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path(MESH:"Huntington Disease")

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Entity

Name
Huntington Disease
Namespace
mesh
Namespace Version
20180828
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/1b20f0637c395f8aa89c2e2e342d7b704062c242/external/mesh-names.belns

Appears in Networks 9

Functional aspects of meningeal lymphatics in ageing and Alzheimer’s disease v1.0.0

Alzheimer's Disease: Targeting the Cholinergic System v1.0.0

A chaperome subnetwork safeguards proteostasis in aging and neurodegenerative disease. v1.0.0

The Ubiquitin Proteasome System in Neurodegenerative Diseases: Sometimes the Chicken, Sometimes the Egg v1.0.0

The Biology of Proteostasis in Aging and Disease v1.0.0

Interplay of pathogenic forms of human tau with different autophagic pathways v1.0.1

Imbalances in the Hsp90 Chaperone Machinery: Implications for Tauopathies v1.0.0

Autophagy and the ubiquitin-proteasome system: collaborators in neuroprotection v1.0.0

New insights into the role of microRNAs and long noncoding RNAs in most common neurodegenerative diseases v1.0.0

In-Edges 24

act(a(MESH:"Lymphatic Vessels")) association path(MESH:"Huntington Disease") View Subject | View Object

Notably, although the fold change in significantly altered genes after lymphatic ablation and MWM was moderate (−1.79 < log2(fold change) < 1.69), functional enrichment analysis (Extended Data Fig. 5o, p) revealed changes in gene sets associated with neurodegenerative diseases, such as Huntington’s, Parkinson’s and Alzheimer’s disease (Extended Data Fig. 5o) PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Meninges

act(p(HGNC:CHAT)) negativeCorrelation path(MESH:"Huntington Disease") View Subject | View Object

Moreover, Huntington’s disease appears to be associated with decreased ChAT activity PubMed:26813123

Appears in Networks:

complex(a(GO:"proteasome complex"), a(MESH:"Inclusion Bodies")) 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

Appears in Networks:

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

Appears in Networks:

p(HGNC:HTT, var("?")) increases path(MESH:"Huntington Disease") View Subject | View Object

The disease is caused by a mutation in the gene coding for Huntingtin—a protein of hitherto unknown function, although it has been recently implicated in the control of gene transcription (Zuccato et al., 2003). PubMed:14556719

Appears in Networks:

a(CHEBI:sirolimus) decreases path(MESH:"Huntington Disease") View Subject | View Object

Treatment of cell, Drosophila, and mouse models of HD, SCA3/MJD, AD, PD, and ALS with the mTOR inhibitor rapamycin (or a derivative) reduces aggregation and suppresses disease (140– 143). PubMed:25784053

Appears in Networks:
Annotations
Cell Ontology (CL)
motor neuron

p(FPLX:HSPA) positiveCorrelation path(MESH:"Huntington Disease") View Subject | View Object

Furthermore, increased levels of HSP70 were found in the cerebellar cortex of human HD brain samples but not in tissue from unaffected individuals or from brains of PD patients (57). PubMed:25784053

Appears in Networks:
Annotations
MeSH
Cerebral Cortex

p(HGNC:ATF6) negativeCorrelation path(MESH:"Huntington Disease") View Subject | View Object

Disruption of the ATF6 arm of the UPR(ER) is reported to occur in mouse models of HD and a VAPB cell model of ALS, suggesting that differential changes in UPR arms may be a feature of disease progression (102, 103). PubMed:25784053

Appears in Networks:
Annotations
Cell Ontology (CL)
motor neuron

p(HGNC:STUB1) association path(MESH:"Huntington Disease") View Subject | View Object

CHIP has been linked to several neurodegenerative disorders including Huntington’s disease, Parkinson’s disease and AD as well as other diseases such as cystic fibrosis and cancer (Dickey et al., 2007b; Edkins, 2015). PubMed:29311797

Appears in Networks:
Annotations
MeSH
Cerebral Cortex

a(CHEBI:sirolimus) decreases path(MESH:"Huntington Disease") View Subject | View Object

Indeed, treatment with rapamycin ameliorates the degenerative phenotype in a Drosophila model of SBMA, as well as in Drosophila and mouse models of Huntington’s disease [48,50,52]. PubMed:18930136

