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akt pan c67e7 rabbit mab  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc akt pan c67e7 rabbit mab
    Akt Pan C67e7 Rabbit Mab, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1732 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mouse+monoclonal+anti+akt/IkappaBalpha+Mouse+mAb/pm42834039-574-110-115
    Average 96 stars, based on 1732 article reviews
    akt pan c67e7 rabbit mab - by Bioz Stars, 2026-10
    96/100 stars

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    Related Articles

    other:

    Article Title: Aurora kinase A promotes trained immunity via regulation of endogenous S-adenosylmethionine metabolism
    Article Snippet: Antibody , Mouse monoclonal anti-AKT , Cell Signaling Technology , Cat# 2920, RRID: AB_1147620 , IB (1:1000).

    Article Title: Akt may associate with insulin-responsive vesicles via interaction with sortilin.
    Article Snippet: Edited by Esteban Gurzov Insulin-responsive vesicles (IRVs) deliver the glucose transporter Glut4 to the plasma membrane in response to activation of the insulin signaling cascade: insulin receptor–IRS–PI3 kinase–Akt–TBC1D4–Rab10.. Previous studies have shown that Akt, TBC1D4, and Rab10 are compartmentalized on the IRVs.. Although functionally significant, the mechanism of Akt association with the IRVs remains unknown.

    Article Title: Fructose-1,6-bisphosphatase is a nonenzymatic safety valve that curtails AKT activation to prevent insulin hyperresponsiveness
    Article Snippet: Mouse monoclonal anti-AKT , Cell Signaling , Cat# 2920; RRID:AB_1147620.

    Incubation:

    Article Title: Interleukin-6 mimics insulin-dependent cellular distribution of some cytoskeletal proteins and Glut4 transporter without effect on glucose uptake in 3T3-L1 adipocytes.
    Article Snippet: Interleukin (IL)-6, a known proinflammatory cytokine, is released in both visceral adipose tissue and contracting skeletal muscle.. In this study, we used microRNA profiling as a screening method to identify miRNA species modified by IL-6 treatment in mouse 3T3-L1 adipocytes. miRNA microarray analysis and qRT-PCR revealed increased expression of miR-146b-3p in adipocytes exposed to IL-6 (1 ng/ml) during 8-day differentiation.. On the basis of ontological analysis of potential targets, selected proteins associated with cytoskeleton and transport were examined in the context of adipocyte response to insulin, using immunofluorescence and confocal microscopy.

    Article Title: Blunted type-5 metabotropic glutamate receptor-mediated polyphosphoinositide hydrolysis in two mouse models of monogenic autism.
    Article Snippet: The involvement of the mGlu5 receptors in the pathophysiology of several forms of monogenic autism has been supported by numerous studies following the seminal observation that mGlu5 receptor-dependent long-term depression was enhanced in the hippocampus of mice modeling the fragile-X syndrome (FXS).. Surprisingly, there are no studies examining the canonical signal transduction pathway activated by mGlu5 receptors (i.e. polyphosphoinositide – PI – hydrolysis) in mouse models of autism.. We have developed a method for in vivo assessment of PI hydrolysis based on systemic injection of lithium chloride followed by treatment with the selective mGlu5 receptor PAM, VU0360172, and measurement of endogenous inositolmonophosphate (InsP) in brain tissue.

    Control:

    Article Title: Interleukin-6 mimics insulin-dependent cellular distribution of some cytoskeletal proteins and Glut4 transporter without effect on glucose uptake in 3T3-L1 adipocytes.
    Article Snippet: Interleukin (IL)-6, a known proinflammatory cytokine, is released in both visceral adipose tissue and contracting skeletal muscle.. In this study, we used microRNA profiling as a screening method to identify miRNA species modified by IL-6 treatment in mouse 3T3-L1 adipocytes. miRNA microarray analysis and qRT-PCR revealed increased expression of miR-146b-3p in adipocytes exposed to IL-6 (1 ng/ml) during 8-day differentiation.. On the basis of ontological analysis of potential targets, selected proteins associated with cytoskeleton and transport were examined in the context of adipocyte response to insulin, using immunofluorescence and confocal microscopy.



