Affinage

G0S2

G0/G1 switch protein 2 · UniProt P27469

Length
103 aa
Mass
11.3 kDa
Annotated
2026-06-09
72 papers in source corpus 22 papers cited in narrative 22 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

G0S2 is a small, multi-localized regulatory protein whose dominant characterized role is the suppression of intracellular triglyceride lipolysis through direct, non-competitive inhibition of adipose triglyceride lipase (ATGL) (PMID:20676045, PMID:30953555). G0S2 binds the patatin-domain region of ATGL independently of ATGL's activity state or the co-activator CGI-58, and this inhibition operates by a mechanism distinct from CGI-58-mediated activation (PMID:20676045, PMID:22039468). The minimal inhibitory determinant is a hydrophobic region spanning residues 20–44, with specific residues (Y27, V28, G30, A34, G37, V39, L42) driving ATGL inhibition (PMID:35026402); a hairpin of two hydrophobic sequences with charged hinge residues directs ATGL-independent sorting of G0S2 between the endoplasmic reticulum and lipid droplets (PMID:36420951). In vivo, adipose-specific overexpression suppresses basal and stimulated lipolysis, ketogenesis, and the carbohydrate-to-fat metabolic shift (PMID:24302733), whereas G0s2 deletion produces a lean, lipolysis-enhanced phenotype with improved glucose tolerance and adipose browning (PMID:25381555, PMID:24556704), and abolishes diet-induced hypertriglyceridemia and atherogenesis by coupling intracellular ATGL activity to extracellular LPL-mediated triglyceride clearance (PMID:40100923). Independent of lipolysis inhibition, G0S2 carries an intrinsic lysophosphatidic acid acyltransferase activity that promotes triglyceride synthesis (PMID:30802154). Beyond lipid metabolism, G0S2 antagonizes Bcl-2 antiapoptotic function by disrupting Bcl-2/Bax heterodimers (PMID:19706769), enforces hematopoietic and leukemic cell quiescence by sequestering nucleolin in the cytosol via its hydrophobic domain (PMID:22693613, PMID:24183236), suppresses oncogene-induced transformation through a MYC-dependent mechanism (PMID:26837760), and regulates mitochondrial oxidative phosphorylation and ATP output (PMID:31916304, PMID:25666096). G0S2 transcription is controlled by retinoic acid through RARE elements (PMID:18636162), by the PML/RARα–C/EBPε complex in APL cells (PMID:27605212), and by PPARγ, whose TNF-α-driven degradation lowers G0S2 (PMID:24993166), while G0S2 protein stability is set by K48-linked polyubiquitination at K25 and is stabilized by ATGL binding and triglyceride accumulation (PMID:27248498).

Mechanistic history

Synthesis pass · year-by-year structured walk · 19 steps
  1. 2008 High

    Establishing how G0S2 is induced linked it to retinoic acid signaling, identifying the first defined transcriptional input.

    Evidence RARE-site reporter mutagenesis and RAR co-transfection in APL cells and transgenic mice

    PMID:18636162

    Open questions at the time
    • Did not address G0S2 protein function downstream of induction
    • Other transcriptional inputs unexplored at this stage
  2. 2009 Medium

    The first functional assignment placed G0S2 at mitochondria as a pro-apoptotic antagonist of Bcl-2, establishing a non-metabolic role.

    Evidence Reciprocal Co-IP, subcellular fractionation, and apoptosis assays in cancer cell lines with NF-κB-inhibition expression profiling

    PMID:19706769

    Open questions at the time
    • Structural basis of Bcl-2 binding without BH domains unresolved
    • Relationship to later lipid functions not addressed
  3. 2010 High

    Identification of G0S2 as a direct ATGL inhibitor defined its central metabolic function and distinguished it mechanistically from CGI-58.

    Evidence Co-IP and lipolysis/lipid droplet assays in cells co-expressing G0S2, CGI-58, and ATGL

    PMID:20676045

    Open questions at the time
    • Inhibition mechanism (competitive vs non-competitive) not yet defined
    • Binding interface on ATGL not mapped
  4. 2011 High

    Mapping the ATGL fragment required for inhibition localized the G0S2 interaction to the patatin domain, advancing structural understanding of the inhibitory complex.

    Evidence Truncation mutagenesis, in vitro lipase assays, and 3D homology modeling

    PMID:22039468

    Open questions at the time
    • G0S2 residues mediating contact not yet defined
    • No co-crystal structure
  5. 2012 Medium

    Discovery of nucleolin sequestration explained a lipolysis-independent role in enforcing hematopoietic stem cell quiescence.

