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Abstract
Taeil Kim1, Joonsun Yoon1, Hwansung Cho1, Wook-bin Lee1, Joon Kim1, Young-Hwa Song2, Se Nyun Kim2, Jeong Ho Yoon2, Jeongsil Kim-Ha3 & Young-Joon Kim1
1 Department of Biochemistry, Yonsei University, Seoul 120-749, South Korea.
2 Digital Genomics, Seoul 120-749, South Korea.
3 Department of Molecular Biology, Sejong University, Seoul 143-747, South Korea.
Correspondence should be addressed to Young-Joon Kim
IκB 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-κB. 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-κB target genes.
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