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p akt2  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc p akt2
    P Akt2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 187 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rabbit+anti+akt2/Phospho-Akt2+(Ser474)+Rabbit+mAb/pm41714926-106-23-26
    Average 95 stars, based on 187 article reviews
    p akt2 - by Bioz Stars, 2026-09
    95/100 stars

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    Related Articles

    Membrane:

    Article Title: Investigation of the function of the PI3-Kinase / AKT signaling pathway for leukemogenesis and therapy of acute childhood lymphoblastic leukemia (ALL).
    Article Snippet: Acute lymphoblastic leukemia is the most common cause of cancer-related death in children and, especially for patients in a high-risk group, still represents a poor prognosis.. The PI3K/AKT/mTOR signaling pathway has been identified as a frequently constitutively activated switching point in the disease of ALL.. Despite the knowledge of the therapeutic importance of the signaling pathway, the results of clinically effective treatment strategies have so far been extremely sobering.

    Incubation:

    Article Title: Mitochondrial genome modulates myocardial Akt/Glut/HK salvage pathway in spontaneously hypertensive rats adapted to chronic hypoxia.
    Article Snippet: .. Fixed cryosections were incubated with the following primary monoclonal antibodies: mouse anti-GLUT1 and mouse anti-GLUT4 (Abcam), rabbit anti-HK2 (Abcam) and anti-OXPHOS antibody cocktail (Abcam) as a marker of the mitochondrial compartment, mouse antiSERCA2 (Sigma), and rabbit anti-AKT2 (Cell Signaling). .. Secondary goat anti-mouse IgG conjugated with Alexa Fluor 647 (Invitrogen), donkey anti-rabbit IgG conjugated with Alexa Fluor 488 (Invitrogen, Molecular Probes) or anti-rabbit IgG Cy5 was then used.

    Article Title: Diabetic phenotype in mouse and humans reduces the number of microglia around β-amyloid plaques
    Article Snippet: Unspecific antibody binding was prevented by incubating the blots in blocking solution containing 5% non-fat milk or 5% BSA (Sigma-Aldrich, St. Louis, MO, USA) in 1x Tris-buffered saline with 0.1% Tween 20 (TBST) for 1 h at RT. .. Proteins were detected from the blots using the following primary antibodies diluted in the appropriate ratio with 1x TBST and incubated overnight at + 4 °C: rabbit anti-phospho-Akt1 (S473, 1:1000, #9018, Cell Signaling Technology, Danvers, MA, USA), rabbit anti-phospho-Akt2 (S474, 1:1000, #8599, Cell Signaling Technology, Danvers, MA, USA), rabbit anti-phospho-Akt (Thr308/309/305, 1:1000, #13038, Cell Signaling Technology, Danvers, MA, USA), rabbit anti-Akt1 (1:1000, #75692, Cell Signaling Technology, Danvers, MA, USA), rabbit anti-Akt2 (1:1000, #3063, Cell Signaling Technology, Danvers, MA, USA), rabbit anti-Akt (1:1000, #9272, Cell Signaling Technology, Danvers, MA, USA), rabbit anti-phospho-GSK3β (S9, 1:1000, #9336, Cell Signaling Technology, Danvers, MA, USA), rabbit anti-GSK3β (1:1000, #9315, Cell Signaling Technology, Danvers, MA, USA), custom-made mouse anti-phospho-Tau (B6, 1:1000) [ ], mouse anti-4R-Tau (RD4, 1:1000, 05–804, Millipore), mouse anti-SQSTM1/p62 (1:1000, #5114, Cell Signaling Technology, Danvers, MA, USA), mouse anti-LC3 (1:1000, ab51520, Abcam, Cambridge, UK), mouse anti-Caspase-3 (1:1000, #9662, Cell Signaling Technology, Danvers, MA, USA), mouse anti-phospho-ERK (1:500, sc-7383, Santa Cruz Biotechnology, Dallas, TX, USA), rabbit anti-ERK2 (1:500, sc-154, Santa Cruz Biotechnology, Dallas, TX, USA), mouse anti-p85α (1:1000, ABIN1098111, Antibodies-online GmbH, Aachen, Germany), rabbit anti-phospho-SYK (1:1000, MA5–14918, Invitrogen, Waltham, MA, USA), rabbit anti-SYK (1:1000, #13198, Cell Signaling Technology, Danvers, MA, USA), mouse anti-β-actin (1:1000, ab8226, Abcam, Cambridge, UK) and mouse anti-GAPDH (1:15000, ab8245, Abcam). .. Blots were subsequently probed with the appropriate horseradish peroxidase (HRP)-conjugated secondary antibodies, either sheep anti-mouse-HRP (1:5000, NA931V, GE Healthcare, Chicago, IL, USA) or donkey anti-rabbit-HRP (1:5000, NA934V, GE Healthcare, Chicago, IL, USA) diluted in 1x TBST and incubated for 1 h at room temperature.

