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anti-Mouse (Murine) G0S2 Antibodies:
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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-deficient mice, corroborating the involvement of ATGL in the stabilization of G0S2
G0S2 silencing mediates MYC-induced oncogenesis in other malignancies
G0S2 expression in naive CD8(+) 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 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 resistance.
Proteasomal degradation of PPAR-gamma and the reduction of g0s2 content are permissive for prolonged TNF-alpha 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 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-resistant state.
a novel model of HSC quiescence in which elevated G0S2 expression can sequester nucleolin in the cytosol, precluding its pro-proliferation functions in the nucleolus
minimal fragment of ATGL could still be activated and inhibited by CGI-58 and G0S2, respectively
Lipolysis is differently regulated between perigonadal and mesenteric adipocytes, and these depot-specific differences might be explained by altered regulation of G0S2 and/or perilipin.
overexpression of G0S2 diminishes the rate of lipolysis in both adipocytes and adipose tissue explants
A novel putative target gene of PPARalpha, G0S2 (G0/G1 switch gene 2) was identified and characterized.
Palmitate can induce lipid accumulation in HepG2 cells by activating C/EBPbeta-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/RARalpha synergizes with C/EBPepsilon to reactivate the C/EBPepsilon target G0S2, thereby contributing to All-trans retinoic acid -mediated acute promyelocytic leukemia 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).
Results indicate that G0S2 acts as a prosurvival molecule in endothelial cells.
Data indicate that the peptide corresponding to residues Lys-20 to Ala-52 from G0S2 Inhibits ATGL in the nanomolar range.
reelin expression is altered by Abeta leading to impaired reelin 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.
Gene expression profiles showed that G0/G1 switch 2 was up-regulated in epidermolysis bullosa subtypes.
Reduced mRNA and protein content of Plin and G0S2 and borderline increased ATGL protein in sc adipose tissue from poorly controlled type 2 diabetic subjects.
findings are compatible with the notion that the ATGL-G0S2 complex is an important long-term regulator of lipolysis under physiological conditions such as fasting in humans
DNA methylation of G0S2 can be an important biomarker for squamous lung cancer.
mRNA expression of G0S2 was regulated mainly by DNA methylation in squamous lung cancer cell lines.
G0S2 is an all-trans-retinoic acid target gene
G0S2 encodes a mitochondrial protein that specifically interacts with Bcl-2 and promotes apoptosis by preventing the formation of protective Bcl-2/Bax heterodimers
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