TBC1D4 Antibody

Product Specifications

Background

TBC1D4 Antibody: TBC1D4, also known as the Akt substrate AS160, was initially identified as an Akt substrate containing a GTPase-activating domain that regulates GLUT4 trafficking, with activation following insulin stimulation. TBC1D4 truncations in humans is a major cause of dominant inherited insulin resistance. The loss of TBC1D4 results in the accumulation of GLUT4 in compartments that are primed for fusion in basal adipocytes.

NCBI Gene ID

9882

Swiss Prot

O60343

Accession Number

NP_055647

Host

Rabbit

Reactivity

Human

Clonality

Polyclonal

Conjugation

Unconjugated

Type

Primary Antibodies

Field of Research

Homeostasis

Purification

TBC1D4 Antibody is affinity chromatography purified via peptide column.

Positive Control

Cat. No. 10-635 - Human Prostate Tissue Slide

Concentration

1 mg/mL

Homology

Predicted species reactivity based on immunogen sequence: Mouse: (89%)

Buffer

TBC1D4 Antibody is supplied in PBS containing 0.02% sodium azide.

Modification

None

Shipping Conditions

Blue Ice

Storage Conditions

TBC1D4 antibody can be stored at 4˚ C for three months and -20˚ C, stable for up to one year.

Fragment

IgG

Symbol

TBC1D4

NCBI Official Name

TBC1 domain family, member 4

NCBI Organism

Homo sapiens

Background Reference 01

Kane S, Sano H, Liu SCH, et al. Akt phosphorylates a novel adipocyte protein with a Rab GTPase-activating protein (GAP) domain. J. Biol. Chem. 2002; 277:22115-8.

Background Reference 02

Sano H, Kane S, Sano E, et al. Insulin-stimulated phosphorylation of a Rab GTPase-activating protein regulates GLUT4 translocation. J. Biol. Chem. 2003; 278:14599-602.

Background Reference 03

Dash S, Sano H, Rochford JJ, et al. A truncation mutation in TBC1D4 in a family with acanthosis nigricans and postprandial hyperinsulinemia. Proc. Natl. Acad. Sci. U.S.A. 2009; 106:9350–5.

Background Reference 04

Brewer PD, Romenskaia I, Kanow MA, et al. Loss of AS160 Akt substrate causes Glut4 protein to accumulate in compartments that are primed for fusion in basal adipocytes. J. Biol. Chem. 2011; 286:26287-97.