AKT1 Antibody (YA834)
(Synonyms: KIAA0600, HDAC5, Histone deacetylase 5, HD5, Antigen NY-CO-9)Based on 1 publication(s) in Google Scholar
AKT1 Antibody (YA834) is a Mouse-derived and non-conjugated IgG2b monoclonal antibody, targeting to AKT1.
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Host:
Mouse
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Isotype:
IgG
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Application:
WB, IHC-P, ICC/IF
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Reactivity :
Human
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Formulation:
Supplied in 1*PBS (pH7.4), 0.2% BSA and 40% Glycerol. Preservative: 0.05% Sodium Azide.
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Conjugation:
Non-conjugated
Publications Citing Use of MedChemExpress (MCE) AKT1 Antibody (YA834)
More
Applications
| Application |
WB
WB: Western Blot
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IHC-P
IHC-P: Immunohistochemistry-Paraffin
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ICC/IF
ICC/IF: Immunocytochemistry/
Immunofluorescence |
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| Dilution Ratio | 1:2000 | 1:100-1:200 | 1:100-200 |
Product Details
AKT1 Antibody (YA834) is a Mouse-derived and non-conjugated IgG2b monoclonal antibody, targeting to AKT1.
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Host Mouse
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Clonality Monoclonal
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Species ReactivityHuman
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Observed Molecular WeightObserved band size: 56 kDaNote: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
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Calculated Molecular Weight Predicted band size: 56 kDa
Synthetic peptide corresponding to Human AKT1.AA range:1-80.
Endogenous
Protein A affinity purified.
Non-conjugated
Unmodified
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in 1*PBS (pH7.4), 0.2% BSA and 40% Glycerol. Preservative: 0.05% Sodium Azide.
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Concentration
Batch-dependent, Please check the COA for the concentration of each lot. Check Lot Concentration
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Publications (1)
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Journal Impact Factor
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Most Recent
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ACS Chem Biol
Targeted O-GlcNAcylation of CK2α Triggers Its Ubiquitin-Proteasome Degradation and Alters Downstream Phosphorylation. [Abstract]2025 Jul 18;20(7):1646-1659. PMID: 40521680
Verification Images
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Western blot analysis of extracts from Hela (lane2(20μg), A549(lane3(20μg), K562(lane4(20μg) and HepG2(lane5(20μg) using AKT1 Antibody (HY-P80007). Proteins were transferred to a PVDF membrane and blocked with 5% non-fat milk in TBST at 4°C overnight. The primary antibody (1/2000) and Loading control antibody (Beta Actin, HY-P80993, 1/10,000) was used in 5% non-fat milk in TBST for 2 hour at room temperature. Goat Anti-Mouse IgG-HRP Secondary Antibody (HY-P8004, 1/10,000) was used for 1 hour at room temperature.
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Immunocytochemistry analysis of Hela cells labeling AKT1 with Cleaved AKT1 Antibody (HY-P80007) at 1/50 dilution. Cells were fixed in 4% paraformaldehyde for 15 minutes at room temperature, permeabilized with 0.1% Triton X-100 for 10 minutes at room temperature, then blocked with QuickBlock™ Blocking Buffer for Immunol Staining for 10 min at room temperature. Cells were then incubated with AKT1 Antibody (HY-P80007) at 1/50 dilution in QuickBlock™ Blocking Buffer for Immunol Staining at 4 ℃. Alexa Fluor® 488-conjugated AffiniPure Goat Anti-Mouse IgG H&L(HY-P8005, Green) was used as the secondary antibody at 1/1,000 dilution. PBS instead of the primary antibody was used as the secondary antibody only control. The Nuclear counterstain was DAPI (Blue).
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Immunocytochemistry analysis of Hela cells labeling AKT1 with AKT1 Antibody (HY-P80007) at 1/100 dilution. Cells were fixed in 4% paraformaldehyde for 15 minutes at room temperature, permeabilized with 0.1% Triton X-100 for 10 minutes at room temperature, then blocked with QuickBlock™ Blocking Buffer for Immunol Staining for 10 min at room temperature. Cells were then incubated with AKT1 Antibody (HY-P80007)at 1/100 dilution in QuickBlock™ Blocking Buffer for Immunol Staining at 4 ℃. Alexa Fluor® 488-conjugated AffiniPure Goat Anti-Mouse IgG H&L(HY-P8005, Green) was used as the secondary antibody at 1/1,000 dilution. PBS instead of the primary antibody was used as the secondary antibody only control. The Nuclear counterstain was DAPI (Blue).