    Article Title: Diabetic phenotype in mouse and humans with β-amyloid pathology reduces the number of microglia around β-amyloid plaques
    Article Snippet: Unspecific antibody binding was prevented by incubating the blots in blocking solution containing 5% non-fat milk or 5% BSA (Sigma-Aldrich, St. Louis, MO, USA) in 1x Tris-buffered saline with 0.1 % Tween 20 (TBST) for 1 h at RT. .. Proteins were detected from the blots using the following primary antibodies diluted in the appropriate ratio with 1x TBST and incubated overnight at +4°C: rabbit anti-phospho-Akt1 (S473, 1:1000, #9018, Cell Signaling Technology, Danvers, MA, USA), rabbit anti-phospho-Akt2 (S474, 1:1000, #8599, Cell Signaling Technology, Danvers, MA, USA), rabbit anti-phospho-Akt (Thr308/309/305, 1:1000, #13038, Cell Signaling Technology, Danvers, MA, USA), rabbit anti-Akt1 (1:1000, #75692, Cell Signaling Technology, Danvers, MA, USA), rabbit anti-Akt2 (1:1000, #3063, Cell Signaling Technology, Danvers, MA, USA), rabbit anti-Akt (1:1000, #9272, Cell Signaling Technology, Danvers, MA, USA), rabbit anti-phospho-GSK3β (S9, 1:1000, #9336, Cell Signaling Technology, Danvers, MA, USA), rabbit anti-GSK3β (1:1000, #9315, Cell Signaling Technology, Danvers, MA, USA), custom-made mouse anti-phospho-Tau (B6, 1:1000) [ ], mouse anti-4R-Tau (RD4, 1:1000, 05-804, Millipore), mouse anti-SQSTM1/p62 (1:1000, #5114, Cell Signaling Technology, Danvers, MA, USA), mouse anti-LC3 (1:1000, ab51520, Abcam, Cambridge, UK), mouse anti-Caspase-3 (1:1000, #9662, Cell Signaling Technology, Danvers, MA, USA), mouse anti-phospho-ERK (1:500, sc-7383, Santa Cruz Biotechnology, Dallas, TX, USA), rabbit anti-ERK2 (1:500, sc-154, Santa Cruz Biotechnology, Dallas, TX, USA), mouse anti-p85α (1:1000, ABIN1098111, Antibodies-online GmbH, Aachen, Germany), rabbit anti-phospho-SYK (1:1000, MA5-14918, Invitrogen, Waltham, MA, USA), rabbit anti-SYK (1:1000, #13198, Cell Signaling Technology, Danvers, MA, USA), mouse anti-β-actin (1:1000, ab8226, Abcam, Cambridge, UK) and mouse anti-GAPDH (1:15000, ab8245, Abcam). .. Blots were subsequently probed with the appropriate horseradish peroxidase (HRP)-conjugated secondary antibodies, either sheep anti-mouse-HRP (1:5000, NA931V, GE Healthcare, Chicago, IL, USA) or donkey anti-rabbit-HRP (1:5000, NA934V, GE Healthcare, Chicago, IL, USA) diluted in 1x TBST and incubated for 1 h at room temperature.

    Article Title: Intranasal insulin activates Akt2 signaling pathway in the hippocampus of wild-type but not in APP/PS1 Alzheimer model mice.
    Article Snippet: .. Proteins were detected from the blots using the following primary antibodies diluted in the appropriate ratio with 1x TBST and incubated overnight at þ4 C: rabbit anti- phospho-Akt1 (Ser473, 1:1000, #9018; Cell Signaling Technology), rabbit anti-phospho-Akt2 (Ser474, 1:1000, #8599; Cell Signaling Technology), rabbit anti-phospho-Akt (Thr308/309/305, 1:1000, #13038; Cell Signaling Technology), rabbit anti-Akt1 (1:1000, #75692; Cell Signaling Technology), rabbit anti-Akt2 (1:1000, #3063; Cell Signaling Technology), rabbit anti-Akt (1:1000, #9272; Cell Signaling Technology), rabbit anti-phospho-GSK3b (Ser9, 1:1000, #9336; Cell Signaling Technology), rabbit anti-GSK3b (1:1000, #9315; Cell Signaling Technology), custom-made mouse anti-phospho-tau detecting the Ser202, Thr205, and Ser208 residues (B6, 1:1000), mouse anti-4R-Tau (RD4, 1:1000, 05-804; Millipore), mouse anti-SQSTM1/p62 (1:1000, #5114; Cell Signaling Technology), mouse anti-LC3 (1:1000, ab51520), and mouse antiGAPDH (1:15,000, ab8245; Abcam). .. Blots were subsequently probed with the appropriate horseradish peroxidase (HRP)econjugated secondary antibodies, either sheep anti-mouse-HRP (1:5000, NA931V; GE Healthcare) or donkey anti-rabbit-HRP (1:5000, NA934V; GE Healthcare) diluted in 1x TBST and incubated for 1 hour at room temperature.

