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Human G0S2 Protein expressed in Human - ABIN2721519
Laurens, Badin, Louche, Mairal, Tavernier, Marette, Tremblay, Weisnagel, Joanisse, Langin, Bourlier, Moro: G0/G1 Switch Gene 2 controls adipose triglyceride lipase activity and lipid metabolism in skeletal muscle. in Molecular metabolism 2016
G0S2 silencing mediates MYC (show MYC Proteins)-induced oncogenesis in other malignancies
G0S2 expression in naive CD8 (show CD8A Proteins)(+) T cells decreased immediately after T-cell receptor activation downstream of various signal transduction pathways. G0S2 inhibits energy production by oxidative phosphorylation to fine-tune proliferation in homeostasis.
findings do not rule out the possibility that G0S2 may be playing a role in other forms of leukemia, but clearly show that the commonly used Emu-Myc (show MYC Proteins) transgenic is not the correct model to conduct studies on G0s2
G0s2 is a physiological regulator of adiposity and energy metabolism and is a potential target in the treatment of obesity and insulin (show INS Proteins) resistance.
Proteasomal degradation of PPAR-gamma (show PPARG Proteins) and the reduction of g0s2 content are permissive for prolonged TNF-alpha (show TNF Proteins) induced lipolysis.
G0s2 has an important role in adipogenesis and accumulation of triacylglycerol.
Roles for G0S2 were found in lactation, energy balance, and thermogenesis. This study provides a basis for tumor suppressive effects of G0S2 by regulating lipolysis.
fat-specific G0S2 overexpression uncouples adiposity from insulin (show INS Proteins) sensitivity and overall metabolic health through inhibiting adipose lipolysis and decreasing circulating fatty acids.
Data indicate that downregulation of G0S2 in adipose tissue could represent one of the underlying causes leading to increased lipolysis in the insulin (show INS Proteins)-resistant state.
a novel model of HSC (show FUT1 Proteins) quiescence in which elevated G0S2 expression can sequester nucleolin (show NCL Proteins) in the cytosol, precluding its pro-proliferation functions in the nucleolus
differences in G0S2 expression may explain depot-specific and obesity-associated differences in lipolysis on the molecular level
Data indicate that a tumor suppressor mechanism by which G0/G1 switch gene 2 product (G0S2) directly inhibits activity of a key intracellular adipose triglyceride lipase (ATGL (show PNPLA2 Proteins)).
Results indicate that G0S2 acts as a prosurvival molecule in endothelial cells.
Data indicate that the peptide corresponding to residues Lys (show LYZ Proteins)-20 to Ala-52 from G0S2 Inhibits ATGL (show PNPLA2 Proteins) in the nanomolar range.
reelin (show RELN Proteins) expression is altered by Abeta (show APP Proteins) leading to impaired reelin (show RELN Proteins) signaling.
A new mechanism that controls proliferation in K562 cells, suggesting a possible tumor suppressor function for G0S2 in leukemia cells.
This linked G0S2 subcellular localization to G0S2 transcriptional repression. The potential mechanisms responsible for this G0S2 repression are examined.
Reduced mRNA and protein content of Plin (show PLIN1 Proteins) and G0S2 and borderline increased ATGL (show PNPLA2 Proteins) protein in sc adipose tissue from poorly controlled type 2 diabetic subjects.
findings are compatible with the notion that the ATGL (show PNPLA2 Proteins)-G0S2 complex is an important long-term regulator of lipolysis under physiological conditions such as fasting in humans
Promotes apoptosis by binding to BCL2, hence preventing the formation of protective BCL2-BAX heterodimers.
G0/G1 switch protein 2
, G0S2-like protein
, putative lymphocyte G0/G1 switch protein 2
, G0/G1 switch regulatory protein 2
, G0/G1 switch gene 2
, putative lymphocyte G0/G1 switch