Zobrazeno 1 - 8
of 8
pro vyhledávání: '"Mary Ann Crissey"'
Publikováno v:
PLoS ONE, Vol 6, Iss 4, p e18280 (2011)
Barrett's esophagus (BE) is an intestinal metaplasia that occurs in the setting of chronic acid and bile reflux and is associated with a risk for adenocarcinoma. Expression of intestine-specific transcription factors in the esophagus likely contribut
Externí odkaz:
https://doaj.org/article/7ad67009390340649acaed59a9af978e
Autor:
Mary Ann Crissey, Warren Masker
Publikováno v:
Mutation Research Letters. 301:235-241
Both spontaneous frameshift mutation and deletion mutation were measured in a T7 phage deficient in the 3'-->5' exonuclease of T7 DNA polymerase. It was found that the absence of this exonuclease caused a marked increase in the reversion of both plus
Autor:
Lee, Jennifer J.1 (AUTHOR) jeesoole@sas.upenn.edu, Jain, Vaibhav1 (AUTHOR), Amaravadi, Ravi K.1 (AUTHOR) Ravi.amaravadi@pennmedicine.upenn.edu
Publikováno v:
International Journal of Molecular Sciences. Nov2021, Vol. 22 Issue 22, p12402. 1p.
Autor:
Magness, Scott T., Puthoff, Brent J., Crissey, Mary Ann, Dunn, James, Henning, Susan J., Houchen, Courtney, Kaddis, John S., Kuo, Calvin J., Linheng Li, Lynch, John, Martin, Martin G., May, Randal, Niland, Joyce C., Olack, Barbara, Qian, Dajun, Stelzner, Matthias, Swain, John R., Fengchao Wang, Jiafang Wang, Xinwei Wang
Publikováno v:
American Journal of Physiology: Gastrointestinal & Liver Physiology; Oct2013, Vol. 305 Issue 8, pG542-G551, 10p
Publikováno v:
American Journal of Physiology: Gastrointestinal & Liver Physiology; Nov2010, Vol. 299, pG1054-G1067, 14p
Autor:
Yang, Y., Masker, W.
Publikováno v:
Molecular & General Genetics MGG; Jul1997, Vol. 255 Issue 3, p277-284, 8p
Publikováno v:
Nucleic Acids Research; 7/15/1991, Vol. 19 Issue 14, p3901-3905, 5p
Autor:
Dorottya Laczkó, John P. Lynch, Bradley Johnson, Gary W. Falk, Anil K. Rustgi, Mary Ann S. Crissey, Fang Wang
Publikováno v:
Cancer Research. 76:4253-4253
The molecular pathogenesis of colitis-associated colorectal cancer (CAC) has been suggested to involve oxidative stress-induced DNA damage, resulting in mutations of tumor-suppressor genes and activation of pro-oncogenic pathways. However, the exact