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Appears in Networks 1

In-Edges 6

a(GO:"Bunina body") positiveCorrelation complex(a(MESH:"Inclusion Bodies"), a(MESH:Ubiquitin)) View Subject | View Object

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

a(MESH:"Lewy Bodies") positiveCorrelation complex(a(MESH:"Inclusion Bodies"), a(MESH:Ubiquitin)) View Subject | View Object

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

a(MESH:"Neurofibrillary Tangles") positiveCorrelation complex(a(MESH:"Inclusion Bodies"), a(MESH:Ubiquitin)) View Subject | View Object

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

path(MESH:"Bulbo-Spinal Atrophy, X-Linked") positiveCorrelation complex(a(MESH:"Inclusion Bodies"), a(MESH:Ubiquitin)) View Subject | View Object

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

path(MESH:"Huntington Disease") positiveCorrelation complex(a(MESH:"Inclusion Bodies"), a(MESH:Ubiquitin)) View Subject | View Object

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

path(MESH:"Spinocerebellar Ataxias") positiveCorrelation complex(a(MESH:"Inclusion Bodies"), a(MESH:Ubiquitin)) View Subject | View Object

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

Out-Edges 8

complex(a(MESH:"Inclusion Bodies"), a(MESH:Ubiquitin)) positiveCorrelation a(MESH:"Neurofibrillary Tangles") View Subject | View Object

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

complex(a(MESH:"Inclusion Bodies"), a(MESH:Ubiquitin)) positiveCorrelation a(GO:"Bunina body") View Subject | View Object

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

complex(a(MESH:"Inclusion Bodies"), a(MESH:Ubiquitin)) positiveCorrelation path(MESH:"Huntington Disease") View Subject | View Object

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

complex(a(MESH:"Inclusion Bodies"), a(MESH:Ubiquitin)) positiveCorrelation path(MESH:"Spinocerebellar Ataxias") View Subject | View Object

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

complex(a(MESH:"Inclusion Bodies"), a(MESH:Ubiquitin)) positiveCorrelation path(MESH:"Bulbo-Spinal Atrophy, X-Linked") View Subject | View Object

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

complex(a(MESH:"Inclusion Bodies"), a(MESH:Ubiquitin)) positiveCorrelation a(MESH:"Lewy Bodies") View Subject | View Object

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

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

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.