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May act as a GTPase-activating protein for RAB2A, RAB8A, RAB10 and RAB14. Additionally we are shipping TBC1D4 Proteins (3) and many more products for this protein.
Showing 10 out of 101 products:
Human Polyclonal TBC1D4 Primary Antibody for IHC (p), IHC - ABIN188734
Stöckli, Davey, Hohnen-Behrens, Xu, James, Ramm: Regulation of glucose transporter 4 translocation by the Rab guanosine triphosphatase-activating protein AS160/TBC1D4: role of phosphorylation and membrane association. in Molecular endocrinology (Baltimore, Md.) 2008
Show all 2 references for 188734
Human Polyclonal TBC1D4 Primary Antibody for EIA, WB - ABIN453848
Lee, Obata, Yoshida, Stockert, Williamson, Jungbluth, Chen, Old, Scanlan: Immunomic analysis of human sarcoma. in Proceedings of the National Academy of Sciences of the United States of America 2003
Show all 2 references for 453848
Human Polyclonal TBC1D4 Primary Antibody for IHC, ELISA - ABIN190878
Karlsson, Zierath, Kane, Krook, Lienhard, Wallberg-Henriksson: Insulin-stimulated phosphorylation of the Akt substrate AS160 is impaired in skeletal muscle of type 2 diabetic subjects. in Diabetes 2005
Human Polyclonal TBC1D4 Primary Antibody for IF, ELISA - ABIN1532319
Dunham, Matthews, Burton, Ashurst, Howe, Ashcroft, Beare, Burford, Hunt, Griffiths-Jones, Jones, Keenan, Oliver, Scott, Ainscough, Almeida, Ambrose, Andrews, Ashwell, Babbage, Bagguley, Bailey et al.: The DNA sequence and analysis of human chromosome 13. ... in Nature 2004
AS160 regulates glucose-independent eukaryotic cell proliferation through p21 (show CDKN1A Antibodies)-dependent control of the cell cycle.
AS160 and TBC1D1 (show TBC1D1 Antibodies) phosphorylations were evident 30 min after exercise.
homozygous carriers of a nonsense p.Arg684Ter variant have markedly higher concentrations of plasma glucose and serum insulin 2 hours after an oral glucose load compared with individuals with other genotypes
Findings suggest that a dampening of insulin (show INS Antibodies)-induced phosphorylation of AS160 on specific sites in skeletal muscle contributes to the insulin (show INS Antibodies) resistance evident in a sedentary aging population
insulin (show INS Antibodies) resistance in muscles from healthy individuals is associated with suppression of site-specific phosphorylation of AS160
AS160 interacts with the large cytoplasmic NP domain of the alpha-subunit (show POLG Antibodies) of the Na(+),K(+)-ATPase (show ATP1A1 Antibodies). AMP (show APRT Antibodies)-stimulated protein kinase (show CDK7 Antibodies) (AMPK (show PRKAA1 Antibodies)) and AS160 participate in a common pathway to modulate the cell surface expression of the Na(+),K(+)-ATPase (show ATP1A1 Antibodies).
Crystal structures of human TBC1D1 (show TBC1D1 Antibodies) and TBC1D4 (AS160) RabGTPase-activating protein (RabGAP) domains reveal critical elements for GLUT4 (show SLC2A4 Antibodies) translocation.
AS160 phosphotyrosine-binding domain constructs inhibit insulin (show INS Antibodies)-stimulated GLUT4 (show SLC2A4 Antibodies) vesicle fusion with the plasma membrane
Impaired insulin (show INS Antibodies)-induced site-specific TBC1D4 phosphorylation may contribute to skeletal muscle insulin (show INS Antibodies) resistance in type 2 diabetes.
results show AS160 phosphorylation level is frequently increased in breast cancer; results implicate a possible role of AS160 in breast tumorigenesis and suggest that p-AS160 might be useful as a marker and a potential novel treatment target
AS160 regulates glucose-independent eukaryotic cell proliferation through p21 (show D4S234E Antibodies)-dependent control of the cell cycle.
Findings demonstrate that the RabGAP activity of AS160 maintains GLUT4 (show SLC2A4 Antibodies) protein levels in a cell/tissue-autonomous manner and its inactivation causes lysosomal degradation of GLUT4 (show SLC2A4 Antibodies) and postprandial hyperglycemia and hyperinsulinemia.
Rab28 (show RAB28 Antibodies) is a substrate for the GAP domains of both TBC1D1 (show TBC1D1 Antibodies) and TBC1D4 in vitro.
As160 knockout mice have GLUT4 (show SLC2A4 Antibodies) expression and glucose uptake defects in skeletal muscle and adipose tissue. These defects combine in AS160 KO/Tbc1d1 (show TBC1D1 Antibodies) KO mice, supporting nonredundant functions for AS160 and Tbc1d1 (show TBC1D1 Antibodies).
AS160 has a direct role in linking the trafficking of Na(+),K(+)-ATPase (show ATP1A1 Antibodies) to the energy state of renal epithelial cells
TBC1D4 is dispensable for the regulation of renal Na+ and water transport, but may play a role for GLUT4 (show SLC2A4 Antibodies)-mediated basolateral glucose uptake in distal tubules.
The Thr649 phosphorylation of AS160/TBC1D4 by protein kinase B (show AKT1 Antibodies) plays an important role in the heart electric conduction system through regulating the R-wave amplitude.
AS160 forms a ternary complex with Fsp27 (show CIDEC Antibodies) and Rab8a (show RAB8A Antibodies) to positively regulate lipid droplets fusion.
RAB10 (show RAB10 Antibodies) and its GTPase-activating protein (show RASA1 Antibodies) AS160 comprise the principal signaling module downstream of insulin receptor (show INSR Antibodies) activation that regulates the accumulation of GLUT4 (show SLC2A4 Antibodies) transport vesicles at the plasma membrane.
Data show that the AS160-knockout mice exhibited insulin resistance in both muscle and liver in a euglycaemic clamp study.
A novel isoform of TBC1D4 was detected by Western blotting using protein extracted from pig pancreas.
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.
Acrg embryonic lethality minimal region ortholog
, TBC (Tre-2, BUB2, CDC16) domain-containing protein
, TBC1 domain family member 4
, akt substrate of 160 kDa