    Evidence Retroviral overexpression/shRNA in primary HSCs, proteomic partner identification, fractionation/imaging

    PMID:22693613

    Open questions at the time
    • How nucleolin retention links to cell-cycle machinery unclear
    • Single-lab finding
  6. 2013 Medium

    Extending the quiescence mechanism to leukemia showed G0S2 restrains proliferation by cytosolic nucleolin sequestration in K562 cells.

    Evidence 5-azacytidine demethylation, shRNA rescue, nucleolin interaction assays, and xenografts

    PMID:24183236

    Open questions at the time
    • Generality across leukemia subtypes untested
    • Quantitative contribution vs lipid roles unknown
  7. 2013 High

    An adipose-overexpression mouse confirmed in vivo that G0S2 suppresses lipolysis, ketogenesis, and fuel switching, validating its physiological lipase-inhibitory role.

    Evidence Adipose-specific transgenic mice with lipolysis assays, fasting metabolism, and cold-tolerance tests

    PMID:24302733

    Open questions at the time
    • Endogenous regulation under physiological states not addressed by overexpression
    • Tissue-specific contributions beyond adipose unexamined
  8. 2014 High

    Loss-of-function mouse studies established the reciprocal phenotype, showing G0s2 deletion drives leanness, enhanced lipolysis, browning, and improved glucose handling.

    Evidence Two independent G0s2 knockout mouse lines with metabolic phenotyping and tissue expression profiling

    PMID:24556704 PMID:25381555

    Open questions at the time
    • Mechanism of WAT browning downstream of G0S2 loss not dissected
    • Effects on non-adipose tissues underexplored
  9. 2014 Medium

    Linking TNF-α to PPARγ degradation explained how inflammatory signaling lowers G0S2 transcription and de-represses lipolysis.

    Evidence 3T3-L1 adipocytes, ChIP for PPARγ promoter binding, MG-132 rescue, and lipolysis assays

    PMID:24993166

    Open questions at the time
    • Direct PPARγ response element not finely mapped
    • Interplay with other transcriptional inputs unaddressed
  10. 2015 Medium

    Demonstrating that G0S2 restrains oxidative phosphorylation in naive CD8+ T cells extended its role to mitochondrial bioenergetics and immune cell metabolism.

    Evidence G0s2-null mice, Seahorse respirometry, AMPK phosphorylation, and TCR-pathway analysis

    PMID:25666096

    Open questions at the time
    • Molecular target within OXPHOS machinery unidentified
    • Apparent opposite direction vs cardiac OXPHOS role unresolved
  11. 2016 High

    Defining K48-polyubiquitination at K25 and ATGL/triglyceride-dependent stabilization revealed how G0S2 protein abundance is post-translationally tuned.

    Evidence K25 mutagenesis, ubiquitination and proteasome assays, ATGL co-expression, and ATGL-KO adipose analysis

    PMID:27248498

    Open questions at the time
    • Responsible E3 ligase not identified
    • Mechanism of triglyceride-induced stabilization unresolved
  12. 2016 Medium

    Showing tumor-suppressive activity independent of ATGL via MYC established a lipolysis-uncoupled function in oncogenic transformation.

    Evidence G0s2-null MEFs with HRAS/EGFR transformation assays, rescue, expression profiling, and MYC inhibition

    PMID:26837760

    Open questions at the time
    • Direct molecular link between G0S2 and MYC signaling unknown
    • Relevance to human tumors not established here
  13. 2016 Medium

    Identifying ligand-dependent PML/RARα recruitment with C/EBPε to the G0S2 promoter explained how ATRA induces G0S2 during APL differentiation.

    Evidence ChIP-qPCR and Co-IP in NB4/PR9 and primary APL cells with ATRA treatment

    PMID:27605212

    Open questions at the time
    • Functional consequence of induced G0S2 in differentiation not isolated
    • Single-lab finding
  14. 2019 High

    Discovery of intrinsic LPAAT activity revealed that G0S2 actively promotes triglyceride synthesis, a function entirely separate from lipolysis inhibition.

    Evidence In vitro LPAAT assays, 4-aa motif mutagenesis, and isotopic FA-incorporation in ATGL-deficient hepatocytes/mice

    PMID:30802154

    Open questions at the time
    • Relative contribution of LPAAT vs ATGL-inhibitory function in vivo unclear
    • Structural basis of catalysis undefined
  15. 2019 Medium

    Defining non-competitive patatin-domain inhibition and connecting G0S2-driven lipid droplet accumulation to mTOR-S6K-53BP1 signaling linked it to DNA repair and radioresistance in glioma stem cells.

