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Rabbit Anti-phospho-AKT (Ser473) antibody (bs-0876R)
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说明书: 100ul  
100ul/1980.00元
大包装/询价

产品编号 bs-0876R
英文名称 phospho-AKT (Ser473)
中文名称 磷酸化蛋白激酶B抗体
别    名 Akt(Phospho-Ser473); AKT (phospho-S473); AKT (phospho Ser473); p-AKT (Ser473); AKT 1; AKT; AKT1; AKT-1; AKT1_HUMAN; C AKT; cAKT; MGC9965; MGC99656; Oncogene AKT1; PKB; PKB alpha; PKB-ALPHA; PRKBA; Protein Kinase B Alpha; Protein kinase B; Proto-oncogene c-Akt; RAC Alpha; RAC alpha serine/threonine protein kinase; RAC; RAC PK Alpha; Rac protein kinase alpha; RAC Serine/Threonine Protein Kinase; RAC-alpha serine/threonine-protein kinase; RAC-PK-alpha; v akt murine thymoma viral oncogene homolog 1; vAKT Murine Thymoma Viral Oncogene Homolog 1.  
Specific References  (21)     |     bs-0876R has been referenced in 21 publications.
[IF=0] Tang et al. The cardioprotective effects of citric Acid and L-malic Acid on myocardial ischemia/reperfusion injury. (2013) Evid.Based.Complement.Alternat.Me. 2013:820695  WB ;  Rat.  
[IF=5.17] Liang et al. Histone demethylase RBP2 induced by Helicobactor Pylori CagA participates in the malignant transformation of gastric epithelial cells. (2014) Oncotarge. 5:5798-807  WB ;  Human.  
[IF=1.146] Xu et al. Cardioprotection against experimental myocardial ischemic injury using cornin. (2016) Braz.J.Med.Biol.Re. 49:e5039  WB ;  Rat.  
[IF=3.454] Hao YL et al. The role of microRNA-1 targeting of MAPK3 in myocardial ischemia-reperfusion injury in rats undergoing sevoflurane preconditioning via the PI3K/Akt pathway.Am. J. Physiol., Cell Physiol. 2018 Sep 01;315(3)  WB ;  Rat.  
[IF=2.342] Liu W et al. Glycyrrhizic acid from licorice down-regulates inflammatory responses via blocking MAPK and PI3K/Akt-dependent NF-κB signalling pathways in TPA-induced skin inflammation. Medchemcomm. 2018 Jul 19;9(9):1502-1510.  IHC-P ;  Mouse.  
[IF=1.935] Ou X et al. Desumoylating Isopeptidase 2 (DESI2) Inhibits Proliferation and Promotes Apoptosis of Pancreatic Cancer Cells through Regulating PI3K/AKT/mTOR Signaling Pathway. (2018)Pathol. Oncol. Res. Nov 8.  WB ;  Human .  
[IF=3.448] Zhang H et al. Ginsenoside Rb1 promotes the growth of mink hair follicle via PI3K/AKT/GSK-3β signalingpathway. Life Sci. 2019 Jul 15;229:210-218.   WB ;  Mink.  
[IF=3.266] Ma Q et al. Vitamin B5 inhibit RANKL induced osteoclastogenesis and ovariectomy induced osteoporosis by scavenging ROS generation. Am J Transl Res. 2019 Aug 15;11(8):5008-5018. eCollection 2019.  WB ;  Mouse.  
[IF=3.743] Liu F et al. Clinical and biological significances of heat shock protein 90 (Hsp90) in human nasopharyngeal carcinoma cells and anti-cancer effects of Hsp90 inhibitor. Biomed Pharmacother. 2019 Oct 18;120:109533.   ICF ;  Human.  
[IF=6.67] Santos, Joana, et al. "Uncovering potential downstream targets of oncogenic GRPR overexpression in prostate carcinomas harboring ETS rearrangements." Oncoscience 2.5 (2015): 497.  WB ;  Human.  
[IF=2.35] Li, Guofu, et al. "The neutrophil elastase inhibitor, sivelestat, attenuates sepsis-related kidney injury in rats." International Journal of Molecular Medicine 38.3 (2016): 767-775.  WB ;  Rat.  
[IF=5.714] Zhao H et al. The cardiotoxicity of the common carp (Cyprinus carpio) exposed to environmentally relevant concentrations of arsenic and subsequently relieved by zinc supplementation. Environmental Pollution.2019 Oct; 253:741-748.  WB ;  Carp.  
