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. Author manuscript; available in PMC: 2011 Jan 1.
Published in final edited form as: Cell Mol Neurobiol. 2009 Jul 7;30(1):23. doi: 10.1007/s10571-009-9427-x

Figure 1.

Figure 1

A. The db333/db333 mutation. DNA sequence chromatograms from homozygous mutant db333/db333 mice (TAA/TAA), heterozygous db333/db333 mice (TAA/TAT) and C57Bl/6 WT mice (TAT/TAT). db333/db333 mice have a point mutation in the leptin receptor gene causing a premature stop codon. The db333/db333 mouse has a T to A transversion (TAT→TAA) in the 7th coding exon of the leptin receptor gene, resulting in a premature stop codon at Tyr333 B. Schematic Presentation of Leptin Receptor Mutations in Mouse Models of Obesity with Leptin Signaling Deficiencies. The predicted protein length is shown with the numbers at the end of each receptor representing the amino acid residue at the carboxy terminus. The STAT-3 binding site is located at amino acid 1138 and has an important role in the regulation of energy balance through the JAK/ STAT signaling pathway.