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抗Mouse (Murine) G0S2 抗体:
抗Human G0S2 抗体:
抗Rat (Rattus) G0S2 抗体:
ER+ breast cancer cells with restored G0S2 expression had a relative increased sensitivity to tamoxifen
G0S2 protein but not mRNA levels were reduced in the adipose tissue of ATGL (显示 PNPLA2 抗体)-deficient mice, corroborating the involvement of ATGL (显示 PNPLA2 抗体) in the stabilization of G0S2
G0S2 silencing mediates MYC (显示 MYC 抗体)-induced oncogenesis in other malignancies
G0S2 expression in naive CD8 (显示 CD8A 抗体)(+) 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 (显示 MYC 抗体) 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 (显示 INS 抗体) resistance.
Proteasomal degradation of PPAR-gamma (显示 PPARG 抗体) and the reduction of g0s2 content are permissive for prolonged TNF-alpha (显示 TNF 抗体) 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 (显示 INS 抗体) sensitivity and overall metabolic health through inhibiting adipose lipolysis and decreasing circulating fatty acids.
Palmitate can induce lipid accumulation in HepG2 cells by activating C/EBPbeta (显示 CEBPB 抗体)-mediated G0S2 expression.
G0S2 functions as a master regulator of tissue-specific balance of TG storage vs. mobilization, partitioning of metabolic fuels between adipose and liver, and the whole-body adaptive energy response.
PML (显示 PML 抗体)/RARalpha (显示 RARA 抗体) synergizes with C/EBPepsilon (显示 CEBPE 抗体) to reactivate the C/EBPepsilon (显示 CEBPE 抗体) target G0S2, thereby contributing to All-trans retinoic acid -mediated acute promyelocytic leukemia (显示 PML 抗体) 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 (显示 PNPLA2 抗体)).
Results indicate that G0S2 acts as a prosurvival molecule in endothelial cells.
Data indicate that the peptide corresponding to residues Lys (显示 LYZ 抗体)-20 to Ala-52 from G0S2 Inhibits ATGL (显示 PNPLA2 抗体) in the nanomolar range.
reelin (显示 RELN 抗体) expression is altered by Abeta (显示 APP 抗体) leading to impaired reelin (显示 RELN 抗体) signaling.
A new mechanism that controls proliferation in K562 cells, suggesting a possible tumor suppressor function for G0S2 in leukemia cells.
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