path(MESH:"Spinocerebellar Ataxias")
Accumulation of ubiquitin conjugates and/or inclusion bodies associated with ubiquitin, proteasome, and certain disease-characteristic proteins have been reported in a broad array of chronic neurodegenerative diseases, such as the neurofibrillary tangles of Alzheimer’s disease (AD), brainstem Lewy bodies (LBs) (the neuropathological hallmark in Parkinson’s disease [PD]), Bunina bodies in Amyotrophic Lateral Sclerosis (ALS), and nuclear inclusions in CAG repeat expansion (polyglutamine/Q extension) disorders such as Huntington’s disease, Spinocerebellar Ataxias (SCAs), and Spinal and Bulbar Muscular Atrophy (SBMA; Kennedy’s disease) (reviewed recently by Alves-Rodrigues et al., 1998; Sherman and Goldberg, 2001) (Figure 2) PubMed:14556719
Accumulation of ubiquitin conjugates and/or inclusion bodies associated with ubiquitin, proteasome, and certain disease-characteristic proteins have been reported in a broad array of chronic neurodegenerative diseases, such as the neurofibrillary tangles of Alzheimer’s disease (AD), brainstem Lewy bodies (LBs) (the neuropathological hallmark in Parkinson’s disease [PD]), Bunina bodies in Amyotrophic Lateral Sclerosis (ALS), and nuclear inclusions in CAG repeat expansion (polyglutamine/Q extension) disorders such as Huntington’s disease, Spinocerebellar Ataxias (SCAs), and Spinal and Bulbar Muscular Atrophy (SBMA; Kennedy’s disease) (reviewed recently by Alves-Rodrigues et al., 1998; Sherman and Goldberg, 2001) (Figure 2) PubMed:14556719
Accumulation of ubiquitin conjugates and/or inclusion bodies associated with ubiquitin, proteasome, and certain disease-characteristic proteins have been reported in a broad array of chronic neurodegenerative diseases, such as the neurofibrillary tangles of Alzheimer’s disease (AD), brainstem Lewy bodies (LBs) (the neuropathological hallmark in Parkinson’s disease [PD]), Bunina bodies in Amyotrophic Lateral Sclerosis (ALS), and nuclear inclusions in CAG repeat expansion (polyglutamine/Q extension) disorders such as Huntington’s disease, Spinocerebellar Ataxias (SCAs), and Spinal and Bulbar Muscular Atrophy (SBMA; Kennedy’s disease) (reviewed recently by Alves-Rodrigues et al., 1998; Sherman and Goldberg, 2001) (Figure 2) PubMed:14556719
Accumulation of ubiquitin conjugates and/or inclusion bodies associated with ubiquitin, proteasome, and certain disease-characteristic proteins have been reported in a broad array of chronic neurodegenerative diseases, such as the neurofibrillary tangles of Alzheimer’s disease (AD), brainstem Lewy bodies (LBs) (the neuropathological hallmark in Parkinson’s disease [PD]), Bunina bodies in Amyotrophic Lateral Sclerosis (ALS), and nuclear inclusions in CAG repeat expansion (polyglutamine/Q extension) disorders such as Huntington’s disease, Spinocerebellar Ataxias (SCAs), and Spinal and Bulbar Muscular Atrophy (SBMA; Kennedy’s disease) (reviewed recently by Alves-Rodrigues et al., 1998; Sherman and Goldberg, 2001) (Figure 2) PubMed:14556719
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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.