    Bioprocessing:

    Article Title: Mitochondrial genome modulates myocardial Akt/Glut/HK salvage pathway in spontaneously hypertensive rats adapted to chronic hypoxia.
    Article Snippet: .. Fixed cryosections were incubated with the following primary monoclonal antibodies: mouse anti-GLUT1 and mouse anti-GLUT4 (Abcam), rabbit anti-HK2 (Abcam) and anti-OXPHOS antibody cocktail (Abcam) as a marker of the mitochondrial compartment, mouse antiSERCA2 (Sigma), and rabbit anti-AKT2 (Cell Signaling). .. Secondary goat anti-mouse IgG conjugated with Alexa Fluor 647 (Invitrogen), donkey anti-rabbit IgG conjugated with Alexa Fluor 488 (Invitrogen, Molecular Probes) or anti-rabbit IgG Cy5 was then used.

    Marker:

    Article Title: Mitochondrial genome modulates myocardial Akt/Glut/HK salvage pathway in spontaneously hypertensive rats adapted to chronic hypoxia.
    Article Snippet: .. Fixed cryosections were incubated with the following primary monoclonal antibodies: mouse anti-GLUT1 and mouse anti-GLUT4 (Abcam), rabbit anti-HK2 (Abcam) and anti-OXPHOS antibody cocktail (Abcam) as a marker of the mitochondrial compartment, mouse antiSERCA2 (Sigma), and rabbit anti-AKT2 (Cell Signaling). .. Secondary goat anti-mouse IgG conjugated with Alexa Fluor 647 (Invitrogen), donkey anti-rabbit IgG conjugated with Alexa Fluor 488 (Invitrogen, Molecular Probes) or anti-rabbit IgG Cy5 was then used.

    other:

    Article Title: Integrin and autocrine IGF2 pathways control fasting insulin secretion in β-cells
    Article Snippet: Antibodies and reagents by guest on Septem ber 19, 2020 http://w w w .jbc.org/ D ow nloaded from The following antibodies were used: Cell Signaling Technology: rabbit anti-Akt1 (#2938), rabbit anti-Akt2 (#3063), rabbit anti-ERK1/2 (#9102), rabbit anti-p(Y118) paxillin (#2541), rabbit anti-pS473 Akt (#9271), rabbit anti-Akt (#9272), rabbit anti-Src (#2108).



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    Cell Signaling Technology Inc akt2
    (A) Schematic overview of the canonical signaling events modulating muscle insulin action and its interaction with mTORC1 signaling. (B to D) Canonical insulin signaling as determined by phosphorylation of <t>Akt2</t> on Ser473 and Thr308, and phosphorylation of the Akt substrates GSK3β on Ser9 and TBC1D4 on Thr 642 in whole-muscle lysates from skeletal muscle biopsy samples obtained before (Basal) and immediately after (Insulin) the hyperinsulinemic-euglycemic (HE) clamp. Levels of total Akt2, GSK3β, and TBC1D4 were comparable across groups and unaffected by insulin. (E and F) mTORC1 signaling as determined by phosphorylation of p70 S6 kinase (p70S6K) on Thr389 and S6 on Ser235/236 in whole-muscle lysates from skeletal muscle biopsy samples obtained before (Basal) and immediately after (Insulin) the HE clamp. Levels of total p70S6K and S6 were comparable across groups and unaffected by insulin. Linear mixed models were used to estimate within– and between-group differences. Data are presented as observed individual values (with lines connecting individually matched participants) and estimated means ± 95% confidence limits, unless otherwise stated. For m.3243A>G carriers, individual datapoints are color-shaded to indicate muscle mtDNA heteroplasmy (light red = low, dark red = high). *Different from Basal ( P < 0.05). Basal, n = 30; Insulin, n = 27 (13 in m.3243A>G, 14 in Controls). Illustrations in (A) were created with BioRender.com.
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    Cell Signaling Technology Inc pser474 akt2 8599s
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    Image Search Results


