Investigating the effect of different transducer stiffness values on the contactin complex detachment by steered molecular dynamics

Kianfar, Parnian; Abolfathi, Nabiollah; Karimi, Navid Zarif

doi:10.1016/j.jmgm.2017.05.015

Cited by 2 publications

(1 citation statement)

References 35 publications

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“…PTPR-γ is thought to exist in two conformations: the active monomer and the inactive homodimer brought about by PTPR-γ binding to its endogenous ligand(s) 42 . Several members of the contactin family have been suggested as endogenous PTPR-γ ligands 45 , 46 . Hence, experiments aimed at testing whether these ligands inhibit PTPR-γ 42 , 47 and improve T2DM are warranted.…”

Section: Discussionmentioning

confidence: 99%

Hepatic protein tyrosine phosphatase receptor gamma links obesity-induced inflammation to insulin resistance

et al. 2017

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Obesity-induced inflammation engenders insulin resistance and type 2 diabetes mellitus (T2DM) but the inflammatory effectors linking obesity to insulin resistance are incompletely understood. Here, we show that hepatic expression of Protein Tyrosine Phosphatase Receptor Gamma (PTPR-γ) is stimulated by inflammation in obese/T2DM mice and positively correlates with indices of inflammation and insulin resistance in humans. NF-κB binds to the promoter of Ptprg and is required for inflammation-induced PTPR-γ expression. PTPR-γ loss-of-function lowers glycemia and insulinemia by enhancing insulin-stimulated suppression of endogenous glucose production. These phenotypes are rescued by re-expression of Ptprg only in liver of mice lacking Ptprg globally. Hepatic PTPR-γ overexpression that mimics levels found in obesity is sufficient to cause severe hepatic and systemic insulin resistance. We propose hepatic PTPR-γ as a link between obesity-induced inflammation and insulin resistance and as potential target for treatment of T2DM.

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