We are analyzing https://link.springer.com/article/10.1007/s13205-023-03525-y.

Title:
Vitamin B6, B12 and folate modulate deregulated pathways and protein aggregation in yeast model of Huntington disease | 3 Biotech
Description:
Huntington’s disease (HD) is an incurable and progressive neurodegenerative disease affecting the basal ganglia of the brain. HD is caused due to expansion of the polyglutamine tract in the protein Huntingtin resulting in aggregates. The increased PolyQ length results in aggregation of protein Huntingtin leading to neuronal cell death. Vitamin B6, B12 and folate are deficient in many neurodegenerative diseases. We performed an integrated analysis of transcriptomic, metabolomic and cofactor-protein network of vitamin B6, B12 and folate was performed. Our results show considerable overlap of pathways modulated by Vitamin B6, B12 and folate with those obtained from transcriptomic and metabolomic data of HD patients and model systems. Further, in yeast model of HD we showed treatment of B6, B12 or folate either alone or in combination showed impaired aggregate formation. Transcriptomic analysis of yeast model treated with B6, B12 and folate showed upregulation of pathways like ubiquitin mediated proteolysis, autophagy, peroxisome, fatty acid, lipid and nitrogen metabolism. Metabolomic analysis of yeast model shows deregulation of pathways like aminoacyl-tRNA biosynthesis, metabolism of various amino acids, nitrogen metabolism and glutathione metabolism. Integrated transcriptomic and metabolomic analysis of yeast model showed concordance in the pathways obtained. Knockout of Peroxisomal (PXP1 and PEX7) and Autophagy (ATG5) genes in yeast increased aggregates which is mitigated by vitamin B6, B12 and folate treatment. Taken together our results show a role for Vitamin B6, B12 and folate mediated modulation of pathways important for preventing protein aggregation with potential implications for HD.
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pubmed, article, google, scholar, cas, disease, central, huntingtons, yeast, analysis, model, autophagy, mol, brain, metabolism, biol, httpsdoiorgs, huntington, vitamin, huntingtin, sci, res, httpsdoiorg, protein, neurol, data, research, pathways, cell, gene, diseases, rep, front, expression, metabolic, human, dis, models, mutant, supplementary, folate, aggregation, sai, neurodegenerative, genet, med, science, india, department, acids,

Topics {✒️}

month download article/chapter high-resolution mass spectrometry pyridoxal 5′-phosphate-dependent enzymes dst/inspire fellowship/2016/if160535 wild-type huntingtin dosage integrated multi-omic analysis sequence alignment/map format chen y-ci impaired plp-dependent metabolism defective sphingosine-1-phosphate metabolism central nervous system ubiquitin–proteasome system leads ubiquitin–proteasome system involvement large-brained animal models cofactor-protein network network-based meta-analysis genome-wide expression profiling kanikaram sai phalguna post-mortem human brain full article pdf cofactor-protein interactions early-state transcriptional modulating protein aggregation thota sm 1h nmr analysis oxidative stress analysis privacy choices/manage cookies biomolecular interaction networks la spada ar article pradhan van der westhuyzen rhizomelic chondrodysplasia punctata van den bosch modern biology dbt mutant huntingtin toxicity protein huntingtin resulting protein huntingtin leading biotechnology-basic research gene expression data durga prasad patnana accepted manuscript version preventing protein aggregation gene expression omnibus striatal gene expression sequence count data aggregate-prone proteins amyotrophic lateral sclerosis amyotrophic lateral sclerosis compartment-dependent degradation disease model reveal

Questions {❓}

Crook ZR, Housman D (2011) Huntington’s disease: can mice lead the way to treatment?
Das S, Rajanikant GK (2014) Huntington disease: can a zebrafish trail leave more than a ripple?
Du X, Pang TYC, Hannan AJ (2013) A tale of two maladies?
Ravikumar B, Rubinsztein DC (2006) Role of autophagy in the clearance of mutant huntingtin: a step towards therapy?

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         description:Huntington’s disease (HD) is an incurable and progressive neurodegenerative disease affecting the basal ganglia of the brain. HD is caused due to expansion of the polyglutamine tract in the protein Huntingtin resulting in aggregates. The increased PolyQ length results in aggregation of protein Huntingtin leading to neuronal cell death. Vitamin B6, B12 and folate are deficient in many neurodegenerative diseases. We performed an integrated analysis of transcriptomic, metabolomic and cofactor-protein network of vitamin B6, B12 and folate was performed. Our results show considerable overlap of pathways modulated by Vitamin B6, B12 and folate with those obtained from transcriptomic and metabolomic data of HD patients and model systems. Further, in yeast model of HD we showed treatment of B6, B12 or folate either alone or in combination showed impaired aggregate formation. Transcriptomic analysis of yeast model treated with B6, B12 and folate showed upregulation of pathways like ubiquitin mediated proteolysis, autophagy, peroxisome, fatty acid, lipid and nitrogen metabolism. Metabolomic analysis of yeast model shows deregulation of pathways like aminoacyl-tRNA biosynthesis, metabolism of various amino acids, nitrogen metabolism and glutathione metabolism. Integrated transcriptomic and metabolomic analysis of yeast model showed concordance in the pathways obtained. Knockout of Peroxisomal (PXP1 and PEX7) and Autophagy (ATG5) genes in yeast increased aggregates which is mitigated by vitamin B6, B12 and folate treatment. Taken together our results show a role for Vitamin B6, B12 and folate mediated modulation of pathways important for preventing protein aggregation with potential implications for HD.
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      description:Huntington’s disease (HD) is an incurable and progressive neurodegenerative disease affecting the basal ganglia of the brain. HD is caused due to expansion of the polyglutamine tract in the protein Huntingtin resulting in aggregates. The increased PolyQ length results in aggregation of protein Huntingtin leading to neuronal cell death. Vitamin B6, B12 and folate are deficient in many neurodegenerative diseases. We performed an integrated analysis of transcriptomic, metabolomic and cofactor-protein network of vitamin B6, B12 and folate was performed. Our results show considerable overlap of pathways modulated by Vitamin B6, B12 and folate with those obtained from transcriptomic and metabolomic data of HD patients and model systems. Further, in yeast model of HD we showed treatment of B6, B12 or folate either alone or in combination showed impaired aggregate formation. Transcriptomic analysis of yeast model treated with B6, B12 and folate showed upregulation of pathways like ubiquitin mediated proteolysis, autophagy, peroxisome, fatty acid, lipid and nitrogen metabolism. Metabolomic analysis of yeast model shows deregulation of pathways like aminoacyl-tRNA biosynthesis, metabolism of various amino acids, nitrogen metabolism and glutathione metabolism. Integrated transcriptomic and metabolomic analysis of yeast model showed concordance in the pathways obtained. Knockout of Peroxisomal (PXP1 and PEX7) and Autophagy (ATG5) genes in yeast increased aggregates which is mitigated by vitamin B6, B12 and folate treatment. Taken together our results show a role for Vitamin B6, B12 and folate mediated modulation of pathways important for preventing protein aggregation with potential implications for HD.
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