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    Cell Signaling Technology Inc mouse monoclonal antibodies against phospho akt ser473
    Effect of circ-CCDC134 and linear-CCDC134 overexpression on the phosphorylation of AKT and STAT3. Jurkat cells were transfected with plasmid encoding circ-CCDC134, plasmid encoding linear CCDC134 and respective empty plasmid. Then the cells were further stimulated with PMA (20 ng/mL) and ionomycin (500 ng/mL) for 1 hour. A Overexpression of circ-CCDC134 increased AKT phosphorylation at Thr308. B Overexpression of circ-CCDC134 increased AKT phosphorylation at <t>Ser473.</t> C A representative example. D Overexpression of linear CCDC134 did not affect AKT phosphorylation at Thr308. E Overexpression of linear CCDC134 did not affect AKT phosphorylation at Ser473. F A representative example. G Overexpression of circ-CCDC134 increased STAT3 phosphorylation at Ser727. H Overexpression of circ-CCDC134 did not affect STAT3 phosphorylation at Tyr705. I A representative example. J Overexpression of linear CCDC134 did not affect STAT3 phosphorylation at Ser727. K Overexpression of linear CCDC134 did not affect STAT3 phosphorylation at Tyr705. L A representative example. (ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001)
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    Cell Signaling Technology Inc mouse monoclonal anti akt pan
    Effect of circ-CCDC134 and linear-CCDC134 overexpression on the phosphorylation of AKT and STAT3. Jurkat cells were transfected with plasmid encoding circ-CCDC134, plasmid encoding linear CCDC134 and respective empty plasmid. Then the cells were further stimulated with PMA (20 ng/mL) and ionomycin (500 ng/mL) for 1 hour. A Overexpression of circ-CCDC134 increased AKT phosphorylation at Thr308. B Overexpression of circ-CCDC134 increased AKT phosphorylation at <t>Ser473.</t> C A representative example. D Overexpression of linear CCDC134 did not affect AKT phosphorylation at Thr308. E Overexpression of linear CCDC134 did not affect AKT phosphorylation at Ser473. F A representative example. G Overexpression of circ-CCDC134 increased STAT3 phosphorylation at Ser727. H Overexpression of circ-CCDC134 did not affect STAT3 phosphorylation at Tyr705. I A representative example. J Overexpression of linear CCDC134 did not affect STAT3 phosphorylation at Ser727. K Overexpression of linear CCDC134 did not affect STAT3 phosphorylation at Tyr705. L A representative example. (ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001)
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    Image Search Results


    Effect of circ-CCDC134 and linear-CCDC134 overexpression on the phosphorylation of AKT and STAT3. Jurkat cells were transfected with plasmid encoding circ-CCDC134, plasmid encoding linear CCDC134 and respective empty plasmid. Then the cells were further stimulated with PMA (20 ng/mL) and ionomycin (500 ng/mL) for 1 hour. A Overexpression of circ-CCDC134 increased AKT phosphorylation at Thr308. B Overexpression of circ-CCDC134 increased AKT phosphorylation at Ser473. C A representative example. D Overexpression of linear CCDC134 did not affect AKT phosphorylation at Thr308. E Overexpression of linear CCDC134 did not affect AKT phosphorylation at Ser473. F A representative example. G Overexpression of circ-CCDC134 increased STAT3 phosphorylation at Ser727. H Overexpression of circ-CCDC134 did not affect STAT3 phosphorylation at Tyr705. I A representative example. J Overexpression of linear CCDC134 did not affect STAT3 phosphorylation at Ser727. K Overexpression of linear CCDC134 did not affect STAT3 phosphorylation at Tyr705. L A representative example. (ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001)

    Journal: Arthritis Research & Therapy

    Article Title: Decreased expression of circ-CCDC134 mediated by TNF-α in patients with rheumatoid arthritis affects T cell function via targeting protein phosphatase 2A

    doi: 10.1186/s13075-026-03763-4

    Figure Lengend Snippet: Effect of circ-CCDC134 and linear-CCDC134 overexpression on the phosphorylation of AKT and STAT3. Jurkat cells were transfected with plasmid encoding circ-CCDC134, plasmid encoding linear CCDC134 and respective empty plasmid. Then the cells were further stimulated with PMA (20 ng/mL) and ionomycin (500 ng/mL) for 1 hour. A Overexpression of circ-CCDC134 increased AKT phosphorylation at Thr308. B Overexpression of circ-CCDC134 increased AKT phosphorylation at Ser473. C A representative example. D Overexpression of linear CCDC134 did not affect AKT phosphorylation at Thr308. E Overexpression of linear CCDC134 did not affect AKT phosphorylation at Ser473. F A representative example. G Overexpression of circ-CCDC134 increased STAT3 phosphorylation at Ser727. H Overexpression of circ-CCDC134 did not affect STAT3 phosphorylation at Tyr705. I A representative example. J Overexpression of linear CCDC134 did not affect STAT3 phosphorylation at Ser727. K Overexpression of linear CCDC134 did not affect STAT3 phosphorylation at Tyr705. L A representative example. (ns, not significant; * P < 0.05; ** P < 0.01; *** P < 0.001)

    Article Snippet: The antibodies used for the Western blot analysis included rabbit monoclonal antibodies against Jun N-terminal kinases (JNK), phospho-JNK (Thr183/Tyr185), AKT, phospho-AKT (Thr308), Signal transducer and activator of transcription 3 (STAT3), phospho-STAT3 (Ser727), poly(rC)-binding protein 2 (PCBP2), the alpha isoform of protein phosphatase 2 A (PP2A) scaffold subunit A (PPP2R1A), in addition to mouse monoclonal antibodies against phospho-AKT (Ser473) and phospho-STAT3 (Tyr705) (Cell Signaling Technology, Danvers, MA, USA).

    Techniques: Over Expression, Phospho-proteomics, Transfection, Plasmid Preparation