Background
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Function
AKT1 (protein kinase Bα, PKBα) is a serine/threonine kinase that functions as a central effector of the PI3K/AKT/mTOR signaling pathway, regulating cellular growth, survival, metabolism, proliferation, and differentiation across multiple tissues and cell types[1][2][3]. Activation of AKT1 occurs downstream of PI3K through phosphoinositide-dependent kinase-1 (PDK1) -mediated phosphorylation, enabling downstream regulation of targets involved in protein synthesis, apoptosis control, and metabolic adaptation[4][5]. Mechanistically, AKT1 contributes to angiogenesis, physiological tissue growth, immune-cell function, and stress-response signaling, making it a critical node in both normal physiology and disease-associated signaling networks[2][4][5]. In disease models, dysregulated AKT signaling is strongly associated with cancer, metabolic disorders, cardiovascular pathology, and inflammatory conditions, and constitutive activation of AKT-dependent pathways promotes oncogenic progression and therapeutic resistance[2][6][7]. Compared with related isoforms, AKT1 exhibits distinct biological functions despite substantial structural homology with AKT2 and AKT3; genetic studies demonstrate that AKT1 deficiency primarily causes growth retardation, whereas AKT2 deficiency induces insulin resistance and diabetes, and AKT3 loss predominantly affects brain development[4][5]. Isoform-specific investigations further show that AKT1 and AKT2 can exert non-redundant or even opposing effects on migration, invasion, inflammation, and fibrogenesis depending on cellular context[2][6][8]. For experimental applications, increasing efforts focus on developing AKT1-selective inhibitors and isoform-selective cellular models, which provide valuable tools for dissecting AKT isoform-specific signaling and for evaluating targeted therapeutic strategies with improved selectivity profiles[6][7][9].
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Subcellular Localization
Cytoplasm; Nucleus; Cell membrane; Mitochondrion intermembrane space
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Expression
Tissue_specificity:This protein is expressed in prostate cancer, and its expression level gradually increases from normal to malignant (protein level) . It is expressed in all human cell types analyzed to date. The phosphorylated form of Tyr-176 is significantly increased in the progressive stages of breast cancer (i.e., from normal to hyperplastic (ADH) , ductal carcinoma in situ (DCIS) , invasive ductal carcinoma (IDC) , and lymph node metastasis (LNMM) stages) . -
Isoforms & Post-Translational Modification
P31749 has 2 isomers: P31749-1: 55686 Da (predicted); P31749-2: 48347 Da (predicted).
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 (PubMed:12149249, PubMed:15047712, PubMed:15262962, PubMed:16266983, PubMed:18456494, PubMed:20481595, PubMed:20978158, PubMed:8978681, PubMed:9512493, PubMed:9736715). Phosphorylation of the activation loop at Thr-308 by PDPK1/PDK1 is a prerequisite for full activation (PubMed:9512493). Phosphorylation by mTORC2 in response to growth factors plays a key role in AKT1 activation: mTORC2 phosphorylates different sites depending on the context, such as Thr-450, Ser-473, Ser-477 or Thr-479, thereby facilitating subsequent phosphorylation of the activation loop by PDPK1/PDK1 (PubMed:15718470, PubMed:24670654). Phosphorylation at Ser-473 by mTORC2 promotes ubiquitination and degradation by the proteasome (By similarity). Also phosphorylated at Ser-477 and Thr-479 by CDK2, facilitating subsequent phosphorylation of the activation loop by PDPK1/PDK1 (PubMed:24670654). Activated TNK2 phosphorylates it on Tyr-176 resulting in its binding to the anionic plasma membrane phospholipid PA (PubMed:20333297). 