A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

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Citation Kim, T., Yoon, J., Cho, H., Lee, W.B., Kim, J., Song, Y.H., Kim, S.N., Yoon, J.H., Kim-Ha, J., Kim, Y.J. (2005). Downregulation of lipopolysaccharide response in Drosophila by negative crosstalk between the AP1 and NF-kappaB signaling modules.  Nat. Immunol. 6(2): 211--218. (Export to RIS)
FlyBase ID FBrf0184193
Publication Type Research paper
PubMed ID 15640802
PubMed Abstract IkappaB kinase (IKK) and Jun N-terminal kinase (Jnk) signaling modules are important in the synthesis of immune effector molecules during innate immune responses against lipopolysaccharide and peptidoglycan. However, the regulatory mechanisms required for specificity and termination of these immune responses are unclear. We show here that crosstalk occurred between the drosophila Jnk and IKK pathways, which led to downregulation of each other's activity. The inhibitory action of Jnk was mediated by binding of drosophila activator protein 1 (AP1) to promoters activated by the transcription factor NF-kappaB. This binding led to recruitment of the histone deacetylase dHDAC1 to the promoter of the gene encoding the antibacterial protein Attacin-A and to local modification of histone acetylation content. Thus, AP1 acts as a repressor by recruiting the deacetylase complex to terminate activation of a group of NF-kappaB target genes.
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Language of Publication English
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Publication Type Journal
Abbreviation Nat. Immunol.
Title Nature Immunology
Publication Year 2000-
ISBN/ISSN 1529-2908 1529-2916
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