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MIP-1alpha Induces Binding of Nuclear Factors to the kappaB DNA Element in Human B Cells

O I Omoike, R M Teague, S H Benedict, M A Chan

Mol Cell Biol Res Commun. 2000 Jul;4(1):15-9.

PMID: 11152622

Abstract:

The chemokine macrophage inflammatory protein-1 alpha (MIP-1alpha) stimulates migration of B cells through an unknown mechanism. Furthermore, little is known about signal transduction mechanisms through which MIP-1alpha might signal phenotypic changes in B cells. We are investigating the role of MIP-1alpha in B cell signaling. Here we report that stimulation of the Ramos B cell line or tonsil B or peripheral blood-B (PBL-B) cells with MIP-1alpha caused the transcription factor NF-kappaB to bind to DNA. NF-kappaB induction was dose dependent, and was transient, with peak induction occurring at 30 min. MIP-1alpha treatment stimulated the degradation of IkappaBalpha, a cytoplasmic inhibitor of NF-kappaB. The biological significance of NF-kappaB activation by MIP-1alpha is currently unknown, but it is known that NF-kappaB modulates expression of genes involved in many inflammatory and immune responses. Here we show that NF-kappaB activation is a target of signals sent into B cells by MIP-1alpha.

Chemicals Related in the Paper:

Catalog Number Product Name Structure CAS Number Price
IAR4248673 MIP-1alpha human MIP-1alpha human Price
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