[IF=2.394] Liu W et al. Synergistic effect of tolfenamic acid and glycyrrhizic acid on TPA-induced skin inflammation in mice. MedChemComm.2019.  IHC-P ;  Mouse.  
[IF=2.976] Wang S et al. Girdin regulates the proliferation and apoptosis of pancreatic cancer cells via the PI3K/Akt signalling pathway.Oncol Rep. 2018 Aug;40(2):599-608.   ICF ;  Human.  
[IF=2.154] Wang Y et al. H2S mediates apoptosis in response to inflammation through PI3K/Akt/NFκB signaling pathway. Biotechnol Lett. 2019 Dec 23.   WB ;  bovine.  
[IF=3.329] Zhang Y et al. Overexpressed CES2 has prognostic value in CRC and knockdown CES2 reverses L-OHP-resistance in CRC cells by inhibition of the PI3K signaling pathway. Exp Cell Res. 2020 Jan 22:111856.   WB ;  Human.  
[IF=2.342] Liu W et al. Glycyrrhizic acid from licorice down-regulates inflammatory responses via blocking MAPK and PI3K/Akt-dependent NF-κB signalling pathways in TPA-induced skin inflammation. MedChemComm. 2018.  IHC-P ;  Mouse.  
[IF=3.895] Yin H et al. T-2 Toxin Induces Oxidative Stress, Apoptosis and Cytoprotective Autophagy in Chicken Hepatocytes. Toxins (Basel). 2020 Jan 29;12(2).   WB ;  Chicken.  
[IF=.181] Li S et al. The Effect of YiQiFuMai on Ischemic Heart Failure by Improve Myocardial Microcirculation and Increase eNOS and VEGF Expression. International Journal of Clinical Medicine,2020 11, 84-100.  WB ;  Rabbit.  
[IF=2.868] Liu B et al. MicroRNA‐379 mediates pigmentation, migration, and proliferation of melanocytes by targeting the insulin‐like growth factor 1 receptor. Exp Dermatol. 2020 May;29(5):467-476.  WB ;  alpaca.  
[IF=2.076] Meng C et al. Photobiomodulation with 630-nm LED radiation inhibits the proliferation of human synoviocyte MH7A cells possibly via TRPV4/PI3K/AKT/mTOR signaling pathway. Lasers Med Sci. 2020 Mar 11.  WB ;  human.  
产品类型 磷酸化抗体 
研究领域 肿瘤  细胞生物  神经生物学  信号转导  细胞凋亡  转录调节因子  激酶和磷酸酶  
抗体来源 Rabbit
克隆类型 Polyclonal
交叉反应 Human, Mouse, Rat,  (predicted: Chicken, Dog, Pig, Cow, Rabbit, Sheep, )
产品应用 WB=1:500-2000 ELISA=1:500-1000 IHC-P=1:100-500 IHC-F=1:100-500 Flow-Cyt=2ug/Test IF=1:100-500 (石蜡切片需做抗原修复)
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量 56kDa
细胞定位 细胞核 细胞浆 细胞膜 
性    状 Liquid
浓    度 1mg/ml
免 疫 原 KLH conjugated Synthesised phosphopeptide derived from human AKT around the phosphorylation site of Ser473:QF(p-S)YS 
亚    型 IgG
纯化方法 affinity purified by Protein A
储 存 液 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
保存条件 Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.
PubMed PubMed
产品介绍 The serine-threonine protein kinase encoded by the AKT1 gene is catalytically inactive in serum-starved primary and immortalized fibroblasts. AKT1 and the related AKT2 are activated by platelet-derived growth factor. The activation is rapid and specific, and it is abrogated by mutations in the pleckstrin homology domain of AKT1. It was shown that the activation occurs through phosphatidylinositol 3-kinase. In the developing nervous system AKT is a critical mediator of growth factor-induced neuronal survival. Survival factors can suppress apoptosis in a transcription-independent manner by activating the serine/threonine kinase AKT1, which then phosphorylates and inactivates components of the apoptotic machinery. Mutations in this gene have been associated with the Proteus syndrome. Multiple alternatively spliced transcript variants have been found for this gene. [provided by RefSeq, Jul 2011]

