pubmed-article:18519585 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:18519585 | lifeskim:mentions | umls-concept:C1273518 | lld:lifeskim |
pubmed-article:18519585 | lifeskim:mentions | umls-concept:C0015576 | lld:lifeskim |
pubmed-article:18519585 | lifeskim:mentions | umls-concept:C0680022 | lld:lifeskim |
pubmed-article:18519585 | lifeskim:mentions | umls-concept:C0014520 | lld:lifeskim |
pubmed-article:18519585 | lifeskim:mentions | umls-concept:C0003806 | lld:lifeskim |
pubmed-article:18519585 | lifeskim:mentions | umls-concept:C1120843 | lld:lifeskim |
pubmed-article:18519585 | lifeskim:mentions | umls-concept:C1155265 | lld:lifeskim |
pubmed-article:18519585 | lifeskim:mentions | umls-concept:C0040649 | lld:lifeskim |
pubmed-article:18519585 | lifeskim:mentions | umls-concept:C0013139 | lld:lifeskim |
pubmed-article:18519585 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:18519585 | pubmed:issue | 15 | lld:pubmed |
pubmed-article:18519585 | pubmed:dateCreated | 2008-7-17 | lld:pubmed |
pubmed-article:18519585 | pubmed:abstractText | Drosophila innate immunity is controlled primarily by the activation of IMD (immune deficiency) or Toll signaling leading to the production of antimicrobial peptides (AMPs). IMD signaling also activates the JUN N-terminal kinase (JNK) cascade, which is responsible for immune induction of non-antimicrobial peptide immune gene transcription though the transcription factor AP-1. Transcription of the Dopa decarboxylase (Ddc) gene is induced in response to gram-negative and gram-positive septic injury, but not aseptic wounding. Transcription is induced throughout the epidermis and not specifically at the site of infection. Ddc transcripts are detectible within 2 h and remain high for several hours following infection with either gram-negative or gram-positive bacteria. Using Ddc-green fluorescent protein (GFP) reporter gene constructs, we show that a conserved consensus AP-1 binding site upstream of the Ddc transcription start site is required for induction. However, neither the Toll, IMD, nor JNK pathway is involved. Rather, Ddc transcription depends on a previously uncharacterized member of the p38 mitogen-activated protein kinase family, p38c. We propose that the involvement of DDC in a new pathway involved in Drosophila immunity increases the levels of dopamine, which is metabolized to produce reactive quinones that exert an antimicrobial effect on invading bacteria. | lld:pubmed |
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pubmed-article:18519585 | pubmed:language | eng | lld:pubmed |
pubmed-article:18519585 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18519585 | pubmed:citationSubset | IM | lld:pubmed |