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This study reports an alternative splicing variant of APPL1 (APPL1sv) that is highly expressed in mouse liver, pancreas, and spleen tissues. The expression levels of APPL1sv in liver tissues were enhanced in a mouse model of obesity and diabetic dyslipidemia (i.e. db/db mice) and reduced in calorie-restricted mice compared with ad libitum-fed mice.
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APPL1 enhances glucose uptake by modulating the activation and localization of PKCzeta, as well as its functional interaction with both PP2A and myosin IIa.
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APPL1-SirT1-STAT3 pathway mediated adiponectin signaling in primary hepatocytes.
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Here we establish potential roles for APPL1 and 2 signaling adaptors as regulators of LPS/TLR4-induced signaling, transcription, and cytokine secretion.
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Appl1/2-null mouse embryonic fibroblasts exhibited defects in HGF-induced Akt activation, migration, and invasion.
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In experimental high glucose condition APPL1 acts as a protective factor against podocytes injury through regulating AMPK signaling.
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A role for APPL1 in TLR3/4-dependent TBK1 and IKKepsilon activation in macrophages.
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APPL1 sensitizes insulin signaling by acting at a site downstream of the IR. Study uncovers a mechanism regulating insulin signaling and crosstalk between the insulin and adiponectin pathways.
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Study demonstrates the roles of APPL1 in regulating GSIS and mitochondrial function in pancreatic beta cells, which implicates APPL1 as a therapeutic target in the treatment of type 2 diabetes.
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APPL1 transgenic mice exhibit improved peripheral metabolism, reduced cardiac lipotoxicity, and improved insulin sensitivity.
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Our findings demonstrate that exercise training performed concomitantly to a high-fat diet reduces the degree of insulin resistance and improves adipoR1-2/APPL1 protein levels in the hepatic, adipose, and skeletal muscle tissue
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APPL1 contributes to connecting synaptic NMDA receptors with the intracellular phosphoinositide 3-kinase /Akt cascade in neurons.
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Reduced APPL1 expression in pancreatic islets may serve as a pathological link that couples insulin resistance to beta-cell dysfunction in type 2 diabetes.
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Endurance training was able to increase APPL1 expression.
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APPL1 plays a key role in coordinating the vasodilator and vasoconstrictor effects of insulin by modulating Akt-dependent NO production and ERK1/2-mediated ET-1 secretion in the endothelium.
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Data found that the inhibitory effect of adiponectin on osteoclasts was induced by APPL1-mediated down-regulation of Akt1 activity.
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Appl1 is dispensable for Akt signaling in vivo and T-cell differentiation.
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The promyogenic function of Cdo involves a coordinated activation of p38MAPK and Akt via association with scaffold proteins, JLP and Bnip-2 for p38MAPK and APPL1 for Akt.
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Appl proteins are required for HGF-induced cell survival and migration via activation of Akt
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APPL1 interacts with adiponectin receptors in mammalian cells and the interaction is stimulated by adiponectin.