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.

KOR Druggable Gene Classes

The Knockout Repository

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 treatments(1).

Another example of the power of using the appropriate genetic model comes from a publication around the Limk2 gene(2). 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
TF0075 Pdcd1lg2 NM_021396 Conditional  
TF0269 Adgrg6 NM_001002268 Conditional  
TF0286 Hcn2 NM_008226 Conditional  
TF0902 Gphb5 NM_175644 Conditional  
TF1751 Acsl3 NM_028817 Conditional  
TF4134 Limk2 NM_010718 Trapped 23071748
TF4135 Limk2 NM_010718 Conditional  
TF4136 Adrm1 NM_019822 Trapped  
TF4137 Pomk NM_029037 Trapped  
TF4138 Hdac2 NM_008229 Targeted 23071748
TF4139 Slc5a1 NM_019810 Trapped 23149623
TF4140 Slc5a2 NM_133254 Targeted 23149623
TF4141 Tph1 NM_001136084 Targeted  
TF4142 Nmt1 NM_008707 Trapped  
TF4143 Crb3 NM_177638 Targeted  
TF4144 Slc46a1 NM_026740 Targeted 19204075
TF4145 Tmem218 NM_025464 Trapped 25161209
TF4146 Stk4 NM_021420 Targeted 24852423
TF4147 Cacna1g NM_009783 Targeted  
  1. Am J Physiol Endocrinol Metab. 2013 Jan 15;304(2):E117-30
  2. PLoS One. 2012;7(10):e47168. doi: 10.1371/journal.pone.0047168. Epub 2012 Oct 5.