A fragment of the Escherichia coli ClpB heat-shock protein is a micromolar melanocortin 1 receptor agonist
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Acknowledgement
This work has been supported by NIH Grants R01DK097838 and R01DK091906.
References and notes (38)
J. Biol. Chem.
(1958)- et al.
FEBS Lett.
(1992) - et al.
J. Biol. Chem.
(1993) - et al.
J. Biol. Chem.
(1993) - et al.
Cell
(1997) - et al.
Biochem. Biophys. Res. Commun.
(1994) - et al.
Biochem. Biophys. Res. Commun.
(1994) - et al.
Cell
(1997) - et al.
Biochem. Biophys. Res. Commun.
(1997) - et al.
J. Invest. Dermatol.
(2012)
Chem. Biol.
Eur. J. Pharmacol.
Peptides
J. Biol. Chem.
J. Biomol. Screen.
Gen. Comp. Endocrinol.
Peptides
Peptides
Science
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2021, Psychiatry ResearchCitation Excerpt :One way of modulating appetite-regulating hormones by intestinal microbiota is the production of ClpB protein by E. coli bacteria living in the colon. This protein has a structure similar to alpha-MSH an antigen mimetic to the endogenous melanocortin agonist α-MSH, a hypothalamic hormone that suppresses appetite (Tennoune et al., 2014, Ericson et al., 2015). The ClpB protein provokes the synthesis of alpha-MSH antibodies and may become a risk for an autoimmune response in human body (Breton et al., 2016).
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2020, Clinical NutritionCitation Excerpt :The increased intestinal permeability enables the transport of microbial metabolites into the peripheral circulation. These molecules can be either structurally similar to host molecules, and therefore remained unrecognized by the host immune system, or they differ and then induce immunoglobulin production [109,114]. A “leaky gut” can be provoked by starvation, and an increase in mucin-degrading bacteria contribute to chronic low-grade inflammation presumed to be present in AN patients.
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2019, Current Opinion in PharmacologyCitation Excerpt :Beside its central effects, α-MSH is also able to activate the hormonal satiety pathway in the gut by increasing secretion of peptide YY (PYY) [19], suggesting a direct satietogenic role of ClpB. Indeed, recent reports showed that E. coli ClpB stimulates PYY release [20], and induces MCR-mediated cAMP secretion, although with a micromolar affinity [21]. Importantly, lack of ClpB in E. coli abolishes direct satietogenic effect of these bacteria [22].
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