Insights into the evolutionary features of human neurodegenerative diseases.

Comparative analyses between human disease and non-disease genes are of great interest in understanding human disease gene evolution. However, the progression of neurodegenerative diseases (NDD) involving amyloid formation in specific brain regions is still unknown. Therefore, in this study, we main...

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Autores principales: Arup Panda, Tina Begum, Tapash Chandra Ghosh
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Publicado: Public Library of Science (PLoS) 2012
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Acceso en línea:https://doaj.org/article/973a93fee37049249bc44cda0f537000
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spelling oai:doaj.org-article:973a93fee37049249bc44cda0f5370002021-11-18T08:10:37ZInsights into the evolutionary features of human neurodegenerative diseases.1932-620310.1371/journal.pone.0048336https://doaj.org/article/973a93fee37049249bc44cda0f5370002012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23118989/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Comparative analyses between human disease and non-disease genes are of great interest in understanding human disease gene evolution. However, the progression of neurodegenerative diseases (NDD) involving amyloid formation in specific brain regions is still unknown. Therefore, in this study, we mainly focused our analysis on the evolutionary features of human NDD genes with respect to non-disease genes. Here, we observed that human NDD genes are evolutionarily conserved relative to non-disease genes. To elucidate the conserved nature of NDD genes, we incorporated the evolutionary attributes like gene expression level, number of regulatory miRNAs, protein connectivity, intrinsic disorder content and relative aggregation propensity in our analysis. Our studies demonstrate that NDD genes have higher gene expression levels in favor of their lower evolutionary rates. Additionally, we observed that NDD genes have higher number of different regulatory miRNAs target sites and also have higher interaction partners than the non-disease genes. Moreover, miRNA targeted genes are known to have higher disorder content. In contrast, our analysis exclusively established that NDD genes have lower disorder content. In favor of our analysis, we found that NDD gene encoded proteins are enriched with multi interface hubs (party hubs) with lower disorder contents. Since, proteins with higher disorder content need to adapt special structure to reduce their aggregation propensity, NDD proteins found to have elevated relative aggregation propensity (RAP) in support of their lower disorder content. Finally, our categorical regression analysis confirmed the underlined relative dominance of protein connectivity, 3'UTR length, RAP, nature of hubs (singlish/multi interface) and disorder content for such evolutionary rates variation between human NDD genes and non-disease genes.Arup PandaTina BegumTapash Chandra GhoshPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 10, p e48336 (2012)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Arup Panda
Tina Begum
Tapash Chandra Ghosh
Insights into the evolutionary features of human neurodegenerative diseases.
description Comparative analyses between human disease and non-disease genes are of great interest in understanding human disease gene evolution. However, the progression of neurodegenerative diseases (NDD) involving amyloid formation in specific brain regions is still unknown. Therefore, in this study, we mainly focused our analysis on the evolutionary features of human NDD genes with respect to non-disease genes. Here, we observed that human NDD genes are evolutionarily conserved relative to non-disease genes. To elucidate the conserved nature of NDD genes, we incorporated the evolutionary attributes like gene expression level, number of regulatory miRNAs, protein connectivity, intrinsic disorder content and relative aggregation propensity in our analysis. Our studies demonstrate that NDD genes have higher gene expression levels in favor of their lower evolutionary rates. Additionally, we observed that NDD genes have higher number of different regulatory miRNAs target sites and also have higher interaction partners than the non-disease genes. Moreover, miRNA targeted genes are known to have higher disorder content. In contrast, our analysis exclusively established that NDD genes have lower disorder content. In favor of our analysis, we found that NDD gene encoded proteins are enriched with multi interface hubs (party hubs) with lower disorder contents. Since, proteins with higher disorder content need to adapt special structure to reduce their aggregation propensity, NDD proteins found to have elevated relative aggregation propensity (RAP) in support of their lower disorder content. Finally, our categorical regression analysis confirmed the underlined relative dominance of protein connectivity, 3'UTR length, RAP, nature of hubs (singlish/multi interface) and disorder content for such evolutionary rates variation between human NDD genes and non-disease genes.
format article
author Arup Panda
Tina Begum
Tapash Chandra Ghosh
author_facet Arup Panda
Tina Begum
Tapash Chandra Ghosh
author_sort Arup Panda
title Insights into the evolutionary features of human neurodegenerative diseases.
title_short Insights into the evolutionary features of human neurodegenerative diseases.
title_full Insights into the evolutionary features of human neurodegenerative diseases.
title_fullStr Insights into the evolutionary features of human neurodegenerative diseases.
title_full_unstemmed Insights into the evolutionary features of human neurodegenerative diseases.
title_sort insights into the evolutionary features of human neurodegenerative diseases.
publisher Public Library of Science (PLoS)
publishDate 2012
url https://doaj.org/article/973a93fee37049249bc44cda0f537000
work_keys_str_mv AT aruppanda insightsintotheevolutionaryfeaturesofhumanneurodegenerativediseases
AT tinabegum insightsintotheevolutionaryfeaturesofhumanneurodegenerativediseases
AT tapashchandraghosh insightsintotheevolutionaryfeaturesofhumanneurodegenerativediseases
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