    Evidence Knockdown/overexpression in GSCs, lipid droplet imaging, γ-H2AX foci, 53BP1 ubiquitination assays, and xenografts

    PMID:30953555

    Open questions at the time
    • Mechanistic chain from lipid droplets to mTOR not fully resolved
    • Generality beyond glioma untested
  16. 2020 High

    Zebrafish genetics established G0S2 as a positive regulator of OXPHOS and mitochondrial ATP under hypoxia, conferring ischemic tolerance.

    Evidence TALEN knockout and cardiomyocyte-specific transgenic zebrafish with in vivo FRET ATP biosensor imaging

    PMID:31916304

    Open questions at the time
    • Direction opposite to T-cell OXPHOS finding unreconciled
    • Molecular interaction with OXPHOS machinery unknown
  17. 2022 High

    Per-residue mapping of the 20–44 hydrophobic region and identification of the ER/lipid-droplet sorting hairpin defined the structural determinants of inhibition and localization.

    Evidence Systematic mutagenesis with in vitro ATPL lipase assays and fluorescent-construct imaging of ER/LD sorting

    PMID:35026402 PMID:36420951

    Open questions at the time
    • No high-resolution structure of the G0S2-ATGL complex
    • How ATGL overrides charge-dependent LD sorting unresolved
  18. 2023 Medium

    Identifying JAZF1 repression of G0S2 via the activator Purβ connected G0S2 to apoptosis control during endometrial decidualization.

    Evidence JAZF1 knockdown/overexpression, JAZF1-Purβ Co-IP, promoter analysis, and decidualization/apoptosis assays in hESCs

    PMID:37244968

    Open questions at the time
    • Mechanism by which G0S2 drives hESC apoptosis here not detailed
    • Single tissue context
  19. 2025 High

    WAT transplantation and LPL epistasis showed that intracellular ATGL activity controlled by G0S2 governs extracellular LPL-mediated plasma triglyceride clearance and atherogenesis.

    Evidence G0S2 global KO mice, WAT transplantation rescue, LPL activity measurement, and ATGL inhibitor reversal under dietary lipid challenge

    PMID:40100923

    Open questions at the time
    • Molecular link between intracellular lipolysis and LPL stability not defined
    • Human relevance of the WAT-LPL axis untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • The unifying biochemical basis reconciling G0S2's opposing roles in OXPHOS, its non-lipid partners (Bcl-2, nucleolin), and its ATGL-independent functions remains undefined.
  • No structure of any G0S2 complex
  • Opposing OXPHOS phenotypes across systems unreconciled
  • E3 ligase for K25 ubiquitination unidentified

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 4 GO:0016740 transferase activity 1
Localization
GO:0005739 mitochondrion 2 GO:0005783 endoplasmic reticulum 2 GO:0005829 cytosol 2 GO:0005768 endosome 1 GO:0005811 lipid droplet 1
Pathway
R-HSA-1430728 Metabolism 5 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-5357801 Programmed Cell Death 1
Partners
BCL2NCLPNPLA2

