2013-2014 Seminar Schedule

Computational Biology Branch (CBB) is the research branch of the National Center for Biotechnology Information (NCBI), National Library of Medicine (NLM), National Institutes of Health (NIH).

We hold weekly seminars by CBB members each Tuesday at 11 AM in the Building 38A B2 NCBI Library. Visitors' presentations usually take place in the same room, but are scheduled on a different day of the week. If scheduling a visitor's presentation, please don't forget to book a seminar room.

To schedule a seminar, please click on the appropriate date in the calendar.

Contact Ivan Ovcharenko with questions or if you need help scheduling a seminar.

Upcoming Seminars

Zoya IgnatovaMarch 2, 2015 at 14:00
Affiliation: Biochemistry, University of Potsdam, Potsdam, Germany and Biochemistry and Molecular Biology, University of Hamburg, Hamburg, Germany
Host: Ben Busby
Silent but visible: a common silent polymorphism in CFTR alters physiological function and global protein conformation
“Synonymous single-nucleotide polymorphisms (sSNPs) in the coding sequence are considered neutral for protein function, as by definition they affect only codons, not amino acids. We investigated T2562G, one of the most common sSNPs in the cystic fibrosis transmembrane conductance regulator (CFTR) gene; this silent mutation is associated with the genetic disease cystic fibrosis (CF) and an increased risk of CFTR-related diseases. T2562G, which replaces a frequent Thr854-ACT codon with a Thr854-ACG triplet, altered the physiological function and global conformation of CFTR. Microarray measurements in human bronchial epithelial cell line and primary cells derived from CF-patients reveal that the mutant ACG codon is read by a rare tRNA, suggesting that T2562G sSNP most likely alters the local ribosomal speed along mRNA. Increasing the cellular concentration of tRNAThr cognate to the mutant ACG codon by transient transfection, rescued the folding and functional defects of T2562G-CFTR. These findings reveal an unexpected mechanism for sSNP-associated diseases. Furthermore, we use ribosome profiling and RNA-seq to gain insights into the effect of CFTR misfolding on global, translatome and transcriptome-wide scale. More specifically we address its effect on the ER-folding machinery and its ability to activate the unfolded protein response (UPR). We analyzed CF bronchial epithelial cells and samples derived from lung tissue of CF patients which show distinct behavior. While cells show a robust behavior and lack an induction of UPR, the ER-mediated stress response in patient samples is activated. “

Thomas MadejMarch 3, 2015 at 11:00
Developments in the NCBI Structure Group
Lewis Y GeerMarch 10, 2015 at 11:00
TBD