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MIF — PRKAB1
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Jorgensen et al., Bioorg Med Chem Lett 2010
:
MIF also
promotes AMPK activation with potential benefits for response to myocardial infarction and ischemia-reperfusion
Mount et al., PloS one 2012
(Reperfusion Injury) :
In the heart,
macrophage migration inhibitory factor ( MIF ) released during IRI
contributes to
AMPK activation and protects from injury
Brock et al., J Biol Chem 2012
(Carcinoma, Non-Small-Cell Lung...) :
Our data now suggest that, in contrast to MIF and d-DTs AMPK activating properties in nontransformed cells,
MIF and d-DT act cooperatively to
inhibit steady-state phosphorylation and activation of
AMPK in LKB1 wild type and LKB1 mutant human NSCLC cell lines ... Our data further indicate that
MIF and d-DT, acting through their shared cell surface receptor, CD74, antagonize NSCLC AMPK activation by maintaining glucose uptake, ATP production, and redox balance,
resulting in reduced Ca ( 2+ ) /calmodulin dependent kinase kinase ß-dependent
AMPK activation
Wang et al., Circulation 2013
(Myocardial Infarction...) :
By contrast, small-molecule MIF agonism was not effective in cells or tissues genetically deficient in MIF or the MIF receptor, verifying the specificity of MIF20 for
MIF dependent
AMPK signaling