Antisense modulation of MyD88 expression

Details Antisense modulation of MyD88 expression Antisense modulation of MyD88 expression

2006-04-25

2006-04-25

Schultz, J. D. (Department: 1635)

Chemistry: molecular biology and microbiology

Animal cell, per se ; composition thereof; process of...

Method of regulating cell metabolism or physiology

C435S006120, C435S325000, C514S04400A, C536S023100, C536S024500

Reexamination Certificate

active

07033830

ABSTRACT:
Antisense compounds, compositions and methods are provided for modulating the expression of MyD88. The compositions comprise antisense compounds, particularly antisense oligonucleotides, targeted to nucleic acids encoding MyD88. Methods of using these compounds for modulation of MyD88 expression and for treatment of diseases associated with expression of MyD88 are provided.

REFERENCES:
Adachi et al.,Targeted disruption of the MyD88 gene results in loss of IL-1- and IL-18-mediated function, Immunity, 1998, 9:143-150.
Akira et al.,The role of Toll-like receptors and MyD88 in innate immune responses, J. Endotoxin Res., 2000, 6:383-387.
Akira et al.,Toll-like receptors: critical proteins linking innate and acquired immunity, Nat. Immunol., 2001, 2:675-680.
Bonnert et al.,The cloning and characterization of human MyD88: a member of an IL-1 receptor related family, FEBS Lett., 1997, 402:81-84.
Burns et al.,MyD88, an adapter protein involved in interleukin-1 signaling, J. Biol. Chem., 1998, 273:12203-12209.
Dupraz et al.,Dominant negative MyD88 proteins inhibit interleukin-1beta /interferon-gamma -mediated induction of nuclear factor kappa B-dependent nitrite production and apoptosis in beta cells, J. Biol. Chem., 2000, 275:37672-37678.
Hardiman et al.,Molecular characterization and modular analysis of human MyD88, Oncogene, 1996, 13:2467-2475.
Lord et al.,Complexity of the immediate early response of myeloid cells to terminal differentiation and growth arrest includes ICAM-1, Jun-B and histone variants, Oncogene, 1990, 5:387-396.
Medzhitov et al.,MyD88 is an adaptor protein in the hToll/IL-1 receptor family signaling pathways, Mol. Cell, 1998, 2:253-258.
Muzio et al.,IRAK(Pelle)family member IRAK-2 and MyD88 as proximal mediators of IL-1 signaling, Science, 1997, 278:1612-1615.
Schmidt et al.,Lipopolysaccharide-induced activation of beta2-integrin function in macrophages requires Irak kinase activity, p38 mitogen- activated protein kinase, and the Rapl GTPase, Mol. Cell. Biol., 2001, 21:438-448.
Schnare et al.,Recognition of CpG DNA is mediated by signaling pathways dependent on the adaptor protein MyD88, Curr. Biol., 2000, 10:1139-1142.
Takeuchi et al.,Toll-like receptors; their physiological role and signal transduction system, Int. Immunopharmacol., 2001, 1:625-635.
Takeuchi et al.,Cutting edge: TLR2-deficient and MyD88-deficient mice are highly susceptible to Staphylococcus aureus infection, J. Immunol., 2000, 165:5392-5396.
Wang et al.,Micrococci and peptidoglycan activate TLR2—>MyD88—>IRAK—>TRAF—>NIK—>IKK—>NF-kappaB signal transduction pathway that induces transcription of interleukin-8, Infect. Immun., 2001, 69:2270-2276.

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