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Results indicate that AKT2 modulates pulmonary fibrosis through inducing TGF-beta1 (show TGFB1 Proteins) and IL-13 (show IL13 Proteins) production by macrophages, and inhibition of AKT2 may be a potential strategy for treating Idiopathic pulmonary fibrosis.
Sirt1 (show SIRT1 Proteins) significantly reduced the levels of raptor (show RPTOR Proteins) and inactivated mammalian target of rapamycin (mTOR (show FRAP1 Proteins))C1 signal by interacting with Akt2.
This review summarises and discusses the consequences of genetic deletions of Akt (show AKT1 Proteins) isoforms in adult mice and their implications for cancer therapy. Whereas combined Akt1 (show AKT1 Proteins) and Akt2 rapidly induced mortality, hepatic Akt (show AKT1 Proteins) inhibition induced liver injury that promotes hepatocellular carcinoma.
Rac1 activation is caused by membrane translocation of a guanine nucleotide exchange factor (show ARHGEF12 Proteins) FLJ00068 in Akt2-mediated insulin (show INS Proteins) signaling in mouse skeletal muscle.
BAY 1125976 is a potent and highly selective allosteric AKT1 (show AKT1 Proteins)/2 inhibitor.
AKT2 inhibition induces a unique mitochondrial-dependent DNA degradation pathway by activating nucleus translocation of AIF (show AIFM1 Proteins) and EndoG (show ENDOG Proteins) during cardiac ischemia.
Akt2 ablation may protect against paraquat toxicity-induced cardiac contractile defect and apoptosis possibly via regulation of Nrf2 (show NFE2L2 Proteins) activation and mitochondrial homeostasis.
Loss of Akt2 enhanced lung tumor development.
Akt2(-/-) mice survive hepatic Akt1 (show AKT1 Proteins) deletion but all develop spontaneous hepatocellular carcinoma. They are insulin (show INS Proteins) resistant. Akt2(-/-) mice are not resistant to diethylnitrosamine hepatocarcinogenesis. They have a high incidence of lung metastasis.
rescued the hepatic regenerative capability in Akt1 (show AKT1 Proteins)-deficient and Akt2-deficient mice
the direct interaction of AKT2 and EF2 (show EEF2 Proteins) was found to be dynamically regulated in embryonic rat cardiomyocytes
Data identify MTSS1 (show MTSS1 Proteins) as a new Akt2-regulated gene, and point to suppression of MTSS1 (show MTSS1 Proteins) as a key step in the metastasis-promoting effects of Akt2 in CRC (show CALR Proteins) cells.
Akt2, Erk2 (show MAPK1 Proteins), and IKK1 (show CHUK Proteins)/2 phosphorylate Bcl3 (show BCL3 Proteins), converting Bcl3 (show BCL3 Proteins) into a transcriptional coregulator by facilitating its recruitment to DNA.
The p.Glu17Lys mutation of AKT2 confers low-level constitutive activity upon the kinase and produces hypoglycemia with suppressed fatty acid release from adipose tissue, but not fatty liver, hypertriglyceridemia, or elevated hepatic de novo lipogenesis.
Studies provide evidence that AKT2 counteracts oxidative-stress-induced (show SQSTM1 Proteins) apoptosis and is required for alpha-beta thymocyte survival and differentiation. Also, it plays a critical role in antagonizing cardiomyocyte apoptosis. [review]
Akt2 role in the human lung cancer cell proliferation, growth, motility, invasion and endothelial cell tube formation
High expressions of AKT1 (show AKT1 Proteins) and AKT2 through possible relation with androgen may cause granulosa cells dysfunction in the +HA PCOS patients.
This study demonstrates novel regulatory circuits involving miR (show MLXIP Proteins)-148a-3p/ERBB3 (show ERBB3 Proteins)/AKT2/c-myc (show MYC Proteins) and DNMT1 (show DNMT1 Proteins) that controls bladder cancer progression, which may be useful in the development of more effective therapies against bladder cancer.
Both in our animal model and in human Age-related macular degeneration (AMD (show AMD1 Proteins)), the AKT2-NF-kappaB (show NFKB1 Proteins)-LCN-2 (show LCN2 Proteins) signalling axis is involved in activating the inflammatory response.
Study reports that Appl1 (show APPL1 Proteins) regulates the activity of Akt (show AKT1 Proteins) and, importantly, its downstream signaling specificity from an endosomal compartment, with profound implications for development.
EDN1 plays an important role in hepatocellular carcinoma progression by activating the PI3K/AKT pathway and is regulated by miR-1.
akt2 has a role in an integrative pathway directly linking glucose, Glut1 (show SLC2A1 Proteins) expression, and activation of apoptosis
Profilin (show PFN1 Proteins)-dependent dissociation of G-actin (show ACTB Proteins)-Tbeta4 complexes simultaneously liberates actin for filament assembly and facilitates Tbeta4 binding to integrin-linked kinase (ILK (show ILK Proteins)) in the lamellipodia.
This gene is a putative oncogene encoding a protein belonging to a subfamily of serine/threonine kinases containing SH2-like (Src homology 2-like) domains. The gene was shown to be amplified and overexpressed in 2 of 8 ovarian carcinoma cell lines and 2 of 15 primary ovarian tumors. Overexpression contributes to the malignant phenotype of a subset of human ductal pancreatic cancers. The encoded protein is a general protein kinase capable of phophorylating several known proteins.
v-akt murine thymoma viral oncogene homolog 2
, RAC-beta serine/threonine-protein kinase
, AKT2 kinase
, RAC-beta serine/threonine-protein kinase-like
, serine/threonine protein kinase
, PKB beta
, RAC-beta serine/threonine protein kinase
, protein kinase Akt-2
, protein kinase B beta
, protein kinase B, beta
, murine thymoma viral (v-akt) homolog-2
, rac protein kinase beta
, RAC protein kinase beta RAC-PK beta
, murine thymoma viral (v-akt) oncogene homolog 2
, thymoma viral proto-oncogene 2
, PKB beta-A
, RAC-beta serine/threonine-protein kinase A
, protein kinase Akt-2-A
, protein kinase B, beta-A
, protein kinase B