Appears in Networks:

a(GO:autolysosome) positiveCorrelation path(MESH:"Huntington Disease") View Subject | View Object

In Huntington’s disease, affected neurons show accumulation of huntingtin in cathepsin-D-positive vacuoles [24]. Cathepsin-D is a lysosomal protease enriched in neuronal tissues, suggesting that these are autolysosomes PubMed:18930136

Appears in Networks:

g(HGNC:MIR196A1) association path(MESH:"Huntington Disease") View Subject | View Object

A case in point is miR‐196a that affects HD PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

p(HGNC:HTT, var("?")) increases path(MESH:"Huntington Disease") View Subject | View Object

This disease is inherited by autosomal dominant alleles due to a mutation in the huntingtin gene (HTT). PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

g(HGNC:MIR206) association path(MESH:"Huntington Disease") View Subject | View Object

Also, a significant relationship has been found between the number of copies of CAG and some miRNAs in the striatum and cortex of mice with Huntington. These miRNAs include miR‐206, miR‐301b, miR‐92b, miR‐378b, miR‐208b, and miR‐449a. PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

g(HGNC:MIR208B) association path(MESH:"Huntington Disease") View Subject | View Object

Also, a significant relationship has been found between the number of copies of CAG and some miRNAs in the striatum and cortex of mice with Huntington. These miRNAs include miR‐206, miR‐301b, miR‐92b, miR‐378b, miR‐208b, and miR‐449a. PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

g(HGNC:MIR301B) association path(MESH:"Huntington Disease") View Subject | View Object

Also, a significant relationship has been found between the number of copies of CAG and some miRNAs in the striatum and cortex of mice with Huntington. These miRNAs include miR‐206, miR‐301b, miR‐92b, miR‐378b, miR‐208b, and miR‐449a. PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

g(HGNC:MIR378B) association path(MESH:"Huntington Disease") View Subject | View Object

Also, a significant relationship has been found between the number of copies of CAG and some miRNAs in the striatum and cortex of mice with Huntington. These miRNAs include miR‐206, miR‐301b, miR‐92b, miR‐378b, miR‐208b, and miR‐449a. PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

g(HGNC:MIR449A) association path(MESH:"Huntington Disease") View Subject | View Object

Also, a significant relationship has been found between the number of copies of CAG and some miRNAs in the striatum and cortex of mice with Huntington. These miRNAs include miR‐206, miR‐301b, miR‐92b, miR‐378b, miR‐208b, and miR‐449a. PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

g(HGNC:MIR92B) association path(MESH:"Huntington Disease") View Subject | View Object

Also, a significant relationship has been found between the number of copies of CAG and some miRNAs in the striatum and cortex of mice with Huntington. These miRNAs include miR‐206, miR‐301b, miR‐92b, miR‐378b, miR‐208b, and miR‐449a. PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:"Deglutition Disorders") association path(MESH:"Huntington Disease") View Subject | View Object

Dysphagia, dysphasia, and seizures are common symptoms in HD PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:Aphasia) association path(MESH:"Huntington Disease") View Subject | View Object

Dysphagia, dysphasia, and seizures are common symptoms in HD PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:Chorea) association path(MESH:"Huntington Disease") View Subject | View Object

HD is a neurodegenerative disease characterized by an insidious onset and subsequent progression of chorea and dementia, which usually presents at the ages of 30 to 50, and its symptoms increase with age. PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:Dementia) association path(MESH:"Huntington Disease") View Subject | View Object

HD is a neurodegenerative disease characterized by an insidious onset and subsequent progression of chorea and dementia, which usually presents at the ages of 30 to 50, and its symptoms increase with age. PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:Seizures) association path(MESH:"Huntington Disease") View Subject | View Object

Dysphagia, dysphasia, and seizures are common symptoms in HD PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

Out-Edges 40

path(MESH:"Huntington Disease") association act(a(MESH:"Lymphatic Vessels")) View Subject | View Object

Notably, although the fold change in significantly altered genes after lymphatic ablation and MWM was moderate (−1.79 < log2(fold change) < 1.69), functional enrichment analysis (Extended Data Fig. 5o, p) revealed changes in gene sets associated with neurodegenerative diseases, such as Huntington’s, Parkinson’s and Alzheimer’s disease (Extended Data Fig. 5o) PubMed:30046111

