CD33 Null Mice: Murine Model for Alzheimer's Disease
- Technology Benefits
- The CD33 null mouse were first developed in 2001 and in the past thirteen years these have been well-studied and characterized. Commercial entities please use “Ready-to-sign License”
- Technology Application
- May be useful as a tool to investigate Alzheimer's disease and inflammation that is mediated by CD33-positive cells.
- Detailed Technology Description
- B6.129-Cd33tm1Ajv/J (“CD33 null”) mice are maintained at Jackson Laboratory and a full description of the mice is found at Jackson’s website (see “State of Development”, below). Mice were generated using a targeting vector containing a PGK-neomycin resistance cassette to disrupt 3.8kb of sequence encoding exons 1 through 5. The construct was electroporated into (129X1/SvJ x 129S1/Sv)F1-Kitl+ derived R1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into recipient blastocysts. The resulting chimeric animals were crossed to C57BL/6 mice, and then backcrossed to the same for 13 generations before arriving at The Jackson Laboratory.
- Others
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State Of Development
A complete description, including genotyping, disease features, phenotyping, etc. is found at 006942 (also see “General Information”, below).
Intellectual Property Info
Non-exclusive license to property rights enables commercial entities to order from Jackson Laboratory.
General Information
Jackson Laboratory Stock Number 006942
Related Materials
Brinkman-Van Der Linden EC, et al., (2003) CD33/Siglec-3 Binding Specificity, Expression Pattern, and Consequences of Gene Deletion in Mice, Mol Cell Biol 23(12):4199-206.
Griciuc A., et al., (2013) Alzheimer's disease risk gene CD33 inhibits microglial uptake of amyloid beta,. Neuron 78(4):631-43.Tech ID/UC Case
24144/2014-105-0
Related Cases
2014-105-0
License online
- *Abstract
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Although the CD33 null mouse was originally developed as a means of understanding the basic biology of human CD33 (hCD33 or Siglec-3), recent studies have identified the CD33 gene is a primary risk factor for Alzheimer’s disease and allelic variants of CD33 may play a primary role in the clearance of amyloid beta by microglial cell in the brain.
- *Principal Investigator
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Name: Ajit Varki
Department:
- Country/Region
- USA
