Anti-TBC1D4 monoclonal antibody (DCABH-849)

Mouse anti-Human TBC1D4 monoclonal antibody for WB, FC, ICC/IF Datasheet

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Specifications


Host Species
Mouse
Antibody Isotype
IgG2b
Clone
6F7
Species Reactivity
Human
Immunogen
Recombinant full length Human TBC1D4 protein produced in HEK293T cells (NP_055647.2).
Conjugate
Unconjugated

Applications


Application Notes
WB: 1/2000; Flow Cyt: 1/100; ICC/IF: 1/100;
*Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.

Target


Alternative Names
TBC1D4; TBC1 domain family, member 4; TBC1 domain family member 4; Akt substrate of 160 kDa; AS160; DKFZp779C0666
Entrez Gene ID
UniProt ID

Product Background


Gene summary
TBC1D4 (TBC1 Domain Family Member 4) is a Protein Coding gene. Diseases associated with TBC1D4 include diabetes mellitus, noninsulin-dependent, 5. Among its related pathways are Translation Insulin regulation of translation and Thyroid hormone signaling pathway. GO annotations related to this gene include GTPase activator activity. An important paralog of this gene is EVI5L. This gene is a member of the Tre-2/BUB2/CDC16 domain family. The protein encoded by this gene is a Rab-GTPase-activating protein, and contains two phopshotyrosine-binding domains (PTB1 and PTB2), a calmodulin-binding domain (CBD), a Rab-GTPase domain, and multiple AKT phosphomotifs. This protein is thought to play an important role in glucose homeostasis by regulating the insulin-dependent trafficking of the glucose transporter 4 (GLUT4), important for removing glucose from the bloodstream into skeletal muscle and fat tissues. Reduced expression of this gene results in an increase in GLUT4 levels at the plasma membrane, suggesting that this protein is important in intracellular retention of GLUT4 under basal conditions. When exposed to insulin, this protein is phosphorylated, dissociates from GLUT4 vesicles, resulting in increased GLUT4 at the cell surface, and enhanced glucose transport. Phosphorylation of this protein by AKT is required for proper translocation of GLUT4 to the cell surface. Individuals homozygous for a mutation in this gene are at higher risk for type 2 diabetes and have higher levels of circulating glucose and insulin levels after glucose ingestion. Alternative splicing results in multiple transcript variants encoding different isoforms.
Antigen Description
May 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. Diabetes mellitus, non-insulin-dependent, 5 (NIDDM5) [MIM:616087]: A multifactorial disorder of glucose homeostasis caused by a lack of sensitivity to the bodys own insulin. Affected individuals usually have an obese body habitus and manifestations of a metabolic syndrome characterized by diabetes, insulin resistance, hypertension and hypertriglyceridemia. The disease results in long-term complications that affect the eyes, kidneys, nerves, and blood vessels. Note=Disease susceptibility is associated with variations affecting the gene represented in this entry. AS160 (Akt substrate of 160 kDa), which was originally known as TBC1 domain family member 4 (TBC1D4), is a Rab GTPase-activating protein that in humans is encoded by the TBC1D4 gene. 0The function about TBC1D4 antigen include GTPase activator activity; Rab GTPase activator activity.
Pathway
Class I PI3K signaling events mediated by Akt, organism-specific biosystem; Insulin Signaling, organism-specific biosystem; Insulin-mediated glucose transport, organism-specific biosystem.

Citations


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References


Funai, K; Schweitzer, GG; et al. In vivo exercise followed by in vitro contraction additively elevates subsequent insulin-stimulated glucose transport by rat skeletal muscle. AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM 298:E999-E1010(2010).
Treebak, JT; Taylor, EB; et al. Identification of a novel phosphorylation site on TBC1D4 regulated by AMP-activated protein kinase in skeletal muscle. AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY 298:C377-C385(2010).

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