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Alan A. Dombkowski
Researcher at Wayne State University
Publications - 62
Citations - 2464
Alan A. Dombkowski is an academic researcher from Wayne State University. The author has contributed to research in topics: Gene & Gene expression. The author has an hindex of 24, co-authored 60 publications receiving 2143 citations. Previous affiliations of Alan A. Dombkowski include Boston Children's Hospital.
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Disulfide by Design 2.0: a web-based tool for disulfide engineering in proteins
TL;DR: DbD2 provides platform-independent access and significantly extends the original functionality of DbD, a web-based, platform- independent application that significantly extends functionality, visualization, and analysis capabilities beyond the original program.
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Protein disulfide engineering.
TL;DR: Progress in disulfide engineering is reviewed, with an emphasis on the issue of stability and computational methods that facilitate engineering efforts.
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Transcriptional profiling of human liver identifies sex-biased genes associated with polygenic dyslipidemia and coronary artery disease
Yijing Zhang,Kathrin Klein,Aarathi Sugathan,Najlla Nassery,Alan A. Dombkowski,Ulrich M. Zanger,David J. Waxman +6 more
TL;DR: It is established that human hepatic sex differences are widespread and affect diverse cell metabolic processes, and may help explain sex differences in lipid profiles associated with sex differential risk of coronary artery disease.
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Disulfide by Design™: a computational method for the rational design of disulfide bonds in proteins
TL;DR: Disulfide by Design is a program for the design of novel disulfide bonds in proteins that provides automated generation of modified PDB files including modeled disulfides.
Journal Article
Genomic amplification and a role in drug-resistance for the KDM5A histone demethylase in breast cancer
Jinling Hou,Jack Wu,Alan A. Dombkowski,Kezhong Zhang,Andreana N. Holowatyj,Julie L. Boerner,Zeng-Quan Yang +6 more
TL;DR: This study finds that the KDM5A gene was significantly amplified and over-expressed in various human tumors, including breast cancer, and demonstrates that K DM5A over-expression was associated with breast cancer drug resistance and suggests KDM 5A is a potential target for breast cancer therapy.