Anti-TBC1D4 (phospho T642) antibody (ab59173)


  • Product nameAnti-TBC1D4 (phospho T642) antibody
    See all TBC1D4 primary antibodies
  • Description
    Rabbit polyclonal to TBC1D4 (phospho T642)
  • SpecificityDetects endogenous levels of TBC1D4 only when phosphorylated ar theonine 642. Recognises phosphorylation at threonine 642 in human and threonine 649 in mouse.
  • Tested applicationsSuitable for: IHC-P, ELISAmore details
  • Species reactivity
    Reacts with: Human
    Predicted to work with: Mouse
  • Immunogen

    Synthetic phosphopeptide (Human) from around the phosphorylation site of threonine 642 (AHTPFS)

  • Positive control
    • Human lung carcinoma tissue


  • FormLiquid
  • Storage instructionsShipped at 4°C. Store at -20°C. Stable for 12 months at -20°C.
  • Storage bufferPreservative: 0.02% Sodium Azide
    Constituents: 50% Glycerol, PBS (without Mg2+ and Ca2+), 150mM Sodium chloride, pH 7.4
  • Concentration information loading...
  • PurityImmunogen affinity purified
  • Purification notesAffinity purified from rabbit antiserum by affinity chromatography using epitope specific phosphopeptide. The antibody against non phosphopeptide was removed by chromatography using non phosphopeptide corresponding to the phosphorylation site
  • ClonalityPolyclonal
  • IsotypeIgG
  • Research areas


Our Abpromise guarantee covers the use of ab59173 in the following tested applications.

The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.

Application Abreviews Notes
IHC-P Use at an assay dependent concentration.
ELISA 1/5000.


  • FunctionMay act as a GTPase-activating protein for RAB2A, RAB8A, RAB10 and RAB14. Isoform 2 promotes insulin-induced glucose transporter SLC2A4/GLUT4 translocation at the plasma membrane, thus increasing glucose uptake.
  • Tissue specificityWidely expressed. Isoform 2 is the highest overexpressed in most tissues. Isoform 1 is highly expressed in skeletal muscle and heart, but was not detectable in the liver nor in adipose tissue. Isoform 2 is strongly expressed in adrenal and thyroid gland, and also in lung, kidney, colon, brain and adipose tissue. Isoform 2 is moderately expressed in skeletal muscle. Expressed in pancreatic Langerhans islets, including beta cells (at protein level). Expression is decreased by twofold in pancreatic islets in type 2 diabetes patients compared to control subjects. Up-regulated in T cells from patients with atopic dermatitis.
  • Sequence similaritiesContains 2 PID domains.
    Contains 1 Rab-GAP TBC domain.
  • Post-translational
    Phosphorylated by AKT1; insulin-induced.
    Insulin-stimulated phosphorylation is required for SLC2A4/GLUT4 translocation.
    Physiological hyperinsulinemia increases phosphorylation in skeletal muscle. Insulin-stimulated phosphorylation is reduced by 39% in type 2 diabetic patients.
  • Cellular localizationCytoplasm. Isoform 2 shows a cytoplasmic perinuclear localization in a myoblastic cell line in resting and insulin-stimulated cells.
  • Information by UniProt
  • Database links
  • Alternative names
    • Acrg embryonic lethality (mouse) minimal region ortholog antibody
    • Acrg embryonic lethality minimal region ortholog antibody
    • Acrg embryonic lethality mouse minimal region ortholog antibody
    • Akt substrate of 160 kDa antibody
    • AS 160 antibody
    • AS160 antibody
    • BUB2 antibody
    • CDC16 antibody
    • KIAA0603 antibody
    • TBC (Tre 2 BUB2 CDC16) domain containing protein antibody
    • TBC Tre 2 BUB2 CDC16 domain containing protein antibody
    • TBC1 D4 antibody
    • TBC1 domain family member 4 antibody
    • Tbc1d4 antibody
    • TBCD4_HUMAN antibody
    • Tre-2 antibody
    see all

Anti-TBC1D4 (phospho T642) antibody images

  • Immunohistochemical analysis of paraffin embedded human lung carcinoma tissue labelled with ab59173 at 1/50-1/100 dilution. Samples were treated with(+) or without(-) peptide.

References for Anti-TBC1D4 (phospho T642) antibody (ab59173)

ab59173 has not yet been referenced specifically in any publications.

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