ab11466 AKT2 Antibody

Western blot analysis of extracts from B16F10, using Akt2 Antibody. The lane on the left was treated with blocking peptide.
Western blot analysis of extracts from various samples, using Akt2 Antibody. Lane 1: Rat spleen lysates; Lane 2: Mouse brain lysates; Lane 3: Mouse brain lysates treated with blocking peptide;
ab11466 at 1/100 staining Human kidney tissue by IHC-P. The sample was formaldehyde fixed and a heat mediated antigen retrieval step in citrate buffer was performed. The sample was then blocked and incubated with the antibody for 1.5 hours at 22°C. An HRP conjugated goat anti-rabbit antibody was used as the secondary antibody.
ab11466 staining A549 cells by IF/ICC. The samples were fixed with PFA and permeabilized in 0.1% Triton X-100,then blocked in 10% serum for 45 minutes at 25°C. Samples were then incubated with primary Ab(ab11466) and mouse anti-beta tubulin Ab(T0023) for 1 hour at 37°C. An AlexaFluor594 conjugated goat anti-rabbit IgG(H+L) Ab(Red) and an AlexaFluor488 conjugated goat anti-mouse IgG(H+L) Ab(Green) were used as the secondary antibody. The nuclear counter stain is DAPI(blue).
Fig. 4 | LINC00460 acts as a competing endogenous RNA of miR503-5p in SiHa and HeLa cells.d–h Expressions of AKT2,HMGA2 and SHOX2 in SiHa and HeLa cells by western blotting.**p<0.01 versus cells co-transfected with wild-type LINC00460 and miR-503-5p mimic. ##p<0.01 versus cells transfected with NC shRNA. WT wild-type LINC00460, MUT mutated LINC00460
Figure 5 Measurement of expression levels of DEPs, oxidative stress markers and proinflammatory cytokines production. (a) Validation of representative inflammation and autophagy-related DEPs by western blots in the control group (n = 3) and noise group (n = 3). (b) Comparison of MDA level and SOD activity in cochlea between the control group (n = 3) and noise group (n = 3). (c) Comparison of proinflammatory cytokines TNF-α and IL-6 in cochlea between the control group (n = 3) and noise group (n = 3). Data are represented as mean ± SD. * p < 0.05, ** p < 0.01.
Figure 8 RAC prevented the activation of the PI3K/AKT/mTOR and MAPK pathway. The phosphorylation of PI3K, AKT, and mTOR (a) and P38 and ERK (b) was measured by western blot. ▲P < 0.05 and ▲▲P < 0.01vs. the model. Results were presented as mean ± SD. n = 3. Note: RAC: Radix Actinidia chinensis; RCC: renal cell carcinoma.
Figure 5 Effect of LBAG on the expression of autophagy and PI3K/AKT pathway-related proteins in rats. (a) Representative protein blots of p62, LC3, and Beclin 1. (b) Quantitative analysis of p62, LC3, and Beclin 1 proteins. (c) Representative protein blots of PI3K/AKT pathway-related proteins. (d) Quantitative analysis of PI3K pathway-related targets in each group. ∗P < 0.05 and ∗∗P < 0.01 vs. sham group. ▲P < 0.05 and ▲▲P < 0.01 vs. IR group.

品牌

产品货号

来源种属

Rabbit

抗体克隆

Polyclonal

来源亚型

IgG

实验方法

WB,IHC,IF,ICC

实验种属

Human,Mouse,Rat,Rabbit,Pig,Dog,Chicken,Bovine,Horse,Sheep

偶联标记

Unconjugated

目的蛋白

AKT2

产品规格

50μl,100μl,200μl

产品报价

¥1500/¥2750/¥3600

实验应用

Western blotting

Recommended dilution: 1:500-1:2000


Immunofluorescence

Recommended dilution: 1:100-1:500


immunocytochemistry

Recommended dilution: 1:100-1:500


Immunohistochemistry

Recommended dilution: 1:50-1:200




最佳稀释倍数与浓度应由实验研究人员确认

产品说明



产品背景

AKT2 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. Phosphorylation of GSK3 isoforms by AKT is also thought to be one mechanism by which cell proliferation is driven. AKT regulates also cell survival via the phosphorylation of MAP3K5 (apoptosis signal-related kinase). Phosphorylation of 'Ser-83' decreases MAP3K5 kinase activity stimulated by oxidative stress and thereby prevents apoptosis. AKT mediates insulin-stimulated protein synthesis by phosphorylating TSC2 at 'Ser-939' and 'Thr-1462', thereby activating mTORC1 signaling and leading to both phosphorylation of 4E-BP1 and in activation of RPS6KB1. AKT is involved in the phosphorylation of members of the FOXO factors (Forkhead family of transcription factors), leading to binding of 14-3-3 proteins and cytoplasmic localization. In particular, FOXO1 is phosphorylated at 'Thr-24', 'Ser-256' and 'Ser-319'. FOXO3 and FOXO4 are phosphorylated on equivalent sites. AKT has an important role in the regulation of NF-kappa-B-dependent gene transcription and positively regulates the activity of CREB1 (cyclic AMP (cAMP)-response element binding protein). The phosphorylation of CREB1 induces the binding of accessory proteins that are necessary for the transcription of pro-survival genes such as BCL2 and MCL1. AKT phosphorylates 'Ser-454' on ATP citrate lyase (ACLY), thereby potentially regulating ACLY activity and fatty acid synthesis. Activates the 3B isoform of cyclic nucleotide phosphodiesterase (PDE3B) via phosphorylation of 'Ser-273', resulting in reduced cyclic AMP levels and inhibition of lipolysis. Phosphorylates PIKFYVE on 'Ser-318', which results in increased PI(3)P-5 activity. The Rho GTPase-activating protein DLC1 is another substrate and its phosphorylation is implicated in the regulation cell proliferation and cell growth. AKT plays a role as key modulator of the AKT-mTOR signaling pathway controlling the tempo of the process of newborn neurons integration during adult neurogenesis, including correct neuron positioning, dendritic development and synapse formation. Signals downstream of phosphatidylinositol 3-kinase (PI(3)K) to mediate the effects of various growth factors such as platelet-derived growth factor (PDGF), epidermal growth factor (EGF), insulin and insulin-like growth factor I (IGF-I). AKT mediates the antiapoptotic effects of IGF-I. Essential for the SPATA13-mediated regulation of cell migration and adhesion assembly and disassembly. May be involved in the regulation of the placental development.

