Use your antibodies-online credentials, if available.
Keine Produkte auf Ihrer Vergleichsliste.
Ihr Warenkorb ist leer.
Weitere Synonyme anzeigen
Wählen Sie die gewünschte Spezies
this study shows that over-expressed miRNA-200b ameliorates ulcerative colitis-related colorectal cancer in mice through orchestrating epithelial-mesenchymal transition and inflammatory responses by channel of AKT2
Fkbp5 knockouts are protected from high-fat diet-induced weight gain, show improved glucose tolerance and increased insulin signaling in skeletal muscle. We identify a novel association between FKBP51 and AS160, a substrate of AKT2 that is involved in glucose uptake. FKBP51 antagonism increases the phosphorylation of AS160.
IL17A promoted osteoblast differentiation and calcification in a partly AKT2dependent manner in MC3T3E1 cells in vitro, possibly reflecting compensation by other signaling pathways. The results of the present study may offer novel perspectives to guide the clinical strategy for the prevention and treatment of periodontitis
The authors find in Mus musculus, each AKT isoform has a unique expression pattern in the hippocampus. AKT1, but not AKT2 or AKT3, is required for late long term potetiation (LTD) through regulating activity-induced protein synthesis. Interestingly, AKT activity inhibits mGluR-LTD, with overlapping functions for AKT1 and AKT3.
At 3days after the first tamoxifen injection, Akt1(-/-)/iAkt2 KO hearts showed decreased expression of connexin43 (Cx43) and connexin-interacting protein zonula occludens-1 (ZO-1). Furthermore, Akt1/2 silencing significantly decreased both Cx43 and ZO-1 expression
Data (including data from studies in transgenic and mutant mice) suggest that Akt2 plays critical role in type 1 diabetes in metallothionein-mediated preservation of cardiac insulin-stimulated metabolic signaling (insulin resistance) and preservation of cardiac function; this mechanism appear to involve inhibition of cardiac Trb3. (Akt2 = protein kinase Akt-2; Trb3 = tribbles pseudokinase 3)
The data indicate that Akt2 ablation protects against cardiac aging through restored Foxo1-related autophagy and mitochondrial integrity.
AKT1 and AKT2 isoforms have opposing roles in smooth muscle cell proliferation, migration, differentiation, and rapamycin response in vitro and in vascular injury in vivo.
IRF5 and IRF5 disease-risk variants increase glycolysis and human m1 macrophage polarization by regulating proximal signaling and Akt2 activation.
Deficiency of AKT2 in myocardium results in diminished MEF2A abundance, which induced decreased size of cardiomyocytes. We additionally confirmed that EndoG, which is also regulated by AKT2, is a suppressor of MEF2A in myocardium.
Results indicate that AKT2 modulates pulmonary fibrosis through inducing TGF-beta1 and IL-13 production by macrophages, and inhibition of AKT2 may be a potential strategy for treating Idiopathic pulmonary fibrosis.
Sirt1 significantly reduced the levels of raptor and inactivated mammalian target of rapamycin (mTOR)C1 signal by interacting with Akt2.
This review summarises and discusses the consequences of genetic deletions of Akt isoforms in adult mice and their implications for cancer therapy. Whereas combined Akt1 and Akt2 rapidly induced mortality, hepatic Akt inhibition induced liver injury that promotes hepatocellular carcinoma.
Rac1 activation is caused by membrane translocation of a guanine nucleotide exchange factor FLJ00068 in Akt2-mediated insulin signaling in mouse skeletal muscle.
BAY 1125976 is a potent and highly selective allosteric AKT1/2 inhibitor.
AKT2 inhibition induces a unique mitochondrial-dependent DNA degradation pathway by activating nucleus translocation of AIF and EndoG during cardiac ischemia.
Akt2 ablation may protect against paraquat toxicity-induced cardiac contractile defect and apoptosis possibly via regulation of Nrf2 activation and mitochondrial homeostasis.
Loss of Akt2 enhanced lung tumor development.
