Orders by weight:
- Carries a deletion of exon 2 and 3 of Myd88 gene.
- The deletion removes the intermediate domain and part of the TIR domain, generating a frameshift from exon 1 to exon 4 (premature Stop codon in exon 5).
- Homozygous mice should not produce any Myd88 protein.
- This model is useful for studying an innate and adaptive immune response as Myd88 is part of the IL-1 receptor (IL-1R), IL-18R, and most of Toll-like receptor (TLR) signaling pathways regulating pro-inflammatory response.
- Deletion of Myd88 in the central nervous system (CNS) protects from HFD-induced impairment of peripheral glucose metabolism (Cell Metabolism 2009, 10 (4), 249-259).
- TLR4 signaling dependence on Myd88 varies between NASH (Myd88-dependent) and ASH (Myd88-independent) (JCI Insight 2017, 2 (17), 95354).
- Lack of Myd88 in Sjögren's syndrome mice reduces inflammation and prevents a loss of saliva (Journal of Leukocyte Biology 2017, 102 (6), 1411-1420).
- Humans with lack of MYD88 suffer from recurrent pyogenic bacterial infections (Science 2008, 321 (5889), 691-696).
Taconic cannot accept orders by weight for this model. Please note that shipments may contain animals with a larger weight variation.
The Myd88 knockout mouse was developed by Taconic Biosciences. The model was created through CRISPR/Cas9-mediated gene editing to delete exons 2 and 3 of Myd88. Targeting occurred in C57BL/6NTac embryos. The selected G1 founder was screened for off-target effects and the targeted locus was sequenced to confirm targeting specificity. Heterozygous animals were intercrossed to generate homozygous mice. Homozygous matings are possible.
There is no specific publication describing the generation of these mice, but multiple publications exist demonstrating applications using similar models. See reference list.
- Kleinridders, A.; Schenten, D.; Könner, A. C.; Belgardt, B. F.; Mauer, J.; Okamura, T.; Wunderlich, F. T.; Medzhitov, R.; Brüning, J. C. Cell Metabolism 2009, 10 (4), 249–259.
- Greuter, T.; Malhi, H.; Gores, G. J.; Shah, V. H. JCI Insight 2017, 2 (17), 95354.
- Kiripolsky, J.; Mccabe, L. G.; Gaile, D. P.; Kramer, J. M. Journal of Leukocyte Biology 2017, 102 (6), 1411–1420.
- von Bernuth, H.; Picard, C.; Jin, Z.; Pankla, R.; Xiao, H.; Ku, CL.; Chrabieh, M.; Mustapha, I.B.; Ghandil, P.; Camcioglu, Y.; Vasconcelos, J.; Sirvent, N.; Guedes, M.; Vitor, A.B.; Herrero-Mata, M.J.; Aróstegui, J.I.; Rodrigo, C.; Alsina, L.; Ruiz-Ortiz, E.; Juan, M.; Fortuny, C.; Yagüe, J.; Antón, J.; Pascal, M.; Chang, H.H.; Janniere, L.; Rose, Y.; Garty, B.Z.; Chapel, H.; Issekutz, A.; Maródi, L.; Rodriguez-Gallego, C.; Banchereau, J.; Abel, L.; Li, X.; Chaussabel, D.; Puel, A.; Casanova, J.L. Science 2008, 321 (5889), 691-696.