@article {759966,
	title = {Differential requirement for STAT by gain-of-function and wild-type receptor tyrosine kinase Torso in Drosophila.},
	journal = {Development},
	volume = {129},
	number = {18},
	year = {2002},
	month = {2002 Sep},
	pages = {4241-8},
	abstract = {
	Malignant transformation frequently involves aberrant signaling from receptor tyrosine kinases (RTKs). These receptors commonly activate Ras/Raf/MEK/MAPK signaling but when overactivated can also induce the JAK/STAT pathway, originally identified as the signaling cascade downstream of cytokine receptors. Inappropriate activation of STAT has been found in many human cancers. However, the contribution of the JAK/STAT pathway in RTK signaling remains unclear. We have investigated the requirement of the JAK/STAT pathway for signaling by wild-type and mutant forms of the RTK Torso (Tor) using a genetic approach in Drosophila. Our results indicate that the JAK/STAT pathway plays little or no role in signaling by wild-type Tor. In contrast, we find that STAT, encoded by marelle (mrl; DStat92E), is essential for the gain-of-function mutant Tor (Tor(GOF)) to activate ectopic gene expression. Our findings indicate that the Ras/Raf/MEK/MAPK signaling pathway is sufficient to mediate the normal functions of wild-type RTK, whereas the effects of gain-of-function mutant RTK additionally require STAT activation.

},
	keywords = {Animals, Base Sequence, Consensus Sequence, DNA-Binding Proteins, Drosophila melanogaster, Drosophila Proteins, Embryo, Nonmammalian, Gene Expression Regulation, Developmental, MAP Kinase Signaling System, Mutation, Plasmids, Polymerase Chain Reaction, Receptor Protein-Tyrosine Kinases, STAT Transcription Factors, Trans-Activators},
	issn = {0950-1991},
	author = {Li, Willis X and Agaisse, Herve and Mathey-Prevot, Bernard and Perrimon, Norbert}
}