Evidence

Reading pass · 22 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2009 G0S2 encodes a mitochondria-localized protein that directly binds Bcl-2 and promotes apoptosis by preventing the formation of protective Bcl-2/Bax heterodimers; G0S2 lacks Bcl-2 homology domains but antagonizes Bcl-2 antiapoptotic activity. Expression is induced by TNF-alpha through NF-κB. Co-immunoprecipitation, subcellular fractionation, ectopic expression in cancer cell lines, expression profiling with NF-κB inhibition Cancer research Medium 19706769
2010 G0S2 acts as a direct inhibitor of adipose triglyceride lipase (ATGL) activity and ATGL-mediated lipolysis. G0S2 binds ATGL independently of ATGL's activity state or the presence of CGI-58. Combined expression of CGI-58 and ATGL cannot stimulate lipid droplet turnover in G0S2-expressing cells, indicating G0S2 and CGI-58 regulate ATGL via non-competing mechanisms. Co-immunoprecipitation, lipid droplet morphology assays, lipolysis assays in cells overexpressing G0S2, CGI-58 and ATGL constructs Cell cycle (Georgetown, Tex.) High 20676045
2011 The minimal active domain of ATGL required for inhibition by G0S2 ranges from amino acids Ile10 to Leu254. This minimal fragment retains both protein-protein interaction with G0S2 and susceptibility to G0S2-mediated inhibition, implying G0S2 interacts with the patatin-domain region of ATGL. Truncation mutagenesis, in vitro lipase activity assays, protein-protein interaction assays, 3D homology modeling PloS one High 22039468
2008 G0S2 is a direct transcriptional target of retinoic acid (RA) signaling. Retinoic acid response element (RARE) half-sites in the G0S2 promoter are required for RA-mediated transcriptional activation; mutation of these sites blocks activation. RAR co-transfection assays confirmed transcriptional activation after RA treatment. G0S2 protein is rapidly induced in APL cells and APL transgenic mice treated with RA in an RAR-dependent manner. Reporter gene assays with RARE site mutagenesis, RAR co-transfection, actinomycin D/cycloheximide treatment, RT-PCR, polyclonal antibody detection of protein International journal of oncology High 18636162
2012 G0S2 localizes to mitochondria, endoplasmic reticulum, and early endosomes in hematopoietic cells. The hydrophobic domain of G0S2 interacts with the RGG-repeat domain of nucleolin, retaining nucleolin in the cytosol; this cytosolic retention of nucleolin occurs in resting but not proliferating hematopoietic stem cells. G0S2 overexpression increases HSC quiescence while G0S2 knockdown promotes HSC division. Retroviral overexpression, shRNA knockdown, bone marrow transplantation, cell cycle analysis, proteomic identification of binding partners (nucleolin), subcellular fractionation/imaging PloS one Medium 22693613
2013 G0S2 inhibits proliferation of K562 leukemia cells by sequestering nucleolin in the cytosol, preventing its pro-proliferative functions in the nucleolus. Knockdown of G0S2 by shRNA in 5-azacytidine-treated K562 cells restores proliferation. 5-azacytidine demethylation, shRNA knockdown, xenograft models, co-immunoprecipitation/interaction assays with nucleolin, proliferation assays Leukemia research Medium 24183236
2013 Adipose-specific overexpression of G0S2 in transgenic mice inhibits basal and adrenergically stimulated lipolysis in adipose explants, reduces in vivo lipolysis and ketogenesis during fasting, impairs the metabolic shift from carbohydrates to fatty acids, and promotes lipid droplet accumulation in brown adipocytes with defective cold adaptation. Adipose-specific transgenic mouse model, lipolysis assays in adipose explants, in vivo metabolic measurements, β3-adrenergic agonist injection, cold tolerance tests, high-fat diet feeding The Journal of biological chemistry High 24302733
2014 Deletion of G0s2 in mice leads to a lean phenotype with enhanced adipose lipase activity, increased stimulated lipolysis in adipocytes, resistance to high-fat diet weight gain, improved glucose and insulin tolerance, and enhanced 'browning' of white adipose tissue with upregulation of thermoregulatory genes. G0s2 knockout mouse generation, lipolysis assays, metabolic phenotyping (body composition, glucose/insulin tolerance tests, energy metabolism), gene expression analysis Diabetologia High 25381555