    (A) Schematic overview of the canonical signaling events modulating muscle insulin action and its interaction with mTORC1 signaling. (B to D) Canonical insulin signaling as determined by phosphorylation of Akt2 on Ser473 and Thr308, and phosphorylation of the Akt substrates GSK3β on Ser9 and TBC1D4 on Thr 642 in whole-muscle lysates from skeletal muscle biopsy samples obtained before (Basal) and immediately after (Insulin) the hyperinsulinemic-euglycemic (HE) clamp. Levels of total Akt2, GSK3β, and TBC1D4 were comparable across groups and unaffected by insulin. (E and F) mTORC1 signaling as determined by phosphorylation of p70 S6 kinase (p70S6K) on Thr389 and S6 on Ser235/236 in whole-muscle lysates from skeletal muscle biopsy samples obtained before (Basal) and immediately after (Insulin) the HE clamp. Levels of total p70S6K and S6 were comparable across groups and unaffected by insulin. Linear mixed models were used to estimate within– and between-group differences. Data are presented as observed individual values (with lines connecting individually matched participants) and estimated means ± 95% confidence limits, unless otherwise stated. For m.3243A>G carriers, individual datapoints are color-shaded to indicate muscle mtDNA heteroplasmy (light red = low, dark red = high). *Different from Basal ( P < 0.05). Basal, n = 30; Insulin, n = 27 (13 in m.3243A>G, 14 in Controls). Illustrations in (A) were created with BioRender.com.

    Journal: medRxiv

    Article Title: Physiological and molecular characterization of individuals carrying a diabetogenic mtDNA mutation establishes a mitochondrial basis for insulin resistance in humans

    doi: 10.64898/2025.12.17.25342274

    Figure Lengend Snippet: (A) Schematic overview of the canonical signaling events modulating muscle insulin action and its interaction with mTORC1 signaling. (B to D) Canonical insulin signaling as determined by phosphorylation of Akt2 on Ser473 and Thr308, and phosphorylation of the Akt substrates GSK3β on Ser9 and TBC1D4 on Thr 642 in whole-muscle lysates from skeletal muscle biopsy samples obtained before (Basal) and immediately after (Insulin) the hyperinsulinemic-euglycemic (HE) clamp. Levels of total Akt2, GSK3β, and TBC1D4 were comparable across groups and unaffected by insulin. (E and F) mTORC1 signaling as determined by phosphorylation of p70 S6 kinase (p70S6K) on Thr389 and S6 on Ser235/236 in whole-muscle lysates from skeletal muscle biopsy samples obtained before (Basal) and immediately after (Insulin) the HE clamp. Levels of total p70S6K and S6 were comparable across groups and unaffected by insulin. Linear mixed models were used to estimate within– and between-group differences. Data are presented as observed individual values (with lines connecting individually matched participants) and estimated means ± 95% confidence limits, unless otherwise stated. For m.3243A>G carriers, individual datapoints are color-shaded to indicate muscle mtDNA heteroplasmy (light red = low, dark red = high). *Different from Basal ( P < 0.05). Basal, n = 30; Insulin, n = 27 (13 in m.3243A>G, 14 in Controls). Illustrations in (A) were created with BioRender.com.

    Article Snippet: The following antibodies were used: Phospho-Akt (Thr308) (Cell Signaling, catalog no. 9275); Phospho-Akt (Ser473) (Cell Signaling, catalog no. 9271); Akt2 (Cell Signaling, catalog no. 3063); Phospho-GSK-3β (Ser9) (Cell Signaling, catalog no. 5558); GSK-3β (BD Transduction Laboratories, catalog no. 610202); Phospho-TBC1D4 (Thr642) (Cell Signaling, catalog no. 8881); TBC1D4 (Abcam, catalog no. ab189890); Phospho-p70S6K (Thr389) (Cell Signaling, catalog no. 9205); p70S6K (Cell Signaling, catalog no. 9202); Phospho-S6 (Ser235/236) (Cell Signaling, catalog no. 4858); S6 (Cell Signaling, catalog no. 2217); PRDX2 (Abcam, catalog no. ab109367); PRDX3 (Abcam, catalog no. ab73349).

    Techniques: Phospho-proteomics