Appears in Networks:
Annotations
Confidence
High
MeSH
Meninges

path(MESH:"Huntington Disease") negativeCorrelation act(p(HGNC:CHAT)) View Subject | View Object

Moreover, Huntington’s disease appears to be associated with decreased ChAT activity PubMed:26813123

Appears in Networks:

path(MESH:"Huntington Disease") decreases p(HGNC:HSP90AB1) View Subject | View Object

Four genes that are significantly repressed both in AD and HD (HSP90AB1, HSPA8, HSPA14, and TCP1) are also repressed in aging (Figure 6B). PubMed:25437566

Appears in Networks:
Annotations
MeSH
Brain
MeSH
Alzheimer Disease
MeSH
Huntington Disease
MeSH
Parkinson Disease

path(MESH:"Huntington Disease") decreases p(HGNC:HSPA8) View Subject | View Object

Four genes that are significantly repressed both in AD and HD (HSP90AB1, HSPA8, HSPA14, and TCP1) are also repressed in aging (Figure 6B). PubMed:25437566

Appears in Networks:
Annotations
MeSH
Brain
MeSH
Alzheimer Disease
MeSH
Huntington Disease
MeSH
Parkinson Disease

path(MESH:"Huntington Disease") decreases p(HGNC:HSPA14) View Subject | View Object

Four genes that are significantly repressed both in AD and HD (HSP90AB1, HSPA8, HSPA14, and TCP1) are also repressed in aging (Figure 6B). PubMed:25437566

Appears in Networks:
Annotations
MeSH
Brain
MeSH
Alzheimer Disease
MeSH
Huntington Disease
MeSH
Parkinson Disease

path(MESH:"Huntington Disease") decreases p(HGNC:TCP1) View Subject | View Object

Four genes that are significantly repressed both in AD and HD (HSP90AB1, HSPA8, HSPA14, and TCP1) are also repressed in aging (Figure 6B). PubMed:25437566

Appears in Networks:
Annotations
MeSH
Brain
MeSH
Alzheimer Disease
MeSH
Huntington Disease
MeSH
Parkinson Disease

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

Appears in Networks:

path(MESH:"Huntington Disease") positiveCorrelation complex(a(GO:"proteasome complex"), a(MESH:"Inclusion 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

Appears in Networks:

path(MESH:"Huntington Disease") positiveCorrelation p(FPLX:HSPA) View Subject | View Object

Furthermore, increased levels of HSP70 were found in the cerebellar cortex of human HD brain samples but not in tissue from unaffected individuals or from brains of PD patients (57). PubMed:25784053

Appears in Networks:
Annotations
MeSH
Cerebral Cortex

path(MESH:"Huntington Disease") negativeCorrelation p(HGNC:ATF6) View Subject | View Object

Disruption of the ATF6 arm of the UPR(ER) is reported to occur in mouse models of HD and a VAPB cell model of ALS, suggesting that differential changes in UPR arms may be a feature of disease progression (102, 103). PubMed:25784053

Appears in Networks:
Annotations
Cell Ontology (CL)
motor neuron

path(MESH:"Huntington Disease") increases path(MESH:"Proteostasis Deficiencies") View Subject | View Object

It is well accepted that loss of proteostasis occurs gradually with age and underlies the basis of severe neurodegenerative disorders such as Parkinson’s disease, Huntington’s disease, Alzheimer’s disease, and other types of frontotemporal dementia (Prahlad & Morimoto, 2009; Voisine et al., 2010; Morimoto & Cuervo, 2014) PubMed:29024336

Appears in Networks:
Annotations
Confidence
High
MeSH
Brain
MeSH
Neurons

path(MESH:"Huntington Disease") association p(HGNC:STUB1) View Subject | View Object

CHIP has been linked to several neurodegenerative disorders including Huntington’s disease, Parkinson’s disease and AD as well as other diseases such as cystic fibrosis and cancer (Dickey et al., 2007b; Edkins, 2015). PubMed:29311797

Appears in Networks:
Annotations
MeSH
Cerebral Cortex

path(MESH:"Huntington Disease") positiveCorrelation a(GO:autolysosome) View Subject | View Object

