci, Alessio Torcinaro, Giacomo Giacovazzo, Aniello Primiano, Michela Gloriani, Niccolò Candelise, Luisa Pieroni, Jean-Philippe Loeffler, Frederique Renè, Cyril Quessada, Tesfaye W Tefera, Hao Wang, Frederik J Steyn, Shyuan T Ngo, Gabriella Dobrowolny, Elisa Lepore, Andrea Urbani, Antonio Musarò, Cinzia Volonté, Elisabetta Ferraro, Roberto Coccurello, Cristiana Valle, Alberto Ferr. Repurposing of Trimetazidine for Amyotrophic Lateral Sclerosis: a study in SOD1 British journal of pharmacology. 2021-11-16. PMID:34783031. |
repurposing of trimetazidine for amyotrophic lateral sclerosis: a study in sod1 amyotrophic lateral sclerosis (als), a neurodegenerative disease characterized by the degeneration of upper and lower motor neurons, progressive wasting and paralysis of voluntary muscles is currently incurable despite intense research and numerous unsuccessful clinical trials. |
2021-11-16 |
2023-08-13 |
Not clear |
| Bridget Martinez, Philip V Peplo. MicroRNA expression in animal models of amyotrophic lateral sclerosis and potential therapeutic approaches. Neural regeneration research. vol 17. issue 4. 2021-11-10. PMID:34472458. |
further studies with animal models of amyotrophic lateral sclerosis are warranted to validate these findings and identify specific mirnas whose suppression or directed against hsod1 results in increased lifespan, improved muscle strength, reduced neuromuscular junction degeneration, and improved motor neuron survival in sod1(g93a) animals. |
2021-11-10 |
2023-08-13 |
mouse |
| Guillem Mòdol-Caballero, Belén García-Lareu, Mireia Herrando-Grabulosa, Sergi Verdés, Rubén López-Vales, Gemma Pagès, Miguel Chillón, Xavier Navarro, Assumpció Bosc. Specific Expression of Glial-Derived Neurotrophic Factor in Muscles as Gene Therapy Strategy for Amyotrophic Lateral Sclerosis. Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics. vol 18. issue 2. 2021-11-02. PMID:33786805. |
to specifically target most skeletal muscles in the mouse model of amyotrophic lateral sclerosis (als), sod1 |
2021-11-02 |
2023-08-13 |
mouse |