Function:
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. 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. Phosphorylates STK4/MST1 at 'Thr-120' and 'Thr-387' leading to inhibition of its: kinase activity, nuclear translocation, autophosphorylation and ability to phosphorylate FOXO3. Phosphorylates STK3/MST2 at 'Thr-117' and 'Thr-384' leading to inhibition of its: cleavage, kinase activity, autophosphorylation at Thr-180, binding to RASSF1 and nuclear translocation. Phosphorylates SRPK2 and enhances its kinase activity towards SRSF2 and ACIN1 and promotes its nuclear translocation. Phosphorylates RAF1 at 'Ser-259' and negatively regulates its activity. Phosphorylation of BAD stimulates its pro-apoptotic activity.
AKT1-specific substrates have been recently identified, including palladin (PALLD), which phosphorylation modulates cytoskeletal organization and cell motility; prohibitin (PHB), playing an important role in cell metabolism and proliferation; and CDKN1A, for which phosphorylation at 'Thr-145' induces its release from CDK2 and cytoplasmic relocalization. These recent findings indicate that the AKT1 isoform has a more specific role in cell motility and proliferation. Phosphorylates CLK2 thereby controlling cell survival to ionizing radiation.

Subunit:
Interacts (via the C-terminus) with CCDC88A (via its C-terminus). Interacts with GRB10; the interaction leads to GRB10 phosphorylation thus promoting YWHAE-binding. Interacts with AGAP2 (isoform 2/PIKE-A); the interaction occurs in the presence of guanine nucleotides. Interacts with AKTIP. Interacts (via PH domain) with MTCP1, TCL1A AND TCL1B. Interacts with CDKN1B; the interaction phosphorylates CDKN1B promoting 14-3-3 binding and cell-cycle progression. Interacts with MAP3K5 and TRAF6. Interacts with BAD, PPP2R5B, STK3 and STK4. Interacts (via PH domain) with SIRT1. Interacts with SRPK2 in a phosphorylation-dependent manner. Interacts with RAF1. Interacts with TRIM13; the interaction ubiquitinates AKT1 leading to its proteasomal degradation. Interacts with TNK2 and CLK2. Interacts (via the C-terminus) with THEM4 (via its C-terminus). Interacts with and phosphorylated by PDPK1.

Subcellular Location:
Cytoplasm. Nucleus. Cell membrane. Note=Nucleus after activation by integrin-linked protein kinase 1 (ILK1). Nuclear translocation is enhanced by interaction with TCL1A. Phosphorylation on Tyr-176 by TNK2 results in its localization to the cell membrane where it is targeted for further phosphorylations on Thr-308 and Ser-473 leading to its activation and the activated form translocates to the nucleus.

Tissue Specificity:
Expressed in prostate cancer and levels increase from the normal to the malignant state (at protein level). Expressed in all human cell types so far analyzed. The Tyr-176 phosphorylated form shows a significant increase in expression in breast cancers during the progressive stages i.e. normal to hyperplasia (ADH), ductal carcinoma in situ (DCIS), invasive ductal carcinoma (IDC) and lymph node metastatic (LNMM) stages.

