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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 (Montrer FKBP5 Protéines) knockouts are protected from high-fat diet-induced weight gain, show improved glucose tolerance and increased insulin (Montrer INS Protéines) signaling in skeletal muscle. We identify a novel association between FKBP51 (Montrer FKBP5 Protéines) and AS160 (Montrer TBC1D4 Protéines), a substrate of AKT2 that is involved in glucose uptake. FKBP51 (Montrer FKBP5 Protéines) antagonism increases the phosphorylation of AS160 (Montrer TBC1D4 Protéines).
IL17A (Montrer IL17A Protéines) 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 (Montrer TRPV6 Protéines) musculus, each AKT (Montrer AKT1 Protéines) isoform has a unique expression pattern in the hippocampus. AKT1 (Montrer AKT1 Protéines), but not AKT2 or AKT3 (Montrer AKT3 Protéines), is required for late long term potetiation (LTD) through regulating activity-induced protein synthesis. Interestingly, AKT (Montrer AKT1 Protéines) activity inhibits mGluR (Montrer GRM8 Protéines)-LTD, with overlapping functions for AKT1 (Montrer AKT1 Protéines) and AKT3 (Montrer AKT3 Protéines).
At 3days after the first tamoxifen injection, Akt1 (Montrer AKT1 Protéines)(-/-)/iAkt2 KO hearts showed decreased expression of connexin43 (Cx43 (Montrer GJA1 Protéines)) and connexin-interacting protein zonula occludens-1 (ZO-1 (Montrer TJP1 Protéines)). Furthermore, Akt1 (Montrer AKT1 Protéines)/2 silencing significantly decreased both Cx43 (Montrer GJA1 Protéines) and ZO-1 (Montrer TJP1 Protéines) expression
Data (including data from studies in transgenic and mutant mice) suggest that Akt2 plays critical role in type 1 diabetes in metallothionein (Montrer MT Protéines)-mediated preservation of cardiac insulin (Montrer INS Protéines)-stimulated metabolic signaling (insulin (Montrer INS Protéines) resistance) and preservation of cardiac function; this mechanism appear to involve inhibition of cardiac Trb3 (Montrer TRIB3 Protéines). (Akt2 = protein kinase Akt-2; Trb3 (Montrer TRIB3 Protéines) = tribbles (Montrer TRIB1 Protéines) pseudokinase 3)
The data indicate that Akt2 ablation protects against cardiac aging through restored Foxo1 (Montrer FOXO1 Protéines)-related autophagy and mitochondrial integrity.
AKT1 (Montrer AKT1 Protéines) 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 (Montrer IRF5 Protéines) and IRF5 (Montrer IRF5 Protéines) 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 (Montrer MEF2A Protéines) abundance, which induced decreased size of cardiomyocytes. We additionally confirmed that EndoG (Montrer ENDOG Protéines), which is also regulated by AKT2, is a suppressor of MEF2A (Montrer MEF2A Protéines) in myocardium.
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 (Montrer ATP5J Protéines) in colorectal cancer
Authors present the first evidence that miR (Montrer MLXIP Protéines)-608 behaves as a tumour suppressor in A549 and SK-LU-1 cells through the regulation of AKT2.
the present study suggested that PHB2 (Montrer PHB2 Protéines) may promote Prostate cancer cell migration by inhibiting the expression of AKT2. These results provide information regarding the role of PHB2 (Montrer PHB2 Protéines) 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 (Montrer ATM Protéines)- and p53 (Montrer TP53 Protéines)-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 (Montrer INS Protéines)-mediated glucose uptake in multiple insulin (Montrer INS Protéines)-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 (Montrer MLXIP Protéines)-143-3p acts as a novel tumor suppressive miRNA by regulating gastric tumor growth, migration and invasion through directly targeting AKT2 gene
Zebrafish akt2 is essential for survival, growth, bone development, and glucose homeostasis.
Study reports that Appl1 (Montrer APPL1 Protéines) regulates the activity of Akt (Montrer AKT1 Protéines) 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 (Montrer SLC2A1 Protéines) expression, and activation of apoptosis
Profilin (Montrer PFN1 Protéines)-dependent dissociation of G-actin (Montrer ACTB Protéines)-Tbeta4 complexes simultaneously liberates actin for filament assembly and facilitates Tbeta4 binding to integrin-linked kinase (ILK (Montrer ILK Protéines)) 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