AKT3 Antibody (YA4580)(PBS only)
(Synonyms: CDHN; NCAD; CD325; CDw325)AKT3 Antibody (YA4580) is a Mouse-derived and non-conjugated IgG2a monoclonal antibody, targeting to AKT3.
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Host:
Mouse
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Isotype:
IgG
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Application:
ICC/IF, FC, ELISA
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Reactivity :
Human
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Formulation:
Supplied in PBS, pH 7.4.
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Conjugation:
Non-conjugated
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
Applications
| Application |
ICC/IF
ICC/IF: Immunocytochemistry/
Immunofluorescence |
FC
FC: Flow Cytometry
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ELISA
ELISA: Enzyme Linked Immunosorbent Assay
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|---|---|---|---|
| Dilution Ratio | 1:50-1:250 | 1:200-1:400 | 1:10000 |
Product Details
AKT3 Antibody (YA4580) is a Mouse-derived and non-conjugated IgG2a monoclonal antibody, targeting to AKT3.
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Host Mouse
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Species ReactivityHuman
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Observed Molecular WeightObserved band size: 56 kDa
Note: 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
Purified recombinant fragment of human AKT3 (AA: 37-150) expressed in E. Coli.
affinity purified.
Non-conjugated
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in PBS, pH 7.4.
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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.
Background
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Function
AKT serine/threonine kinase 3 (AKT3) is a PI3K-AKT pathway effector that regulates cellular growth, survival, and neurodevelopment, with particularly high expression in the central nervous system[1][2]. Mechanistically, AKT3 contributes to mTOR signaling and postnatal brain growth by controlling both cell size and cell number, and Akt3-deficient mice display selective reductions in brain volume without major disturbances in glucose homeostasis[1][3]. In disease models, somatic activating mutations and copy-number alterations of AKT3 are associated with megalencephaly-spectrum neurodevelopmental disorders and hemispheric brain overgrowth, supporting a central role for AKT3 during cortical development and neural progenitor regulation[4]. Compared with related isoforms, AKT1 primarily regulates organismal growth, whereas AKT2 is closely linked to insulin-responsive metabolic tissues; in contrast, AKT3 shows brain-enriched expression and mediates isoform-specific control of neural growth and signaling outputs[1][2][3]. Beyond developmental biology, genomically amplified AKT3 promotes glioma progression and activates DNA repair programs, identifying AKT3 as a functionally dominant AKT isoform in specific brain tumor contexts[5]. For experimental applications, recent medicinal chemistry efforts have produced isoform-selective AKT3 degraders that induce proteasomal degradation of AKT3 and suppress growth of resistant cancer models, providing tools for dissecting AKT3-specific signaling and therapeutic vulnerabilities[6].
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Subcellular Localization
Nucleus; Cytoplasm; Membrane; Peripheral membrane protein
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Expression
Tissue_specificity:In human tissues, this gene is highly expressed in the brain, lungs, and kidneys, but lowly expressed in the heart, testes, and liver. In fetal tissues, this gene is highly expressed in the heart, liver, and brain, but not in the kidneys. -
Isoforms & Post-Translational Modification
Q9Y243 has 2 isomers: Q9Y243-1: 55775 Da (predicted); Q9Y243-2: 54032 Da (predicted).
Phosphorylation on Thr-305 and Ser-472 is required for full activity (PubMed:12162751, PubMed:9512493). Phosphorylation of the activation loop at Thr-305 by PDPK1/PDK1 is a prerequisite for full activation (PubMed:9512493). Phosphorylation at Ser-472 by mTORC2 in response to growth factors plays a key role in AKT1 activation by facilitating subsequent phosphorylation of the activation loop by PDPK1/PDK1 (By similarity);Ubiquitinated. When fully phosphorylated and translocated into the nucleus, undergoes 'Lys-48'-polyubiquitination catalyzed by TTC3, leading to its degradation by the proteasome;O-GlcNAcylation at Thr-302 and Thr-309 inhibits activating phosphorylation at Thr-305 via disrupting the interaction between AKT and PDPK1/PDK1 -
Subunit
Interacts (via PH domain) with TCL1A; this enhances AKT3 phosphorylation and activation. Interacts with TRAF6.
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SwissProt ID
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Synonyms
CDHN; NCAD; CD325; CDw325
Documentation
References
[1]. Easton RM, et al. Role for Akt3/protein kinase Bgamma in attainment of normal brain size. Mol Cell Biol. 2005 Mar;25(5):1869-78. [Content Brief]
[2]. Khalili M, et al. Underserved Does Not Mean Undeserved: Unfurling the HCV Care in the Safety Net. Dig Dis Sci. 2018 Dec;63(12):3250-3252. [Content Brief]
[3]. Tschopp O, et al. Essential role of protein kinase B gamma (PKB gamma/Akt3) in postnatal brain development but not in glucose homeostasis. Development. 2005 Jul;132(13):2943-54. [Content Brief]
[4]. Poduri A, et al. Somatic activation of AKT3 causes hemispheric developmental brain malformations. Neuron. 2012 Apr 12;74(1):41-8. [Content Brief]
[5]. Turner KM, et al. Genomically amplified Akt3 activates DNA repair pathway and promotes glioma progression. Proc Natl Acad Sci U S A. 2015 Mar 17;112(11):3421-6. [Content Brief]
[6]. Xu F, et al. Discovery of Isoform-Selective Akt3 Degraders Overcoming Osimertinib-Induced Resistance in Non-Small Cell Lung Cancer Cells. J Med Chem. 2022 Oct 27;65(20):14032-14048. [Content Brief]
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