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. Author manuscript; available in PMC: 2017 May 1.
Published in final edited form as: Nat Rev Neurosci. 2016 Apr 7;17(5):282–292. doi: 10.1038/nrn.2016.24

Figure 4. CNTF signalling pathways.

Figure 4

Binding of CNTF to its receptor complex, which is composed of CNTFRα, LIFR and gp130, activates the associated JAK, a tyrosine kinase, which phosphorylates (round dots with P) STAT, LIFR, and gp130 at tyrosine residues. Phosphorylated STAT dimerizes and enters the nucleus to induce gene expression. The consequent change in gene expression is likely to be essential for CNTF-mediated suppression of food intake by increasing the number of ARHPOMC neurons through adult neurogenesis and boosting synthesis of αMSH, the MC4R agonist. The activated receptor complex also activates MAPK, which can suppress STAT phosphorylation, thus providing a negative feedback.