Post-translational modifications:
O-GlcNAcylation at Thr-305 and Thr-312 inhibits activating phosphorylation at Thr-308 via disrupting the interaction between AKT1 and PDPK1. O-GlcNAcylation at Ser-473 also probably interferes with phosphorylation at this site.
Phosphorylation on Thr-308, Ser-473 and Tyr-474 is required for full activity. Activated TNK2 phosphorylates it on Tyr-176 resulting in its binding to the anionic plasma membrane phospholipid PA. This phosphorylated form localizes to the cell membrane, where it is targeted by PDPK1 and PDPK2 for further phosphorylations on Thr-308 and Ser-473 leading to its activation. Ser-473 phosphorylation by mTORC2 favors Thr-308 phosphorylation by PDPK1. Ser-473 phosphorylation is enhanced by interaction with AGAP2 isoform 2 (PIKE-A). Ser-473 phosphorylation is enhanced in focal cortical dysplasias with Taylor-type balloon cells. Ser-473 phosphorylation is enhanced by signaling through activated FLT3. Dephosphorylated at Thr-308 and Ser-473 by PP2A phosphatase. The phosphorylated form of PPP2R5B is required for bridging AKT1 with PP2A phosphatase.
Ubiquitinated via 'Lys-48'-linked polyubiquitination by ZNRF1, leading to its degradation by the proteasome. Ubiquitinated; undergoes both 'Lys-48'- and 'Lys-63'-linked polyubiquitination. TRAF6-induced 'Lys-63'-linked AKT1 ubiquitination is critical for phosphorylation and activation. When ubiquitinated, it translocates to the plasma membrane, where it becomes phosphorylated. When fully phosphorylated and translocated into the nucleus, undergoes 'Lys-48'-polyubiquitination catalyzed by TTC3, leading to its degradation by the proteasome. Also ubiquitinated by TRIM13 leading to its proteasomal degradation.
Acetylated on Lys-14 and Lys-20 by the histone acetyltransferases EP300 and KAT2B. Acetylation results in reduced phosphorylation and inhibition of activity. Deacetylated at Lys-14 and Lys-20 by SIRT1. SIRT1-mediated deacetylation relieves the inhibition.

DISEASE:
Defects in AKT1 are a cause of susceptibility to breast cancer (BC) [MIM:114480]. A common malignancy originating from breast epithelial tissue. Breast neoplasms can be distinguished by their histologic pattern. Invasive ductal carcinoma is by far the most common type. Breast cancer is etiologically and genetically heterogeneous. Important genetic factors have been indicated by familial occurrence and bilateral involvement. Mutations at more than one locus can be involved in different families or even in the same case.
Defects in AKT1 are associated with colorectal cancer (CRC) [MIM:114500].
Note=Genetic variations in AKT1 may play a role in susceptibility to ovarian cancer.
Defects in AKT1 are a cause of Proteus syndrome (PROTEUSS) [MIM:176920]. A highly variable, severe disorder of asymmetric and disproportionate overgrowth of body parts, connective tissue nevi, epidermal nevi, dysregulated adipose tissue, and vascular malformations. Many features of Proteus syndrome overlap with other overgrowth syndromes.

Similarity:
Belongs to the protein kinase superfamily. AGC Ser/Thr protein kinase family. RAC subfamily.
Contains 1 AGC-kinase C-terminal domain.
Contains 1 PH domain.
Contains 1 protein kinase domain.

SWISS:
P47196

Gene ID:
207

Database links:

Entrez Gene: 207 Human

Entrez Gene: 11651 Mouse

Entrez Gene: 24185 Rat

Omim: 164730 Human

SwissProt: O57513 Chicken

SwissProt: P31749 Human

SwissProt: P31750 Mouse

SwissProt: P47196 Rat

Unigene: 525622 Human

Unigene: 6645 Mouse

Unigene: 11422 Rat



Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.

