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  • Identification of common mechanisms by which human and mouse cytomegalovirus seven-transmembrane receptor homologues contribute to in vivo phenotypes in a mouse model.

Identification of common mechanisms by which human and mouse cytomegalovirus seven-transmembrane receptor homologues contribute to in vivo phenotypes in a mouse model.

Journal of virology (2013-01-25)
Helen E Farrell, Alexander M Abraham, Rhonda D Cardin, Ann-Sofie Mølleskov-Jensen, Mette M Rosenkilde, Nicholas Davis-Poynter
ABSTRACT

The mouse cytomegalovirus chemokine receptor homologue (CKR) M33 is required for salivary gland tropism and efficient reactivation from latency, phenotypes partially rescued by the human cytomegalovirus CKR US28. Herein, we demonstrate that complementation of salivary gland tropism is mediated predominantly by G protein-dependent signaling conserved with that of M33; in contrast, both G protein-dependent and -independent pathways contribute to the latency phenotypes. A novel M33-dependent replication phenotype in cultured bone marrow macrophages is also described.

MATERIALS
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Octoxinol 10, European Pharmacopoeia (EP) Reference Standard
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Triton X-100 solution, BioUltra, for molecular biology, ~10% in H2O
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Triton X-102
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Triton X-305 solution, 70% in H2O
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Triton X-45
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Triton X-100, for molecular biology
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Triton X-100, peroxide- and carbonyl-free
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Triton X-100, laboratory grade
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Triton X-100, BioXtra