Additional Mouse Models Added to the Knockout Repository

Taconic Biosciences has recently added an additional 19 mouse models to the Knockout Repository (KOR). The KOR's more than 4,100 lines provide academic and commercial researchers worldwide with unparalleled access to fully licensed knockout mouse models.

The Knockout Repository

gene classes This repository offers the scientific community immediate access to expertly designed, highly valuable research tools that rapidly accelerate translational research and the drug discovery and development processes. Mutations are focused on the 'druggable' gene classes and were generated using two complementary, proven technologies: Gene Targeting and Gene Trapping.

The KOR lines are maintained as frozen germplasm (sperm and/or embryos) allowing both academic and commercial researchers on demand access with rapid recovery times. Eliminating the time associated with the design and development of these mouse models provides a tremendous competitive advantage.

In Addition to the KOR

The addition of new lines to this massive collection makes the KOR an even more valuable tool to the drug discovery researcher. The new mouse models knock out gene function either constitutively (by gene targeting or gene trapping) or conditionally. These newly introduced models can be useful tools in studies focused on different therapeutic areas including diabetes, proliferation, retinal degeneration, behavior, and inflammation.

Noteworthy Knockout Repository Additions

Some noteworthy additions to the collection include knockouts of two highly related sodium-glucose co-transporters, Slc5a1 and Slc5a2. A publication using these models individually and in combination was able to precisely define each gene's role in urinary glucose excretion and show how pharmacologic inhibition of both transporters could lead to better diabetes treatments1.

Another example of the power of using the appropriate genetic model comes from a publication around the Limk2 gene2. In vitro studies have suggested a role for Limk2 in cell morphology, but its function in the context of the whole animal was lacking. Using a gene trap mutation of Limk2, Rice demonstrate a role for Limk2 in actin dynamics and specifically in keratinocyte migration in the developing eyelid. Mice lacking Limk2 function have an eyes open at birth (EOB) phenotype.

New Model Details

The information on the newly added lines is summarized below:

Catalog number Gene Name Accession Number Mutation Type Publication ID
TF0075Pdcd1lg2 NM_021396 Conditional  
TF0269Adgrg6 NM_001002268 Conditional  
TF0286Hcn2 NM_008226 Conditional  
TF0902Gphb5 NM_175644 Conditional  
TF1751Acsl3 NM_028817 Conditional  
TF4134Limk2 NM_010718 Trapped 23071748
TF4135Limk2 NM_010718 Conditional  
TF4136Adrm1 NM_019822 Trapped  
TF4137Pomk NM_029037 Trapped  
TF4138Hdac2 NM_008229 Targeted 23071748
TF4139Slc5a1 NM_019810 Trapped 23149623
TF4140Slc5a2 NM_133254 Targeted 23149623
TF4141Tph1 NM_001136084 Targeted  
TF4142Nmt1 NM_008707 Trapped  
TF4143Crb3 NM_177638 Targeted  
TF4144Slc46a1 NM_026740 Targeted 19204075
TF4145Tmem218 NM_025464 Trapped 25161209
TF4146Stk4 NM_021420 Targeted 24852423
TF4147Cacna1g NM_009783 Targeted  
1. David R. Powell, Christopher M. DaCosta, Jason Gay, Zhi-Ming Ding, Melinda Smith, Jennifer Greer, Deon Doree, Sabrina Jeter-Jones, Faika Mseeh, Lawrence A. Rodriguez, Angela Harris, Lindsey Buhring, Kenneth A. Platt, Peter Vogel, Robert Brommage, Melanie K. Shadoan, Arthur T. Sands, Brian Zambrowicz. (2013) Improved glycemic control in mice lacking Sglt1 and Sglt2. Am J Physiol Endocrinol Metab. 2013 Jan 15;304(2):E117-30.
2. Dennis S. Rice, Gwenn M. Hansen, Feng Liu, Mike J. Crist, Matthew M. Newhouse, David Potter, Nianhua Xu, Alejandro Abuin, Peter J. Vogel, and Brian P. Zambrowicz. (2012) Keratinocyte Migration in the Developing Eyelid Requires LIMK2. PLoS One. 2012;7(10):e47168.

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