Ignet

Gene Pair Information

Gene Pair: AKT1, MAPK8

Related Sentences

#	PMID	Sentence
1	21896669	Western blotting was used to quantify the expression and phosphorylation of insulin receptor, insulin receptor substrate 1, and Akt and of inflammatory mediators that modulate insulin signaling in a negative manner (IKK?, JNK, and inducible nitric oxide synthase).
2	17550900	At the molecular level, JNK1 knockdown mice had sustained and significant increase of hepatic Akt phosphorylation.
3	21073655	Furthermore, high glucose concentrations led to apoptosis of ?-cells by activation of p38MAPK and p53, and dysfunction of ?-cells through phosphatase and tensih homolog (PTEN)-dependent Jun N-terminal kinase (JNK) activation and protein kinase B (AKT/PKB) inhibition, which induced the translocation of forkhead box O1 and pancreatic duodenal homeobox-1, followed by reduced insulin expression and secretion.
4	21073655	In conclusion, NOX2-derived ROS could play a critical role in high glucose-induced ?-cell dysfunction through PTEN-dependent JNK activation and AKT inhibition.
5	21209957	Our results show that palmitate and oleate (0.5 mmol/L, 48 h) induced JNK activation and AKT inhibition which resulted in decreased phosphorylation of FOXO1 following nuclear localization and the nucleocytoplasmic translocation of PDX-1, leading to the reducing of insulin and ultimately dysfunction of pancreatic NIT-1 cells.
6	18174526	Fatty acids induced nuclear localization of Foxo1 at 4 h when Akt activity was increased, indicating that FoxO1 activation was not mediated by JNK inhibition of Akt.
7	21090814	Medicinal chemistry studies resulted in an improved Jnk-1 ligand able to increase adiponectin secretion in human adipocytes and increase insulin-induced protein kinase PKB phosphorylation in human hepatocytes, in similar fashion to Jnk-1 siRNA and to rosiglitazone treatment.
8	21460183	The increased superoxide content induces c-Jun N-terminal kinase 1 (JNK1) kinase activity, which in turn affects FOXO localization through a compensatory dephosphorylation of Akt.