Myd88

Constitutive knockout

Myd88 - Constitutive knockout
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This model is cryopreserved and available for immediate cryorecovery.

C57BL/6NTac Background

  • Model #
  • Genotype
  • Nomenclature
  • 16356
    C57BL/6NTac-Myd88em1Tac
  • 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).

Orders by weight: Taconic cannot accept orders by weight for this model. Please note that shipments may contain animals with a larger weight variation.

Origin:

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.


Color:

Black

Species:

Mouse

Initial Publication:

There is no specific publication describing the generation of these mice, but multiple publications exist demonstrating applications using similar models. See reference list.

Other Publications:

  • 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.


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This model is sold under terms which grant perpetual use rights.