Project description:Wild-type (WT) C57Bl/6 and akt2-/- male mice. Keywords: RNA Expression Array Left ventricles (LV) from 12-16 week-old male wild type mice and age-matched akt2-/- mice
Project description:Finding diffrential gene expression gene expression in the livers of male mice after the deletion of Akt1 in th eliver of Akt2-/- mice.
Project description:Germ free (GF) and conventionalized (CONV-D) wild-type C57Bl/6 male mice in the CARB-fed, 24h fasted, and 30d trained states; plus GF and CONV-D CARB-fed Ppara-/- mice. CARB-fed indicates a standard polysaccharide-rich mouse chow diet. CONV-D mice are those that received a microbiota transplant from conventionally raised mice 2-3 weeks before experiment was initiated Keywords: RNA Expression Array
Project description:Insulin resistance and Type 2 diabetes are marked by an aberrant response in the insulin signaling network. The phosphoinositide-dependent serine/threonine kinase, Akt2, plays a key role in insulin signaling and glucose uptake, most notably within skeletal muscle. Protein-protein interaction regulates the functional consequence of Akt2 and in turn, Akt2’s role in glucose uptake. However, only few insulin-responsive Akt2 interaction partners have been identified in skeletal muscle cells. In the present work, rat L6 myoblasts, a widely used insulin sensitive skeletal muscle cell line, were used to examine endogenous, insulin-stimulated Akt2 protein interaction partners. Akt2 co-immunoprecipitation was coupled with 1D-SDS-PAGE and fractions were analyzed by HPLC-ESI-MS/MS to reveal Akt2 protein-protein interactions. The pull-down assay displayed specificity for the Akt2 isoform; Akt1 and Akt3 unique peptides were not detected. A total of 330 proteins were significantly enriched as bonafide Akt2 protein interaction partners. Among them, 226 were novel for any cell types. Furthermore, 59 were detected with a significantly increased (57) or decreased (2) association with Akt2 following insulin administration (n=4; p<0.05). Multiple pathways were identified for the novel Akt2 interaction partners, such as the EIF2 and ubiquitination pathways. These data suggest that multiple new endogenous proteins may associate with Akt2 under basal as well as insulin-stimulated conditions, providing further insight into the insulin signaling network.
Project description:Akt1 and Akt2, isoforms of the serine threonine kinase Akt, are essential for T cell development. However, their role in peripheral T cell differentiation remains undefined. Using mice with germline deletions of either Akt1 or Akt2, we found that both isoforms are important for Th17 differentiation, although Akt2 loss had a greater impact than Akt1. To better understand the consequences of Akt2 deficiency in the setting of in vitro Th17 differentiation, we used microarray analysis to compare the transcriptional landscape of Akt2â/â and WT cells that had been cultured in Th17 polarizing conditions for 36 hours.
Project description:In the mammalian heart AKT1 and AKT2 are the isoforms of the protein kinase AKT (protein kinase B) which are predominantly expressed. AKT isoforms exert common and specific functions in the field of metabolism, cellular growth, apoptosis and cell migration. To identify specific and common functions of AKT1 and AKT2 isoforms, we generated tamoxifen-inducible, cardiomyocyte-specific AKT1, AKT2, and AKT1+AKT2 double knockout mice (iCMAKT – KO mice). Inactivation of AKT isoforms was achieved by application of 4-OH-tamoxifen, which activates an OH-Tx inducible cre-recombinase expressed under the control of the αMHC-promoter (αMHC-mercremer). Transgenic mice expressing only the αMHCmercremer construct were also treated with OH-Tx and served as controls. To identify alterations in cardiac gene expression due to AKT deletion we analyzed gene expression profiles of control hearts, iCMAKT1, iCMAKT2 and iCMAKT1+2 hearts.
Project description:We are reporting here the effects of adaptation to different ambient temperatures in the whole genome gene expression of interscapular BAT of BAT specific Akt2 knockout mice
Project description:We found that hepatic injury induced by PTEN loss establishes a selection pressure for tumorinitiating cells (TICs) to proliferate and form mixed lineage tumors. The Pten null mice demonstrate escalating levels of hepatic injury prior to proliferation of hepatic progenitors. Attenuation of hepatic injury by deleting Akt2 reduces progenitor cell proliferation and delays tumor development. Treatment of double mutant mice with 3,5-dietoxycarbonyl-1,4 dihydrocollidine (DDC) shows that the primary effect of AKT2 loss is attenuation of hepatic injury and not inhibition of progenitor cell proliferation in response to injury. Pten/Akt2 double mutant (PtenloxP/loxP; Akt2-/-; Alb-Cre+) (Dm) were generated by crossing the PtenloxP/loxP; Alb-Cre+ (Pm) with the Akt2-/- mice [19]. Control animals are PtenloxP/loxP; Albumin (Alb)-Cre-.
Project description:We report RNA sequencing data from tibialis anterior muscles of 4 month old male wild type C57Bl/6 mice and mdx/mTR mice (generated in the C57Bl/6 background), which lack the dystrophin and telomerase RNA component genes.