Akt2(-/-) mice survive hepatic Akt1 deletion but all develop spontaneous hepatocellular carcinoma. They are insulin resistant. Akt2(-/-) mice are not resistant to diethylnitrosamine hepatocarcinogenesis. They have a high incidence of lung metastasis.
rescued the hepatic regenerative capability in Akt1-deficient and Akt2-deficient mice
MiR-92a inhibits fibroblast-like synoviocyte proliferation and migration in rheumatoid arthritis by targeting AKT2.
Data show while overexpression of AKT serine/threonine kinase 1 (AKT1) promoted local tumor growth, downregulation of AKT1 or overexpression of AKT serine/threonine kinase 2 (AKT2) promoted peritumoral invasion and lung metastasis.
AKT2 inhibition as a powerful therapeutic target against CSC.
AKT2 and XIST expression was identified as a potential biomarker participating in the effect of ATP5J in colorectal cancer
Authors present the first evidence that miR-608 behaves as a tumour suppressor in A549 and SK-LU-1 cells through the regulation of AKT2.
the present study suggested that PHB2 may promote Prostate cancer cell migration by inhibiting the expression of AKT2. These results provide information regarding the role of PHB2 in Prostate cancer migration and malignancy
Data found that S131 of Akt2 is not phosphorylated by CK2 although the consensus sequence recognized by CK2 (S/T-x-x-E/D/pS/pT) is conserved. A single sequence element, a T at position n+1, hampers phosphorylation, causing an alpha-helix structure preventing the recognition of its own consensus by CK2. Using synthetic peptides, study suggests that Akt2 S131 could be phosphorylated by kinases of the Plk family.
Findings demonstrate that DSBs trigger pro-survival autophagy in an ATM- and p53-dependent manner, which is curtailed by AKT2 signaling.
genetic association studies in population of men in Finland: Data suggest that a partial loss-of-function variant in AKT2 (p.Pro50Thr) is associated with type 2 diabetes in the population studied; this AKT2 variant is associated with reduced insulin-mediated glucose uptake in multiple insulin-sensitive tissues.
miR2965p/AKT2 axis serves important roles in Hepatocellular carcinoma carcinogenesis and progression.
miR296 is downregulated in tissue from patients with pancreatic cancer and pancreatic carcinoma cell lines. These findings suggested that it may function as a tumor suppressor via inhibiting the growth, migration and invasion of pancreatic cancer cells. AKT2 was validated as a direct target of miR296 in pancreatic cancer cells.
miR-143-3p acts as a novel tumor suppressive miRNA by regulating gastric tumor growth, migration and invasion through directly targeting AKT2 gene
Our findings suggest that Akt2 might be associated with the resistance to anti-EGFR therapies, especially the use of erlotinib against PC, and that this resistance can be overcome by combined treatment with a PI3K inhibitor. Akt2 expression could become a predictive biomarker for erlotinib resistance in PC.
Studied action of linoleic acid (LA) on cell migration and neoplasm invasiveness of breast cancer cells. Findings show Akt2 activation requires EGFR and PI3K activity, whereas migration and invasion are dependent on FFAR4, EGFR and PI3K/Akt activity.
Analysis of genomic data from TCGA demonstrated coamplification of CCNE1 and AKT2 Overexpression of Cyclin E1 and AKT isoforms, in addition to mutant TP53, imparted malignant characteristics in untransformed fallopian tube secretory cells, the dominant site of origin of high-grade serous ovarian cancer
Akt1-Akt3 activity (according to Thr308 phosphorylation) is not associated with proliferative processes in the tumor tissue of the thyroid.
Recent studies reveal that AKT2-NOX2 signaling has critical roles in Ca mobilization, ROS generation, degranulation, and control of the ligand-binding function of cell surface molecules, thereby promoting heterotypic cell-cell interactions in thromboinflammation.
The expression levels of AKT2 and CDC25C showed lower expression in neural tube defects. And the percentage of methylated region of AKT2 promoter were increased in neural tube defects.
Report frequency of genetic variation in Akt2 and discuss link to type 2 diabetes.
Zebrafish akt2 is essential for survival, growth, bone development, and glucose homeostasis.
Study reports that Appl1 regulates the activity of Akt 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 expression, and activation of apoptosis
Profilin-dependent dissociation of G-actin-Tbeta4 complexes simultaneously liberates actin for filament assembly and facilitates Tbeta4 binding to integrin-linked kinase (ILK) 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