Anti-Phospho-Akt (Ser473) AKT1 Rabbit Monoclonal Antibody

Overview

Anti-Phospho-Akt (Ser473) AKT1 Rabbit Monoclonal Antibody is an antibody targeting AKT1. Common applications include WB, IHC, ICC, IF. Key specifications include host: Rabbit; clonality: Monoclonal; clone: Clone: IFD-1; isotype: Rabbit IgG; reactivity: Human,Mouse,Rat; observed MW: 65 kDa; calculated MW: 55686 MW.

Boster Bio Anti-Phospho-Akt (Ser473) AKT1 Rabbit Monoclonal Antibody catalog # P00024-5. Tested in WB, IHC, ICC/IF applications. This antibody reacts with Human, Mouse, Rat.

Key elements and design rationale

• Target: AKT1 — RAC-alpha serine/threonine-protein kinase
• Antibody format: Host: Rabbit; Clonality: Monoclonal; Clone: Clone: IFD-1; Isotype: Rabbit IgG
• Species reactivity: Human,Mouse,Rat
• Molecular weight guidance: Observed: 65 kDa; Calculated: 55686 MW
• Phospho site(s): Ser473

Biological background

Protein function (datasheet): 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. Phosphorylates KAT6A at 'Thr-369' and this phosphorylation inhibits the interaction of KAT6A with PML and negatively regulates its acetylation activity towards p53/TP53.

Cellular localization (datasheet): Cytoplasm. Nucleus. Cell membrane. 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 details (datasheet): 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. .

Research relevance and current trends

• Commonly studied in contexts related to Metabolism,Metabolism Processes,Nuclear,Pathways and Processes,Protein Phosphorylation,Ser/Thr Kinases,Serine/Threonine Kinases,Signal Transduction.
• Supports comparative expression analysis across conditions, genotypes, or treatments when paired with appropriate controls.
• Useful for confirming target presence and subcellular distribution using orthogonal readouts (e.g., microscopy vs. immunoblotting).

Common research applications

• Western blot (WB): Compare relative target abundance and apparent size/isoforms across samples; interpret bands in light of expected MW and potential PTMs.
• Immunohistochemistry (IHC): Assess tissue distribution and cell-type patterns; interpret staining with appropriate negative controls and antigen context.
• Immunofluorescence / ICC: Visualize subcellular localization and co-localization patterns; consider fixation/permeabilization compatibility and controls.

Notes for experimental interpretation

• Consider isoforms, post-translational modifications, and processing that can shift apparent molecular weight or localization.
• Use appropriate positive and negative controls (e.g., KO/KD, blocking peptide, or isotype controls) to support specificity interpretation.

As a monoclonal antibody, this reagent is expected to recognize a defined epitope, which can support consistency across lots when epitope accessibility is preserved.

Customization & Add-ons: Can’t find the antibody you need—or require a custom format for your assay? We can help you source the best match or support custom antibody solutions for diverse research needs, including species and isotype selection, conjugations and labeling (e.g., HRP/AP, biotin, fluorophores), purification grade options (Protein A/G, affinity purified), formulation preferences (buffer selection, carrier-free, glycerol-free), custom concentrations and aliquoting, low-endotoxin options for cell-based work, and application-focused QC/validation support (project dependent). Click Talk to a Scientist to submit a request, email us at support@biohippo.com, or explore our Research Services for additional support—our team will follow up with feasibility details and next steps.