Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.11.18 (MAP)
 7,412 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Torso signal transduction pathway exhibits two opposite effects on the activity of the Bicoid (Bcd) morphogen: (i) Bcd function is repressed by Torso (Tor) at the anterior pole of the embryo leading to a retraction of the expression of many Bcd targets from the most anterior region of the embryo, where the Tor tyrosine kinase receptor is activated, and (ii) Bcd function is strengthened by Tor in a broader anterior region, as indicated by a shift of the posterior border of Bcd targets towards the anterior pole in embryos deprived from Tor activity. Anterior repression of Bcd targets was not observed in embryos lacking maternal contribution of D-sor, which acts downstream of Tor and encodes a MAP-kinase kinase. This indicates that the Ras signalling cascade is directly involved in this process, although the known transcriptional effectors of the Tor pathway, tll and hkb, are not (Ronchi, E., Treisman, J., Dostatni, N., Struhl, G. and Desplan, C. (1993) Cell 74, 347-355). Bcd is a good in vitro substrate for phosphorylation by MAP-kinase and phosphorylation of the protein occur in vivo on MAP-kinase sites. In the presence of a Bcd mutant that could no longer be phosphorylated by MAP-kinase, expression of Bcd targets remained repressed by Tor at the pole while strengthening of Bcd activity was reduced. These experiments indicate that phosphorylation of Bcd by MAP-kinase is likely to be required for the Tor pathway to induce its full positive effect on Bcd. This suggests that Tor signalling acts at a distance from the anterior pole by direct modification of the diffusing Bcd morphogen.
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PMID:Phosphorylation of bicoid on MAP-kinase sites: contribution to its interaction with the torso pathway. 1060 46

Spatially and temporally regulated activity of Branchless/Breathless signaling is essential for trachea development in Drosophila. Early ubiquitous breathless (btl) expression is controlled by binding of Trachealess/Tango heterodimers to the btl minimum enhancer. Branchless/Breathless signaling includes a Sprouty-dependent negative feedback loop. We show that late btl expression is a target of Branchless/Breathless signaling and hence, Branchless/Breathless signaling contains a positive feedback loop, which may guarantee a continuous supply of fresh receptors to membranes of growing tracheal branch cells. Branchless/Breathless signaling activates MAP-kinase, which in turn, activates late btl expression and destabilizes Anterior-open, a repressor for late btl expression. Biochemical and genetic analysis indicated that the minimum btl enhancer includes binding sites of Anterior-open.
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PMID:Ligand-dependent activation of breathless FGF receptor gene in Drosophila developing trachea. 1217 85