产品图片
Sample:
Heart (Mouse) Lysate at 40 ug
Primary: Anti-phospho-AKT (Ser473) (bs-0876R) at 1/300 dilution
Secondary: IRDye800CW Goat Anti-Rabbit IgG at 1/20000 dilution
Predicted band size: 56 kD
Observed band size: 56 kD
Sample:
U937 Cell (Human) Lysate at 30 ug
Primary: Anti-phospho-AKT (Ser473) (bs-0876R) at 1/300 dilution
Secondary: IRDye800CW Goat Anti-Rabbit IgG at 1/20000 dilution
Predicted band size: 56 kD
Observed band size: 56 kD
Sample:Liver(Mouse) Lysate at 30 ug
Primary: Anti-phospho-AKT(Ser473) (bs-0876R) at 1:300 dilution;
Secondary: HRP conjugated Goat Anti-Rabbit IgG(bs-0295G-HRP) at 1: 5000 dilution;
Predicted band size : 56kD
Observed band size : 56kD
Tissue/cell: Human breast; 4% Paraformaldehyde-fixed and paraffin-embedded;
Antigen retrieval: citrate buffer ( 0.01M, pH 6.0 ), Boiling bathing for 15min; Block endogenous peroxidase by 3% Hydrogen peroxide for 30min; Blocking buffer (normal goat serum,C-0005) at 37℃ for 20 min;
Incubation: Anti-phospho-AKT/PKB(Ser473) Polyclonal Antibody, Unconjugated(bs-0876R) 1:600, overnight at 4°C, followed by conjugation to the secondary antibody(SP-0023) and DAB(C-0010) staining
Tissue/cell: Transplanted tumor in mice; 4% Paraformaldehyde-fixed and paraffin-embedded;
Antigen retrieval: citrate buffer ( 0.01M, pH 6.0 ), Boiling bathing for 15min; Block endogenous peroxidase by 3% Hydrogen peroxide for 30min; Blocking buffer (normal goat serum,C-0005) at 37℃ for 20 min;
Incubation: Anti-phospho-AKT/PKB(Ser473) Polyclonal Antibody, Unconjugated(bs-0876R) 1:600, overnight at 4°C, followed by conjugation to the secondary antibody(SP-0023) and DAB(C-0010) staining
Tissue/cell: Transplanted tumor in mice; 4% Paraformaldehyde-fixed and paraffin-embedded;
Antigen retrieval: citrate buffer ( 0.01M, pH 6.0 ), Boiling bathing for 15min; Block endogenous peroxidase by 3% Hydrogen peroxide for 30min; Blocking buffer (normal goat serum,C-0005) at 37℃ for 20 min;
Incubation: Anti-phospho-AKT/PKB(Ser473) Polyclonal Antibody, Unconjugated(bs-0876R) 1:600, overnight at 4°C, followed by conjugation to the secondary antibody(SP-0023) and DAB(C-0010) staining
Blank control:A549.
Primary Antibody (green line): Rabbit Anti-phospho-AKT (Ser473) antibody (bs-0876R)
Dilution: 2μg /10^6 cells;
Isotype Control Antibody (orange line): Rabbit IgG .
Secondary Antibody : Goat anti-rabbit IgG-FITC
Dilution: 1μg /test.
Protocol
The cells were incubated in 5%BSA to block non-specific protein-protein interactions for 30 min at room temperature .Cells stained with Primary Antibody for 30 min at room temperature. The secondary antibody used for 40 min at room temperature. Acquisition of 20,000 events was performed.
Blank control:A549.
Primary Antibody (green line): Rabbit Anti-phospho-AKT (Ser473) antibody (bs-0876R)
Dilution: 2μg /10^6 cells;
Isotype Control Antibody (orange line): Rabbit IgG .
Secondary Antibody : Goat anti-rabbit IgG-FITC
Dilution: 1μg /test.
Protocol
The cells were incubated in 5%BSA to block non-specific protein-protein interactions for 30 min at room temperature .Cells stained with Primary Antibody for 30 min at room temperature. The secondary antibody used for 40 min at room temperature. Acquisition of 20,000 events was performed.
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