Zobrazeno 1 - 10
of 14
pro vyhledávání: '"Jill M, Beaver"'
Autor:
Yanhao Lai, Helen Budworth, Jill M. Beaver, Nelson L. S. Chan, Zunzhen Zhang, Cynthia T. McMurray, Yuan Liu
Publikováno v:
Nature Communications, Vol 7, Iss 1, Pp 1-15 (2016)
The expansion of trinucleotide repeats can have detrimental effects and give rise to a range of human diseases. Here the authors report that the mismatch repair and the base excision repair machinery can operate together to promote expansion during l
Externí odkaz:
https://doaj.org/article/3879ba8a8aee40aca671630c5cc0af1e
Autor:
Zhongliang Jiang, Yanhao Lai, Jill M. Beaver, Pawlos S. Tsegay, Ming-Lang Zhao, Julie K. Horton, Marco Zamora, Hayley L. Rein, Frank Miralles, Mohammad Shaver, Joshua D. Hutcheson, Irina Agoulnik, Samuel H. Wilson, Yuan Liu
Publikováno v:
Cells, Vol 9, Iss 1, p 225 (2020)
DNA damage and base excision repair (BER) are actively involved in the modulation of DNA methylation and demethylation. However, the underlying molecular mechanisms remain unclear. In this study, we seek to understand the mechanisms by exploring the
Externí odkaz:
https://doaj.org/article/788c11cb8b9c443193a8998431ba13e9
Publikováno v:
PLoS ONE, Vol 13, Iss 2, p e0192148 (2018)
Oxidative DNA damage and base excision repair (BER) play important roles in modulating trinucleotide repeat (TNR) instability that is associated with human neurodegenerative diseases and cancer. We have reported that BER of base lesions can lead to T
Externí odkaz:
https://doaj.org/article/bd2f798d46a6491e8d72cd5f4fed059a
Autor:
Yanhao Lai, Jill M Beaver, Karla Lorente, Jonathan Melo, Shyama Ramjagsingh, Irina U Agoulnik, Zunzhen Zhang, Yuan Liu
Publikováno v:
PLoS ONE, Vol 9, Iss 4, p e93464 (2014)
Expansion of GAA·TTC repeats within the first intron of the frataxin gene is the cause of Friedreich's ataxia (FRDA), an autosomal recessive neurodegenerative disorder. However, no effective treatment for the disease has been developed as yet. In th
Externí odkaz:
https://doaj.org/article/8542abc33b1d4c1db464a473956f4000
Autor:
Zhongliang, Jiang, Yanhao, Lai, Jill M, Beaver, Pawlos S, Tsegay, Ming-Lang, Zhao, Julie K, Horton, Marco, Zamora, Hayley L, Rein, Frank, Miralles, Mohammad, Shaver, Joshua D, Hutcheson, Irina, Agoulnik, Samuel H, Wilson, Yuan, Liu
Publikováno v:
Cells
DNA damage and base excision repair (BER) are actively involved in the modulation of DNA methylation and demethylation. However, the underlying molecular mechanisms remain unclear. In this study, we seek to understand the mechanisms by exploring the
Autor:
James M. Anderson, Frederick L. Tyson, Linda S. Birnbaum, Lisa H. Chadwick, John S. Satterlee, Kim McAllister, Ananda L. Roy, Elizabeth L. Wilder, Nora D. Volkow, Jill M. Beaver
Publikováno v:
Science Advances
We outline the reasons why the Roadmap Epigenomics Program, as a group science effort, is a success story.
The NIH Roadmap Epigenomics Program was launched to deliver reference epigenomic data from human tissues and cells, develop tools and meth
The NIH Roadmap Epigenomics Program was launched to deliver reference epigenomic data from human tissues and cells, develop tools and meth
Publikováno v:
DNA Repair (Amst)
Trinucleotide repeat (TNR) instability is the cause of over 40 human neurodegenerative diseases and certain types of cancer. TNR instability can result from DNA replication, repair, recombination, and gene transcription. Emerging evidence indicates t
Publikováno v:
Nucleic Acids Research
Base excision repair (BER) of an oxidized base within a trinucleotide repeat (TNR) tract can lead to TNR expansions that are associated with over 40 human neurodegenerative diseases. This occurs as a result of DNA secondary structures such as hairpin
Publikováno v:
PLoS ONE
PLoS ONE, Vol 13, Iss 2, p e0192148 (2018)
PLoS ONE, Vol 13, Iss 2, p e0192148 (2018)
Oxidative DNA damage and base excision repair (BER) play important roles in modulating trinucleotide repeat (TNR) instability that is associated with human neurodegenerative diseases and cancer. We have reported that BER of base lesions can lead to T