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anti-Mouse (Murine) G0S2 Antibodies:
anti-Human G0S2 Antibodies:
anti-Rat (Rattus) G0S2 Antibodies:
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G0S2 protein but not mRNA levels were reduced in the adipose tissue of ATGL (show PNPLA2 Antibodies)-deficient mice, corroborating the involvement of ATGL (show PNPLA2 Antibodies) in the stabilization of G0S2
G0S2 silencing mediates MYC (show MYC Antibodies)-induced oncogenesis in other malignancies
G0S2 expression in naive CD8 (show CD8A Antibodies)(+) 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 Antibodies) 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 Antibodies) resistance.
Proteasomal degradation of PPAR-gamma (show PPARG Antibodies) and the reduction of g0s2 content are permissive for prolonged TNF-alpha (show TNF Antibodies) 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 Antibodies) 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 Antibodies)-resistant state.
PML (show PML Antibodies)/RARalpha (show RARA Antibodies) synergizes with C/EBPepsilon (show CEBPE Antibodies) to reactivate the C/EBPepsilon (show CEBPE Antibodies) target G0S2, thereby contributing to All-trans retinoic acid -mediated acute promyelocytic leukemia (show PML Antibodies) differentiation and potentially, clinical remission.
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 Antibodies)).
Results indicate that G0S2 acts as a prosurvival molecule in endothelial cells.
Data indicate that the peptide corresponding to residues Lys (show LYZ Antibodies)-20 to Ala-52 from G0S2 Inhibits ATGL (show PNPLA2 Antibodies) in the nanomolar range.
reelin (show RELN Antibodies) expression is altered by Abeta (show APP Antibodies) leading to impaired reelin (show RELN Antibodies) 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 Antibodies) and G0S2 and borderline increased ATGL (show PNPLA2 Antibodies) protein in sc adipose tissue from poorly controlled type 2 diabetic subjects.
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