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 (PubMed:20333297). Phosphorylated at Thr-308 and Ser-473 by IKBKE and TBK1 (PubMed:21464307). Ser-473 phosphorylation is enhanced by interaction with AGAP2 isoform 2 (PIKE-A) (PubMed:14761976). Ser-473 phosphorylation is enhanced in focal cortical dysplasias with Taylor-type balloon cells (PubMed:17013611). Ser-473 phosphorylation is enhanced by signaling through activated FLT3 (PubMed:16266983). Ser-473 is dephosphorylated by PHLPP (PubMed:28147277). Dephosphorylated at Thr-308 and Ser-473 by PP2A phosphatase (PubMed:21329884). The phosphorylated form of PPP2R5B is required for bridging AKT1 with PP2A phosphatase (PubMed:21329884). Ser-473 is dephosphorylated by CPPED1, leading to termination of signaling (PubMed:23799035). AIM2 acts as an inhibitor of AKT1 by inhibiting phosphorylation Ser-473: AIM2 acts both by inhibiting the activity of PRKDC/DNA-PK kinase and promoting dephosphorylation by PP2A phosphatase (By similarity);Ubiquitinated; undergoes both 'Lys-48'- and 'Lys-63'-linked polyubiquitination. TRAF6-induced 'Lys-63'-linked AKT1 ubiquitination is critical for phosphorylation and activation (PubMed:19713527). When ubiquitinated, it translocates to the plasma membrane, where it becomes phosphorylated (PubMed:20059950). When fully phosphorylated and translocated into the nucleus, undergoes 'Lys-48'-polyubiquitination catalyzed by TTC3, leading to its degradation by the proteasome (PubMed:20059950). Also ubiquitinated by TRIM13 leading to its proteasomal degradation (PubMed:21333377). Phosphorylated, undergoes 'Lys-48'-linked polyubiquitination preferentially at Lys-284 catalyzed by MUL1, leading to its proteasomal degradation (PubMed:22410793). Ubiquitinated via 'Lys-48'-linked polyubiquitination by ZNRF1, leading to its degradation by the proteasome (By similarity);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;Cleavage by caspase-3/CASP3 (By similarity). Cleaved at the caspase-3 consensus site Asp-462 during apoptosis, resulting in down-regulation of the AKT signaling pathway and decreased cell survival (PubMed:23152800) -
Subunit
Interacts with BTBD10 (By similarity). Interacts with KCTD20 (By similarity). 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. Interacts with PA2G4 (By similarity). Interacts with KIF14; the interaction is detected in the plasma membrane upon INS stimulation and promotes AKT1 phosphorylation (PubMed:24784001). Interacts with FAM83B; activates the PI3K/AKT signaling cascade (PubMed:23676467). Interacts with WDFY2 (via WD repeats 1-3) (PubMed:16792529). Forms a complex with WDFY2 and FOXO1 (By similarity). Interacts with FAM168A (PubMed:23251525). Interacts with SYAP1 (via phosphorylated form and BSD domain); this interaction is enhanced in a mTORC2-mediated manner in response to epidermal growth factor (EGF) stimulation and activates AKT1 (PubMed:23300339). Interacts with PKHM3 (By similarity). Interacts with FKBP5/FKBP51; promoting interaction between Akt/AKT1 and PHLPP1, thereby enhancing dephosphorylation and subsequent activation of Akt/AKT1 (PubMed:28147277). Interacts with TMEM175; leading to formation of the lysoK(GF) complex (PubMed:32228865). Acts as a negative regulator of the cGAS-STING pathway by mediating phosphorylation of CGAS during mitosis, leading to its inhibition (PubMed:26440888)
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SwissProt ID
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Synonyms
KIAA0600, HDAC5, Histone deacetylase 5, HD5, Antigen NY-CO-9
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Research Field
Signal Transduction
Documentation
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Data Sheet (263 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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User Guide for Antibodies (1077 KB)
[1]. Guerau-de-Arellano M, et al. Akt isoforms in the immune system. Front Immunol. 2022 Aug 23;13:990874. [Content Brief]
[2]. Reyes-Gordillo K, et al. Akt1 and Akt2 Isoforms Play Distinct Roles in Regulating the Development of Inflammation and Fibrosis Associated with Alcoholic Liver Disease. Cells. 2019 Oct 29;8(11):1337. [Content Brief]
[3]. O'Neill BT, et al. Akt1 in the cardiovascular system: friend or foe? J Clin Invest. 2005 Aug;115(8):2059-64. [Content Brief]
[4]. Tellai AD, et al. The complex post-transcriptional regulation of genes coding for methionine adenosyl transferase: New insights for liver cancer. Biochimie. 2025 Nov;238(Pt A):19-28. [Content Brief]
[5]. Quambusch L, et al. Cellular model system to dissect the isoform-selectivity of Akt inhibitors. Nat Commun. 2021 Sep 6;12(1):5297. [Content Brief]