| 产品详情 |
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| Antigenic Specificity | V-Akt Murine Thymoma Viral Oncogene Homolog 1 (AKT1) (pan) |
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| Clone | 2A4-D4-D11 |
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| Host Species | Mouse |
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| Reactive Species | human |
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| Isotype | IgG2b |
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| Format | affinity purified |
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| Size | 100 µL |
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| Concentration | n/a |
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| Applications | Western Blotting (WB) |
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| Reviews / Ratings | If you have used this antibody, please help fellow researchers by submitting reviews to pAbmAbs and antYbuddY. |
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| Description | Akt1 is involved in cellular survival pathways,by inhibiting apoptotic processes. Akt1 is also able to induce protein synthesis pathways,and is therefore a key signaling protein in the cellular pathways that lead to skeletal muscle hypertrophy, and general tissue growth. Since it can block apoptosis,and thereby promote cell survival,Akt1 has been implicated as a major factor in many types of cancer. Akt(now also called Akt1)was originally identified as the oncogene in the transforming retrovirus,AKT8. Akt2 is an important signaling molecule in the Insulin signaling pathway. It is required to induce glucose transport. In a mouse which is null for Akt1 but normal for Akt2,glucose homeostasis is unperturbed,but the animals are smaller,consistent with a role for Akt1 in growth. In contrast,mice which do not have Akt2,but have normal Akt1,have mild growth deficiency and display a diabetic phenotype(insulin resistance),again consistent with the idea that Akt2 is more specific for the insulin receptor signaling pathway. The role of Akt3 is less clear,though it appears to be predominantly expressed in the brain. It has been reported that mice lacking Akt3 have small brains. 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 PI3P-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 (PI3K) 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. Subunit structure: AKT1 interacts (via the C-terminus) with CCDC88A (via its C-terminus). Interacts with GRB10, the interaction leads to GRB10 phosphorylation thus promoting YWHAE-binding By similarity. 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. AKT2 interacts (via PH domain) with MTCP1, TCL1A AND TCL1B. Interacts with CLK2, PBH2 and TRAF6. AKT3 interacts (via PH domain) with TCL1A, this enhances AKT3 phosphorylation and activation. Interacts with TRAF6. Subcellular location: Cytoplasm. Nucleus. Cell membrane. Sequence similarities: 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. |
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| Immunogen | Purified recombinant human AKT1 protein fragments expressed in E.coli. |
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| Other Names | AKT|AKT1|pkb|xAct|v-akt|v-akt1|akt-1|AKT/PKB|Akt|Akt/PKB|Akt1|PKB|CG4006|D-Akt|DAKT1|DAKT1/PKB|DAkt|DAkt1|DPKB|DRAC-PK|DRAC-PK66|DRAC-PK85|Dakt|Dakt1|Dmel\\CG4006|Dpkb|PKB/AKT|PKB/Akt|PKB/dAKT|RAC|RacPK|akt|akt1|dAKT|dAKT/dPKB|dAKT1|dAkt|dAkt/PKB|dAkt1|dPKB|dakt|dakt1|l(3)04226|l(3)89Bq|p-Akt|pAkt|ATAKT1|F18A8.2|F18A8_2|K+ transporter 1|POTASSIUM TRANSPORTER|Rac|PKBalpha|CWS6|PKB-ALPHA|PRKBA|RAC-ALPHA |
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| Gene, Accession # | Gene ID: 207 |
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| Catalog # | ABIN1558165 |
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| Price | |
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| Order / More Info | V-Akt Murine Thymoma Viral Oncogene Homolog 1 (AKT1) (pan) Antibody from ANTIBODIES-ONLINE GmbH |
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| Product Specific References | n/a |
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