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The extensive electrostatic, hydrogen bonding, and hydrophobic interactions on the R-domain explain how mutations distal from phosphorylation sites may nevertheless contribute to dysfunction
doi: 10.1016/s0939-6411(00)00090-4
This hypothesis outlines the failure of an upregulated leptin signal to alter appetite and prevent weight gain
A standardized mouse model of Helicobacter pylori infection: introducing the Sydney strain
