@article {5483,
	title = {Alk is a transcriptional target of LMO4 and ERα that promotes cocaine sensitization and reward.},
	journal = {The Journal of Neuroscience: The Official Journal of the Society for Neuroscience},
	volume = {31},
	year = {2011},
	month = {2011 Oct 5},
	pages = {14134-41},
	abstract = {<p>Previously, we showed that the mouse LIM-domain only 4 (Lmo4) gene, which encodes a protein containing two zinc-finger LIM domains that interact with various DNA-binding transcription factors, attenuates behavioral sensitivity to repeated cocaine administration. Here we show that transcription of anaplastic lymphoma kinase (Alk) is repressed by LMO4 in the striatum and that Alk promotes the development of cocaine sensitization and conditioned place preference, a measure of cocaine reward. Since LMO4 is known to interact with estrogen receptor α (ERα) at the promoters of target genes, we investigated whether Alk expression might be controlled by a similar mechanism. We found that LMO4 and ERα are associated with the Alk promoter by chromatin immunoprecipitation and that Alk is an estrogen-responsive gene in the striatum. Moreover, we show that ERα knock-out mice exhibit enhanced cocaine sensitization and conditioned place preference and an increase in Alk expression in the nucleus accumbens. These data define a novel regulatory network involved in behavioral responses to cocaine. Interestingly, sex differences in several behavioral responses to cocaine in humans and rodents have been described, and estrogen is thought to mediate some of these differences. Our data suggest that estrogen regulation of Alk may be one mechanism responsible for sexually dimorphic responses to cocaine.</p>
},
	keywords = {Adaptor Proteins, Animals, Cells, Cocaine, Cultured, Estrogen Receptor alpha, Gene Targeting, Genetic, HEK293 Cells, Humans, Inbred C57BL, Knockout, LIM Domain Proteins, Male, Mice, Motor Activity, Newborn, Receptor Protein-Tyrosine Kinases, Reward, Signal Transducing, Transcription},
	issn = {1529-2401},
	doi = {10.1523/JNEUROSCI.3415-11.2011},
	author = {Lasek, Amy W and Gesch, Julie and Giorgetti, Francesco and Kharazia, Viktor and Heberlein, Ulrike}
}
@article {5481,
	title = {Happyhour, a Ste20 family kinase, implicates EGFR signaling in ethanol-induced behaviors.},
	journal = {Cell},
	volume = {137},
	year = {2009},
	month = {2009 May 29},
	pages = {949-60},
	abstract = {<p>The consequences of alcohol use disorders (AUDs) are devastating to individuals and society, yet few treatments are currently available. To identify genes regulating the behavioral effects of ethanol, we conducted a genetic screen in Drosophila and identified a mutant, happyhour (hppy), due to its increased resistance to the sedative effects of ethanol. Hppy protein shows strong homology to mammalian Ste20 family kinases of the GCK-1 subfamily. Genetic and biochemical experiments revealed that the epidermal growth factor (EGF)-signaling pathway regulates ethanol sensitivity in Drosophila and that Hppy functions as an inhibitor of the pathway. Acute pharmacological inhibition of the EGF receptor (EGFR) in adult animals altered acute ethanol sensitivity in both flies and mice and reduced ethanol consumption in a preclinical rat model of alcoholism. Inhibitors of the EGFR or components of its signaling pathway are thus potential pharmacotherapies for AUDs.</p>
},
	keywords = {Alcohol-Induced Disorders, Animal, Animals, Crosses, Disease Models, Dopamine, Drosophila melanogaster, Drosophila Proteins, Epidermal Growth Factor, Ethanol, Female, Genetic, Insulin, Male, Mice, Mutation, Phosphorylation, Protein-Serine-Threonine Kinases, Receptor, Signal Transduction},
	issn = {1097-4172},
	doi = {10.1016/j.cell.2009.03.020},
	author = {Corl, Ammon B and Berger, Karen H and Ophir-Shohat, Galit and Gesch, Julie and Simms, Jeffrey A and Bartlett, Selena E and Heberlein, Ulrike}
}
