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Western blot analysis of extracts of NIH3T3 cells using rabbit anti-Akt [pS473] antibody (Cat. no. 44-623G). NIH3T3 cells untreated (lane 1) or treated with PDGF (50 ng/mL, 15 min) (lanes 2-5) were resolved by SDS-PAGE on a 10% polyacrylamide gel and transferred to PVDF. Prior to incubation with the primary antibody, the membrane was incubated with no peptide (lane 1 and 2), the non-phosphorylated peptide corresponding to the phosphopeptide immunogen (lane 3), a generic phosphoserine-containing peptide (lane 4), or the phosphopeptide immunogen (lane 5).
|Tested species reactivity||Human|
|Published species reactivity||Human, Mouse|
|Host / Isotype||Rabbit / IgG|
|Immunogen||The antiserum was produced against a chemically synthesized phosphopeptide derived from the region of human Akt1 that contains serine 473.|
|Purification||Antigen affinity chromatography|
|Storage buffer||Dulbecco's PBS, pH 7.3, with 50% glycerol, 1mg/ml BSA|
|Contains||0.05% sodium azide|
|Tested Applications||Dilution *|
|Flow Cytometry (Flow)||1:100-1:500|
|Western Blot (WB)||Assay Dependent|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
|Western Blot (WB)||See 2 publications below|
AKT1 is one of 3 closely related serine/threonine-protein kinases (AKT1, AKT2 and AKT3) called the AKT kinase, and which regulate many processes including metabolism, proliferation, cell survival, growth and angiogenesis. This is mediated through serine and/or threonine phosphorylation of a range of downstream substrates. Over 100 substrate candidates have been reported so far, but for most of them, no isoform specificity has been reported. AKT is responsible of the regulation of glucose uptake by mediating insulin-induced translocation of the SLC2A4/GLUT4 glucose transporter to the cell surface. Phosphorylation of PTPN1 at 'Ser-50' negatively modulates its phosphatase activity preventing dephosphorylation of the insulin receptor and the attenuation of insulin signaling. Phosphorylation of TBC1D4 triggers the binding of this effector to inhibitory 14-3-3 proteins, which is required for insulin-stimulated glucose transport. AKT regulates also the storage of glucose in the form of glycogen by phosphorylating GSK3A at 'Ser-21' and GSK3B at 'Ser-9', resulting in inhibition of its kinase activity.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
|Differential mTOR and ERK pathway utilization by effector CD4 T cells suggests combinatorial drug therapy of arthritis.||Lin JT,Stein EA,Wong MT,Kalpathy KJ,Su LL,Utz PJ,Robinson WH,Fathman CG||Clinical immunology (Orlando, Fla.) (142:127)||2012|
|Human||Not Cited||Naive CD4 t cell proliferation is controlled by mammalian target of rapamycin regulation of GRAIL expression.||Lin JT,Lineberry NB,Kattah MG,Su LL,Utz PJ,Fathman CG,Wu L||Journal of immunology (Baltimore, Md. : 1950) (182:5919)||2009|
AKT; AKT1m; C-AKT; EC 188.8.131.52; kinase Akt1; PKB; PKB alpha; PKB-alpha; protein kinase B alpha; proto-oncogene c-Akt; RAC; rac protein kinase alpha; RAC-alpha serine/threonine kinase; RAC-PK-alpha; serine-threonine protein kinase; v-akt murine thymoma viral oncogene homolog 1; v-akt murine thymoma viral oncogene-like protein 1
AKT; AKT1; CWS6; PKB; PKB-ALPHA; PRKBA; RAC; RAC-ALPHA