Gene Core
Gene Core

Anthony Orth, Ph.D.
Associate Director, Genomics


Our Gene Core is combining the intrigue of basic genomic research with the excitement of the latest technologies in three lines of investigation.

On the technology side, we identify, test, and deploy systems permitting viral delivery of shRNAs and cDNAs. This enables the screening of primary, difficult-to-transfect human or mouse cell lines and primary cells, supplementing our already broad collections of cDNAs, shRNAs, and siRNAs for transfection-mediated experiments. To generate and maintain our libraries, which now contain a total of over 250,000 unique entities, we employ an advanced suite of automated robotic instruments, permitting high throughput rearraying and preparation of ready-to-assay materials. Our current libraries include:

Plasmid cDNA collections 

• Origene unique human cDNA 

19,823

• MGC unique human cDNA  

20,739

• MGC unique mouse cDNA  

15,652

• Anti-human 5k druggable shRNA (random) 

14,763

• Anti-human 5k druggable shRNA (poolable ) 

14,411 

• Anti-human 474 non-coding shRNA  

    775

• Anti-mouse 616 kinase shRNA 

 2,777

• GNF human ORFs 

 1,441

• MGC mouse+human Kinase cDNA 

    847 

 

 

 

 

 








Viral cDNA collections

• Anti-human 5k druggable shRNA in lenti 14,398
• Anti-mouse kinase shRNA in lenti  2,552
• MGC mouse/human cDNA in retro  8,412


siRNA collections

• GNF anti-human 5k druggable siRNA   10,180
• Novartis anti-human 5k druggable siRNA     9,736
• FGA anti-human 24k whole genome siRNA   49,276
• FGA anti-human 24k whole genome siRNA pooled   24,672


Basic Research
We are interested in genes that play a role in the development or mechanisms of type II diabetes. To date, we have met with success screening for genes which, when over-expressed, block activation of an insulin-sensitive reporter by insulin. Putative hits are being further characterized for their ability to phosphorylate a key pathway kinase, mediate translocation of Glut4 constructs, potentiate adipogenesis, and modulate other aspects of canonical insulin signaling.

Selected Publications

 


Please click here for a full list of group publications