In Huntington’s disease, affected neurons show accumulation of huntingtin in cathepsin-D-positive vacuoles [24]. Cathepsin-D is a lysosomal protease enriched in neuronal tissues, suggesting that these are autolysosomes PubMed:18930136

Appears in Networks:

path(MESH:"Huntington Disease") association path(MESH:Chorea) View Subject | View Object

HD is a neurodegenerative disease characterized by an insidious onset and subsequent progression of chorea and dementia, which usually presents at the ages of 30 to 50, and its symptoms increase with age. PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:"Huntington Disease") association path(MESH:Dementia) View Subject | View Object

HD is a neurodegenerative disease characterized by an insidious onset and subsequent progression of chorea and dementia, which usually presents at the ages of 30 to 50, and its symptoms increase with age. PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:"Huntington Disease") association path(MESH:"Deglutition Disorders") View Subject | View Object

Dysphagia, dysphasia, and seizures are common symptoms in HD PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:"Huntington Disease") association path(MESH:Aphasia) View Subject | View Object

Dysphagia, dysphasia, and seizures are common symptoms in HD PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:"Huntington Disease") association path(MESH:Seizures) View Subject | View Object

Dysphagia, dysphasia, and seizures are common symptoms in HD PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:"Huntington Disease") association g(HGNC:MIR196A1) View Subject | View Object

A case in point is miR‐196a that affects HD PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:"Huntington Disease") increases g(HGNC:MIR196A1) View Subject | View Object

Currently, miR‐10b‐5p, miR‐196a‐5p, miR‐196b‐ 5p, miR‐615‐3p, and miR‐1247‐5p increase in HD, and studies have shown that miR‐196a‐5p, miR‐196b‐5p, and miR‐615‐3p have been almost zero in the control group PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:"Huntington Disease") association g(HGNC:MIR206) View Subject | View Object

Also, a significant relationship has been found between the number of copies of CAG and some miRNAs in the striatum and cortex of mice with Huntington. These miRNAs include miR‐206, miR‐301b, miR‐92b, miR‐378b, miR‐208b, and miR‐449a. PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:"Huntington Disease") association g(HGNC:MIR301B) View Subject | View Object

Also, a significant relationship has been found between the number of copies of CAG and some miRNAs in the striatum and cortex of mice with Huntington. These miRNAs include miR‐206, miR‐301b, miR‐92b, miR‐378b, miR‐208b, and miR‐449a. PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:"Huntington Disease") association g(HGNC:MIR92B) View Subject | View Object

Also, a significant relationship has been found between the number of copies of CAG and some miRNAs in the striatum and cortex of mice with Huntington. These miRNAs include miR‐206, miR‐301b, miR‐92b, miR‐378b, miR‐208b, and miR‐449a. PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:"Huntington Disease") association g(HGNC:MIR378B) View Subject | View Object

Also, a significant relationship has been found between the number of copies of CAG and some miRNAs in the striatum and cortex of mice with Huntington. These miRNAs include miR‐206, miR‐301b, miR‐92b, miR‐378b, miR‐208b, and miR‐449a. PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:"Huntington Disease") association g(HGNC:MIR208B) View Subject | View Object

Also, a significant relationship has been found between the number of copies of CAG and some miRNAs in the striatum and cortex of mice with Huntington. These miRNAs include miR‐206, miR‐301b, miR‐92b, miR‐378b, miR‐208b, and miR‐449a. PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:"Huntington Disease") association g(HGNC:MIR449A) View Subject | View Object

Also, a significant relationship has been found between the number of copies of CAG and some miRNAs in the striatum and cortex of mice with Huntington. These miRNAs include miR‐206, miR‐301b, miR‐92b, miR‐378b, miR‐208b, and miR‐449a. PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:"Huntington Disease") decreases g(NCBIGENE:406915) View Subject | View Object

These experiments show that in apes, miR‐128a levels at birth and during the disease (either in the presymptomatic or postsymptomatic stage) show a significant reduction of this miRNA PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:"Huntington Disease") increases g(MIRBASE:"hsa-mir-10b") View Subject | View Object

Currently, miR‐10b‐5p, miR‐196a‐5p, miR‐196b‐ 5p, miR‐615‐3p, and miR‐1247‐5p increase in HD, and studies have shown that miR‐196a‐5p, miR‐196b‐5p, and miR‐615‐3p have been almost zero in the control group PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:"Huntington Disease") increases g(HGNC:MIR196B) View Subject | View Object