2014 G0s2-null mice are lean with increased serum glycerol (indicating enhanced lipolysis), decreased gonadal fat pad weight, improved cold tolerance, and augmented thermogenic gene expression. G0S2 is most highly expressed in adipose tissue. G0s2 knockout mouse, body composition analysis, serum glycerol measurement, cold tolerance tests, tissue expression profiling Cancer biology & therapy High 24556704
2016 G0S2 protein is degraded via K48-linked polyubiquitination at lysine-25. Mutation of K25 abolishes ubiquitination and increases protein stability. G0S2 protein is stabilized by ATGL expression and by fatty acid-induced triglyceride accumulation through distinct mechanisms. G0S2 protein levels are reduced in adipose tissue of ATGL-deficient mice. Site-directed mutagenesis of K25, ubiquitination assays, proteasome inhibitor treatment, co-expression with ATGL, fatty acid treatment, ATGL-knockout mouse adipose tissue analysis PloS one High 27248498
2016 G0S2 suppresses oncogene-induced transformation independently of ATGL inhibition. G0s2-null MEFs are readily transformed by HRAS or EGFR; restoration of G0S2 reverses HRAS-driven transformation. Gene expression analysis reveals upregulation of MYC target signatures in G0s2-null MEFs; RNAi or pharmacologic inhibition of MYC abrogates transformation. G0s2-null MEFs, oncogene transformation assays (HRAS, EGFR), G0S2 rescue expression, gene expression profiling, MYC RNAi and pharmacologic inhibition Cancer research Medium 26837760
2016 During ATRA-induced APL differentiation, PML/RARα is recruited to the G0S2 promoter in an ATRA-dependent (ligand-dependent) manner and cooperates physically and functionally with C/EBPε (specifically the p30 isoform) to activate G0S2 transcription. ChIP-qPCR demonstrated co-occupancy of PML/RARα and C/EBPε at the G0S2 promoter. Chromatin immunoprecipitation (ChIP)-qPCR in NB4 and PR9 cell lines and primary APL cells, co-immunoprecipitation of PML/RARα and C/EBPε, ATRA treatment Journal of leukocyte biology Medium 27605212
2019 G0S2 possesses an intrinsic lysophosphatidic acid acyltransferase (LPAAT) enzymatic activity, directly catalyzing phosphatidic acid synthesis from lysophosphatidic acid and acyl-CoA. A distinct 4-amino acid motif is required for this LPAAT activity. Knockdown of G0S2 in ATGL-deficient mice still decreases hepatic TG content, and overexpression of G0S2 promotes fatty acid incorporation into TGs even in ATGL-deficient hepatocytes, demonstrating a lipolysis-independent TG synthesis function. In vitro LPAAT activity assay, deletion mutagenesis of 4-aa motif, overexpression/knockdown in ATGL-deficient mice and hepatocytes, isotopic fatty acid incorporation assays FASEB journal : official publication of the Federation of American Societies for Experimental Biology High 30802154
2019 G0S2 inhibits ATGL via non-competitive inhibition by interacting with ATGL's patatin domain. G0S2 inhibition of ATGL reduces lipid droplet turnover and, in glioma stem-like cells, attenuates RNF168-mediated 53BP1 ubiquitination through mTOR-S6K signaling activation and increased 53BP1 protein stability, thereby enhancing DNA repair and radioresistance. G0S2 knockdown/overexpression in GSCs, lipid droplet immunofluorescence, γ-H2AX foci assay, mTOR/S6K pathway analysis, 53BP1 ubiquitination assay, xenograft survival experiments Journal of experimental & clinical cancer research : CR Medium 30953555
2020 In zebrafish, G0s2 functions as a positive regulator of oxidative phosphorylation (OXPHOS) and maintains intra-mitochondrial ATP concentration under hypoxia. TALEN-mediated g0s2 knockout abolishes hypoxic tolerance in zebrafish hearts, while cardiomyocyte-specific overexpression confers strong ischemic tolerance. In vivo FRET-based ATP biosensor imaging showed that g0s2-expressing cardiomyocytes maintain ATP production and contractility during hypoxia. TALEN knockout zebrafish, cardiomyocyte-specific transgenic zebrafish, in vivo mitochondria-targeted FRET ATP biosensor imaging, mosaic overexpression model FASEB journal : official publication of the Federation of American Societies for Experimental Biology High 31916304