 

One of the few specific substrates of AKT2 identified recently is PITX2. Phosphorylation of PITX2 impairs its association with the CCND1 mRNA-stabilizing complex thus shortening the half-life of CCND1. AKT2 seems also to be the principal isoform responsible of the regulation of glucose uptake. Phosphorylates C2CD5 on 'Ser-197' during insulin-stimulated adipocytes. AKT2 is also specifically involved in skeletal muscle differentiation, one of its substrates in this process being ANKRD2. Down-regulation by RNA interference reduces the expression of the phosphorylated form of BAD, resulting in the induction of caspase-dependent apoptosis. Phosphorylates CLK2 on 'Thr-343'.

Description
Rabbit polyclonal antibody to AKT2

Applications 
WB, IF, ICC, IHC.

Immunogen 
AKT2 Antibody detects endogenous levels of total AKT2.

Reactivity 
Human, Mouse, Rat.
可预测:Pig(100%), Zebrafish(%), Bovine(%), Horse(%), Chicken(%), Xenopus(%)

Molecular weight
60kDa; 56kD(Calculated).

Host species 
Rabbit

Ig class 
Immunogen-specific rabbit IgG

Purification 
Antigen affinity purification

Full name 
AKT2

Synonyms 
Akt2; AKT2_HUMAN; HIHGHH; murine thymoma viral (v-akt) homolog-2; PKB; PKB beta; PKBB; PKBBETA; PRKBB; Protein kinase Akt 2; Protein kinase Akt-2; Protein kinase B beta; rac protein kinase beta; RAC-BETA; RAC-beta serine/threonine-protein kinase; RAC-PK-beta; v akt murine thymoma viral oncogene homolog 2;

Storage
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.

Swissprot 
P31751
 

产品图片

Western blot analysis of extracts from B16F10, using Akt2 Antibody. The lane on the left was treated with blocking peptide.

Western blot analysis of extracts from various samples, using Akt2 Antibody. Lane 1: Rat spleen lysates; Lane 2: Mouse brain lysates; Lane 3: Mouse brain lysates treated with blocking peptide;

ab11466 at 1/100 staining Human kidney tissue by IHC-P. The sample was formaldehyde fixed and a heat mediated antigen retrieval step in citrate buffer was performed. The sample was then blocked and incubated with the antibody for 1.5 hours at 22°C. An HRP conjugated goat anti-rabbit antibody was used as the secondary antibody.

ab11466 staining A549 cells by IF/ICC. The samples were fixed with PFA and permeabilized in 0.1% Triton X-100,then blocked in 10% serum for 45 minutes at 25°C. Samples were then incubated with primary Ab(ab11466) and mouse anti-beta tubulin Ab(T0023) for 1 hour at 37°C. An AlexaFluor594 conjugated goat anti-rabbit IgG(H+L) Ab(Red) and an AlexaFluor488 conjugated goat anti-mouse IgG(H+L) Ab(Green) were used as the secondary antibody. The nuclear counter stain is DAPI(blue).

Fig. 4 | LINC00460 acts as a competing endogenous RNA of miR503-5p in SiHa and HeLa cells.d–h Expressions of AKT2,HMGA2 and SHOX2 in SiHa and HeLa cells by western blotting.**p<0.01 versus cells co-transfected with wild-type LINC00460 and miR-503-5p mimic. ##p<0.01 versus cells transfected with NC shRNA. WT wild-type LINC00460, MUT mutated LINC00460

Figure 5 Measurement of expression levels of DEPs, oxidative stress markers and proinflammatory cytokines production. (a) Validation of representative inflammation and autophagy-related DEPs by western blots in the control group (n = 3) and noise group (n = 3). (b) Comparison of MDA level and SOD activity in cochlea between the control group (n = 3) and noise group (n = 3). (c) Comparison of proinflammatory cytokines TNF-α and IL-6 in cochlea between the control group (n = 3) and noise group (n = 3). Data are represented as mean ± SD. * p < 0.05, ** p < 0.01.

Figure 8 RAC prevented the activation of the PI3K/AKT/mTOR and MAPK pathway. The phosphorylation of PI3K, AKT, and mTOR (a) and P38 and ERK (b) was measured by western blot. ▲P < 0.05 and ▲▲P < 0.01vs. the model. Results were presented as mean ± SD. n = 3. Note: RAC: Radix Actinidia chinensis; RCC: renal cell carcinoma.

Figure 5 Effect of LBAG on the expression of autophagy and PI3K/AKT pathway-related proteins in rats. (a) Representative protein blots of p62, LC3, and Beclin 1. (b) Quantitative analysis of p62, LC3, and Beclin 1 proteins. (c) Representative protein blots of PI3K/AKT pathway-related proteins. (d) Quantitative analysis of PI3K pathway-related targets in each group. ∗P < 0.05 and ∗∗P < 0.01 vs. sham group. ▲P < 0.05 and ▲▲P < 0.01 vs. IR group.

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