Currently, miR‐10b‐5p, miR‐196a‐5p, miR‐196b‐ 5p, miR‐615‐3p, and miR‐1247‐5p increase in HD, and studies have shown that miR‐196a‐5p, miR‐196b‐5p, and miR‐615‐3p have been almost zero in the control group PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:"Huntington Disease") increases g(HGNC:MIR615) View Subject | View Object

Currently, miR‐10b‐5p, miR‐196a‐5p, miR‐196b‐ 5p, miR‐615‐3p, and miR‐1247‐5p increase in HD, and studies have shown that miR‐196a‐5p, miR‐196b‐5p, and miR‐615‐3p have been almost zero in the control group PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:"Huntington Disease") increases g(HGNC:MIR1247) View Subject | View Object

Currently, miR‐10b‐5p, miR‐196a‐5p, miR‐196b‐ 5p, miR‐615‐3p, and miR‐1247‐5p increase in HD, and studies have shown that miR‐196a‐5p, miR‐196b‐5p, and miR‐615‐3p have been almost zero in the control group PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:"Huntington Disease") decreases g(MGI:Mir22) View Subject | View Object

In 12‐month‐old HD transgenic mice, downregulation was observed in the expression of the following miRNAs: miR‐ 22, miR‐29c, miR‐128, miR‐132, miR‐138, miR‐218, miR‐ 222, miR‐344, and miR‐674 PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:"Huntington Disease") decreases g(MGI:Mir29c) View Subject | View Object

In 12‐month‐old HD transgenic mice, downregulation was observed in the expression of the following miRNAs: miR‐ 22, miR‐29c, miR‐128, miR‐132, miR‐138, miR‐218, miR‐ 222, miR‐344, and miR‐674 PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:"Huntington Disease") decreases g(MGI:"Mir128-1") View Subject | View Object

In 12‐month‐old HD transgenic mice, downregulation was observed in the expression of the following miRNAs: miR‐ 22, miR‐29c, miR‐128, miR‐132, miR‐138, miR‐218, miR‐ 222, miR‐344, and miR‐674 PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:"Huntington Disease") decreases g(MGI:Mir132) View Subject | View Object

In 12‐month‐old HD transgenic mice, downregulation was observed in the expression of the following miRNAs: miR‐ 22, miR‐29c, miR‐128, miR‐132, miR‐138, miR‐218, miR‐ 222, miR‐344, and miR‐674 PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:"Huntington Disease") decreases g(MGI:"Mir138-1") View Subject | View Object

In 12‐month‐old HD transgenic mice, downregulation was observed in the expression of the following miRNAs: miR‐ 22, miR‐29c, miR‐128, miR‐132, miR‐138, miR‐218, miR‐ 222, miR‐344, and miR‐674 PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:"Huntington Disease") decreases g(MGI:"Mir218-1") View Subject | View Object

In 12‐month‐old HD transgenic mice, downregulation was observed in the expression of the following miRNAs: miR‐ 22, miR‐29c, miR‐128, miR‐132, miR‐138, miR‐218, miR‐ 222, miR‐344, and miR‐674 PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:"Huntington Disease") decreases g(MGI:Mir222) View Subject | View Object

In 12‐month‐old HD transgenic mice, downregulation was observed in the expression of the following miRNAs: miR‐ 22, miR‐29c, miR‐128, miR‐132, miR‐138, miR‐218, miR‐ 222, miR‐344, and miR‐674 PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:"Huntington Disease") decreases g(NCBIGENE:723931) View Subject | View Object

In 12‐month‐old HD transgenic mice, downregulation was observed in the expression of the following miRNAs: miR‐ 22, miR‐29c, miR‐128, miR‐132, miR‐138, miR‐218, miR‐ 222, miR‐344, and miR‐674 PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

path(MESH:"Huntington Disease") decreases g(NCBIGENE:732489) View Subject | View Object

In 12‐month‐old HD transgenic mice, downregulation was observed in the expression of the following miRNAs: miR‐ 22, miR‐29c, miR‐128, miR‐132, miR‐138, miR‐218, miR‐ 222, miR‐344, and miR‐674 PubMed:30663117

Appears in Networks:
Annotations
MeSH
Huntington Disease

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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.