2015 G0S2 inhibits energy production by oxidative phosphorylation in naïve CD8+ T cells. G0S2-null naïve CD8+ T cells display increased basal and spare respiratory capacity associated with increased AMPK-α phosphorylation, not increased mitochondrial biogenesis. G0S2 expression in naïve T cells is suppressed downstream of TCR activation via MAPK, calcium/calmodulin, PI3K, and mTOR pathways. G0s2-null mice, Seahorse respirometry, mitochondrial biogenesis markers, AMPK phosphorylation analysis, T cell activation assays, in vivo lymphopenia-induced proliferation Immunology and cell biology Medium 25666096
2022 The minimal sequence of G0S2 required for ATGL inhibition spans amino acids 20–44, containing a hydrophobic region. Residues Y27, V28, G30, A34, G37, V39, and L42 play substantial roles in ATGL inhibition. N-terminal extensions (aa 20–27) facilitate non-specific interactions that increase binding to ATGL. Full-length G0S2 shows greater tolerance to single amino acid exchanges due to stronger contributions of these flanking interactions. Site-directed mutagenesis, truncation analysis, in vitro ATGL lipase activity assays, binding assays with G0S2 variants Biochimica et biophysica acta. Molecular and cell biology of lipids High 35026402
2022 ATGL-independent localization of G0S2 to both the endoplasmic reticulum (ER) and lipid droplets (LDs) is mediated by a hairpin structure consisting of two hydrophobic sequences. Positively charged residues in the hinge region of this hairpin sort G0S2 from ER to LDs. When ATGL is co-expressed, the role of these positive charges in LD sorting becomes dispensable. Structural prediction, cell imaging with fluorescent-tagged constructs, mutagenesis of hydrophobic sequences and charged residues, co-expression with ATGL Journal of cell science Medium 36420951
2014 TNF-α reduces G0S2 expression in adipocytes through proteasomal degradation of PPARγ, which abolishes PPARγ binding to the G0S2 promoter. Proteasome inhibition (MG-132) maintains PPARγ levels and preserves G0S2 expression. Overexpression of G0S2 or PPARγ partially reverses TNF-α-induced lipolysis. 3T3-L1 adipocyte differentiation, TNF-α treatment, proteasome inhibitor MG-132, ChIP assay for PPARγ binding to G0S2 promoter, G0S2 and PPARγ overexpression, lipolysis assays Cytokine Medium 24993166
2023 JAZF1 represses G0S2 transcription in human endometrial stromal cells (hESCs) by interacting with the G0S2 transcriptional activator Purβ, restricting its activity. JAZF1 depletion leads to increased G0S2 expression, apoptosis, and defective decidualization. G0S2 was identified as a key driver of hESC apoptosis in this context. JAZF1 siRNA/overexpression in hESCs, G0S2 promoter analysis, co-immunoprecipitation of JAZF1 with Purβ, decidualization assays, apoptosis assays, patient tissue analysis Communications biology Medium 37244968
2025 Genetic ablation of G0S2 in mice completely abolishes diet-induced hypertriglyceridemia and attenuates atherogenesis by enhancing whole-body triglyceride clearance. G0S2 deletion increases circulating LPL concentration and activity predominantly from white adipose tissue (WAT), and enhances LPL protein stability in adipocytes. This effect is reversed by ATGL inhibition, linking intracellular ATGL activity (regulated by G0S2) to extracellular LPL-mediated lipolysis. WAT transplantation from G0S2-deficient mice normalizes plasma TG levels in hypertriglyceridemic mice. G0S2 global knockout mice, WAT transplantation, LPL activity and concentration measurement, ATGL inhibitor treatment, dietary lipid challenge, atherosclerosis assessment The Journal of clinical investigation High 40100923
2025 In a mouse model of brain-evoked catabolism of all adipose depots, downregulation of G0s2 (along with Acvr1c and Npr3) is part of the cell-autonomous lipolytic inhibitor suppression that activates catecholamine-independent lipolysis, enabling mobilization of stable adipose stores including bone marrow adipose tissue. This process requires ATGL-dependent lipolysis. Genetic, surgical, and chemical intervention mouse models; adipose-specific gene expression analysis; G0s2 expression profiling during cachexia/starvation models bioRxivpreprint Low bio_10.1101_2024.07.30.605812

