• Contact info@abtriva.com for inquiries and orders.
  • Chinese (Simplified)

  • English

  • German

  • Korean

  • Spanish

United States (English / $ USD)

Rabbit anti-Human AKT3 Polyclonal Antibody

The antibody against AKT3 was raised in rabbit using the Synthetic peptide of Human AKT3 as the immunogen. This antibody exists as a non-conjugated isotype IgG, Antigen affinity purified. This antibody has been validated on ELISA, IHC.

ADC-27301A

The antibody against AKT3 was raised in rabbit using the Synthetic peptide of Human AKT3 as the immunogen. This antibody exists as a non-conjugated isotype IgG, Antigen affinity purified. This antibody has been validated on ELISA, IHC.

$299.00

Number
Order Exclusive Products Now

Request a Quote
High Purity LevelsPrecision and ReliabilityCustomization Options

Specifications


Cat.No ADC-27301A ClonalityPolyclonal
Host SpeciesRabbitTarget NameAKT3
FormLiquidSpecies ReactivityHuman, Mouse, Rat
IsotypeIgGStorage Buffer0.05% NaN3, 40% Glycerol., pH7.4 PBS
Purification MethodAntigen affinity purifiedConjugateNon-conjugated
ApplicationELISA, IHCStorageUpon receipt

Immunogen Information


Immunogen DescriptionSynthetic peptide of Human AKT3Target SpeciesHuman
Immunogen SequenceComplete sequences for the immunogen, target protein, and peptides are available upon request.Uniprot IDQ9Y243
Background Information
  • Uniprot Id

    Q9Y243

  • Target Species

    Human

  • Target Name

    AKT3

  • Target Full Name

    RAC-gamma serine/threonine-protein kinase

  • Target Function

    AKT3 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. AKT3 is the least studied AKT isoform. It plays an important role in brain development and is crucial for the viability of malignant glioma cells. AKT3 isoform may also be the key molecule in up-regulation and down-regulation of MMP13 via IL13. Required for the coordination of mitochondrial biogenesis with growth factor-induced increases in cellular energy demands. Down-regulation by RNA interference reduces the expression of the phosphorylated form of BAD, resulting in the induction of caspase-dependent apoptosis.

  • Target Involvement

    Megalencephaly-polymicrogyria-polydactyly-hydrocephalus syndrome 2 (MPPH2)

  • Target Subcellular Location

    Nucleus. Cytoplasm. Membrane; Peripheral membrane protein. Note=Membrane-associated after cell stimulation leading to its translocation.

  • Target Protein Families

    Protein kinase superfamily, AGC Ser/Thr protein kinase family, RAC subfamily

  • Target Tissue Specificity

    In adult tissues, it is highly expressed in brain, lung and kidney, but weakly in heart, testis and liver. In fetal tissues, it is highly expressed in heart, liver and brain and not at all in kidney.

  • Target Synonyms

    MPPH; PKBG; MPPH2; PRKBG; STK-2; PKB-GAMMA; RAC-gamma; RAC-PK-gamma; AKT3

  • Target Background

    The protein encoded by this gene is a member of the AKT, also called PKB, serine/threonine protein kinase family. AKT kinases are known to be regulators of cell signaling in response to insulin and growth factors. They are involved in a wide variety of biological processes including cell proliferation, differentiation, apoptosis, tumorigenesis, as well as glycogen synthesis and glucose uptake. This kinase has been shown to be stimulated by platelet-derived growth factor (PDGF), insulin, and insulin-like growth factor 1 (IGF1). Alternatively splice transcript variants encoding distinct isoforms have been described.

Inquire Rabbit anti-Human AKT3 Polyclonal Antibody Now



AbTriva respects your privacy and protects your personal data in accordance with AbTriva. For more information, please see our data protection statement. *

Notification