The NPM-ALK tyrosine kinase mimics TCR signalling pathways, inducing NFAT and AP-1 by RAS-dependent mechanisms.

Nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) expression is associated with the lymphoid malignancy anaplastic large cell lymphoma (ALCL) and results from a t(2;5) chromosomal translocation. We show that NPM-ALK induces Ras activation and phosphorylation of the ERK MAP Kinase consistent with activation of the Ras-MAP Kinase pathway. Furthermore, we demonstrate that activation of Ras is necessary for inducing transcription via NFAT/AP-1 composite transcriptional binding sites.

CD2 promoter regulated nucleophosmin-anaplastic lymphoma kinase in transgenic mice causes B lymphoid malignancy.

Background: Nucleophosmin-anaplastic lymphoma kinase expression is associated with a lymphoid malignancy, anaplastic large cell lymphoma, and is characterized by a t(2;5) chromosomal translocation.

Materials And Methods: We describe a novel transgenic mouse line in which NPM-ALK expression is targeted to the T-cell lineage using the CD2 promoter.

Results: Surprisingly, the mice develop B cell lymphomas in the majority of cases.

A comparative study of the central effects of specific proopiomelancortin (POMC)-derived melanocortin peptides on food intake and body weight in pomc null mice.

Functional disruption of either MC3R or MC4R results in obesity, implicating both in the control of energy homeostasis. The ligands for these receptors are derived from the prohormone proopiomelancortin (POMC), which is posttranslationally processed to produce a set of melanocortin peptides with a range of activities at the MC3R and MC4R. The relative importance of each of these peptides alpha-MSH, gamma3-MSH, gamma2-MSH, gamma-lipotropin (gamma-LPH) and, in man but not in rodents, beta-MSH] in the maintenance of energy homeostasis is, as yet, unclear.