Source papers

Stage 0 corpus · 72 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2009 Identification of a protein, G0S2, that lacks Bcl-2 homology domains and interacts with and antagonizes Bcl-2. Cancer research 114 19706769
2012 The G0/G1 switch gene 2 (G0S2): regulating metabolism and beyond. Biochimica et biophysica acta 105 23032787
2010 Differential control of ATGL-mediated lipid droplet degradation by CGI-58 and G0S2. Cell cycle (Georgetown, Tex.) 97 20676045
2011 The minimal domain of adipose triglyceride lipase (ATGL) ranges until leucine 254 and can be activated and inhibited by CGI-58 and G0S2, respectively. PloS one 77 22039468
2011 Fasting, but not exercise, increases adipose triglyceride lipase (ATGL) protein and reduces G(0)/G(1) switch gene 2 (G0S2) protein and mRNA content in human adipose tissue. The Journal of clinical endocrinology and metabolism 73 21613358
2017 G0S2: A small giant controller of lipolysis and adipose-liver fatty acid flux. Biochimica et biophysica acta. Molecular and cell biology of lipids 72 28645852
2015 Inhibition of adipose triglyceride lipase (ATGL) by the putative tumor suppressor G0S2 or a small molecule inhibitor attenuates the growth of cancer cells. Oncotarget 69 26318046
2019 Targeted Assessment of G0S2 Methylation Identifies a Rapidly Recurrent, Routinely Fatal Molecular Subtype of Adrenocortical Carcinoma. Clinical cancer research : an official journal of the American Association for Cancer Research 54 30770352
2010 Identification of G0S2 as a gene frequently methylated in squamous lung cancer by combination of in silico and experimental approaches. International journal of cancer 53 19816938
2013 Defective adipose lipolysis and altered global energy metabolism in mice with adipose overexpression of the lipolytic inhibitor G0/G1 switch gene 2 (G0S2). The Journal of biological chemistry 52 24302733
2012 The cytosolic protein G0S2 maintains quiescence in hematopoietic stem cells. PloS one 49 22693613
2014 TNF-α reduces g0s2 expression and stimulates lipolysis through PPAR-γ inhibition in 3T3-L1 adipocytes. Cytokine 45 24993166
1997 Cyclosporin A inhibits early mRNA expression of G0/G1 switch gene 2 (G0S2) in cultured human blood mononuclear cells. DNA and cell biology 43 9428793
2014 Deletion of the gene encoding G0/G 1 switch protein 2 (G0s2) alleviates high-fat-diet-induced weight gain and insulin resistance, and promotes browning of white adipose tissue in mice. Diabetologia 41 25381555
2016 G0S2 Suppresses Oncogenic Transformation by Repressing a MYC-Regulated Transcriptional Program. Cancer research 38 26837760
2017 Palmitate induces fat accumulation by activating C/EBPβ-mediated G0S2 expression in HepG2 cells. World journal of gastroenterology 37 29209111
2008 G0S2 is an all-trans-retinoic acid target gene. International journal of oncology 37 18636162
2009 Impact of DNA demethylation of the G0S2 gene on the transcription of G0S2 in squamous lung cancer cell lines with or without nuclear receptor agonists. Biochemical and biophysical research communications 36 19878646
2022 Single-Cell Sequencing Analysis and Multiple Machine Learning Methods Identified G0S2 and HPSE as Novel Biomarkers for Abdominal Aortic Aneurysm. Frontiers in immunology 35 35769488
2018 Disruption of G0/G1 switch gene 2 ( G0S2) reduced abdominal fat deposition and altered fatty acid composition in chicken. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 33 30085885
2014 Mice lacking G0S2 are lean and cold-tolerant. Cancer biology & therapy 32 24556704
2019 Lipolytic inhibitor G0S2 modulates glioma stem-like cell radiation response. Journal of experimental & clinical cancer research : CR 31 30953555
2013 G0S2 inhibits the proliferation of K562 cells by interacting with nucleolin in the cytosol. Leukemia research 31 24183236
2020 Cooperative application of transcriptomics and ceRNA hypothesis: LncRNA-107052630/miR-205a/G0S2 crosstalk is involved in ammonia-induced intestinal apoptotic injury in chicken. Journal of hazardous materials 27 32334290
1998 An alternative way of thinking about stem-loops in DNA. A case study of the human G0S2 gene. Journal of theoretical biology 27 9680722
2013 Porcine G₀/G₁ switch gene 2 (G0S2) expression is regulated during adipogenesis and short-term in-vivo nutritional interventions. Lipids 23 23322075
2023 Acidosis-induced regulation of adipocyte G0S2 promotes crosstalk between adipocytes and breast cancer cells as well as tumor progression. Cancer letters 19 37442366
2016 Regulation of G0/G1 Switch Gene 2 (G0S2) Protein Ubiquitination and Stability by Triglyceride Accumulation and ATGL Interaction. PloS one 18 27248498
2022 G0S2 regulates innate immunity in Kawasaki disease via lncRNA HSD11B1-AS1. Pediatric research 16 35292727
2019 Identification of an intrinsic lysophosphatidic acid acyltransferase activity in the lipolytic inhibitor G0/G1 switch gene 2 (G0S2). FASEB journal : official publication of the Federation of American Societies for Experimental Biology 16 30802154
2015 G0S2 modulates homeostatic proliferation of naïve CD8⁺ T cells and inhibits oxidative phosphorylation in mitochondria. Immunology and cell biology 16 25666096
2022 Loss of G0/G1 switch gene 2 (G0S2) promotes disease progression and drug resistance in chronic myeloid leukaemia (CML) by disrupting glycerophospholipid metabolism. Clinical and translational medicine 15 36536477
2017 G0S2 represses PI3K/mTOR signaling and increases sensitivity to PI3K/mTOR pathway inhibitors in breast cancer. Cell cycle (Georgetown, Tex.) 15 28910567
2018 The Nuclear Orphan Receptor Nur77 Alleviates Palmitate-induced Fat Accumulation by Down-regulating G0S2 in HepG2 Cells. Scientific reports 14 29556076
2016 Pronounced expression of the lipolytic inhibitor G0/G1 Switch Gene 2 (G0S2) in adipose tissue from brown bears (Ursus arctos) prior to hibernation. Physiological reports 14 27117803
2014 Progesterone-induced down-regulation of hormone sensitive lipase (Lipe) and up-regulation of G0/G1 switch 2 (G0s2) genes expression in inguinal adipose tissue of female rats is reflected by diminished rate of lipolysis. The Journal of steroid biochemistry and molecular biology 14 25448749
2015 Increases in skeletal muscle ATGL and its inhibitor G0S2 following 8 weeks of endurance training in metabolically different rat skeletal muscles. American journal of physiology. Regulatory, integrative and comparative physiology 13 26511521
2022 Residues of the minimal sequence of G0S2 collectively contribute to ATGL inhibition while C-and N-terminal extensions promote binding to ATGL. Biochimica et biophysica acta. Molecular and cell biology of lipids 11 35026402
2020 In vivo real-time ATP imaging in zebrafish hearts reveals G0s2 induces ischemic tolerance. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 11 31916304
2023 JAZF1 safeguards human endometrial stromal cells survival and decidualization by repressing the transcription of G0S2. Communications biology 10 37244968
2021 Promotion effect of salt on intramuscular neutral lipid hydrolysis during dry-salting process of porcine (biceps femoris) muscles by inducing phosphorylation of ATGL, HSL and their regulatory proteins of Perilipin1, ABHD5 and G0S2. Food chemistry 9 34815115
2016 Liver-specific G0 /G1 switch gene 2 (G0s2) expression promotes hepatic insulin resistance by exacerbating hepatic steatosis in male Wistar rats. Journal of diabetes 9 27624922
2023 G0S2 promotes antiestrogenic and pro-migratory responses in ER+ and ER- breast cancer cells. Translational oncology 8 37086619
2025 FXR as a pivotal role linking JNK and G0s2 mitigates triptolide-induced hepatotoxicity through the regulation of metabolic disorder of liver. Pharmacological research 7 40288593
2022 G0S2 Gene Polymorphism and Its Relationship with Carcass Traits in Chicken. Animals : an open access journal from MDPI 7 35405904
2020 The Expression Pattern and Regulatory Mechanism of the G0/G1 Switch Gene 2 (G0S2) in the Pathogenesis and Treatment of AChR Myasthenia Gravis (MG). Mediators of inflammation 6 33061827
2016 Regulation of G0/G1 switch gene 2 (G0S2) expression in human adipose tissue. Archives of physiology and biochemistry 6 26707160
2022 G0S2 ameliorates oxidized low-density lipoprotein-induced vascular endothelial cell injury by regulating mitochondrial apoptosis. Annals of translational medicine 5 36660674
2015 Characterization of lipolytic inhibitor G(0)/G(1) switch gene-2 protein (G0S2) expression in male Sprague-Dawley rat skeletal muscle compared to relative content of adipose triglyceride lipase (ATGL) and comparitive gene identification-58 (CGI-58). PloS one 5 25811590
2014 Tissue expression pattern and polymorphism of G0S2 gene in porcine. Gene 5 24487091
2025 Absence of the intracellular lipolytic inhibitor G0S2 enhances intravascular triglyceride clearance and abolishes diet-induced hypertriglyceridemia. The Journal of clinical investigation 4 40100923
2022 Identification of motifs and mechanisms for lipid droplet targeting of the lipolytic inhibitors G0S2 and HIG2. Journal of cell science 4 36420951
2016 Activation of G0S2 is coordinated by recruitment of PML/RARα and C/EBPε to its promoter during ATRA-induced APL differentiation. Journal of leukocyte biology 4 27605212
2025 Recent advances on the role of G0S2. Discover oncology 3 40679675
2023 The effect of G0S2 on insulin sensitivity: A proteomic analysis in a G0S2-overexpressed high-fat diet mouse model. Frontiers in endocrinology 3 37033250
2025 BCL2A1‑ and G0S2‑driven neutrophil extracellular traps: A protective mechanism linking preeclampsia to reduced breast cancer risk. Oncology reports 2 40242964
2024 Mutation on JmjC domain of UTX impaired its antitumor effects in pancreatic cancer via inhibiting G0S2 expression and activating the Toll-like signaling pathway. Molecular medicine (Cambridge, Mass.) 2 39707168
2021 Biophysical characterization and a roadmap towards the NMR solution structure of G0S2, a key enzyme in non-alcoholic fatty liver disease. PloS one 2 34260600
2019 Correction to: Lipolytic inhibitor G0S2 modulates glioma stem-like cell radiation response. Journal of experimental & clinical cancer research : CR 2 31358019
2015 Deletion of the putative tumor suppressor gene, G0s2, does not affect progression of Eμ-Myc driven lymphomas in mice. Leukemia research 2 26654706
2026 An Extracellular Matrix-Producing Subset of Cancer-Associated Fibroblasts Drives Chemoresistance in Breast Cancer via SRC Activation and G0S2 Upregulation. Cancer research 1 41223328
2025 The Evaluation of PNPLA2, ATGL, and G0S2 Levels in Serum and PBMCs of the Newly Diagnosed and the Chronic Patients With Rheumatoid Arthritis. International journal of rheumatic diseases 1 39989302
2025 The Effect of G0S2 Gene Knockout on the Proliferation, Apoptosis, and Differentiation of Chicken Preadipocytes. Animals : an open access journal from MDPI 1 40218345
2025 G0S2 Promotes PD-L1 Expression in Monocytes and Influences the Efficacy of PD-1 Inhibitors in Hepatocellular Carcinoma. