Recombinant Human TBC1D1 protein (denatured) (His tag N-Terminus)
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Recombinant Human TBC1D1 protein (denatured) (His tag N-Terminus) is a Human Full Length protein, in the 1 to 265 aa range, expressed in Escherichia coli, with >90%, suitable for SDS-PAGE.
View Alternative Names
KIAA1108, TBC1D1, TBC1 domain family member 1
- SDS-PAGE
Supplier Data
SDS-PAGE - Recombinant Human TBC1D1 protein (denatured) (His tag N-Terminus) (AB176041)
15% SDS-PAGE analysis of ab176041 (3μg).
Reactivity data
Sequence info
Properties and storage information
Shipped at conditions
Appropriate short-term storage duration
Appropriate short-term storage conditions
Appropriate long-term storage conditions
Aliquoting information
Storage information
Supplementary information
This supplementary information is collated from multiple sources and compiled automatically.
Biological function summary
TBC1D1 participates in the regulation of insulin-stimulated glucose uptake. It is not part of a multi-protein complex but it interacts with other proteins to execute its functions. TBC1D1 has a significant role in metabolic processes influencing how cells respond to insulin. By acting on GLUT4 TBC1D1 facilitates glucose entry into cells which is an important step in maintaining glucose levels in the blood.
Pathways
TBC1D1 is critical in the insulin signaling and AMP-activated protein kinase (AMPK) pathways. It interacts with proteins such as Akt and AS160 which are important in mediating the effects of insulin. In the insulin signaling pathway TBC1D1 regulates GLUT4 translocation while in the AMPK pathway it contributes to energy balance and metabolism. These pathways highlight the role of TBC1D1 in maintaining cellular energy efficiency and glucose homeostasis.
Specifications
Form
Liquid
General info
Function
May act as a GTPase-activating protein for Rab family protein(s). May play a role in the cell cycle and differentiation of various tissues. Involved in the trafficking and translocation of GLUT4-containing vesicles and insulin-stimulated glucose uptake into cells (By similarity).
Post-translational modifications
Insulin-stimulated phosphorylation by AKT family kinases stimulates SLC2A4/GLUT4 translocation.
Subcellular localisation
Nucleus
Target data
Complementary Products
Product promise
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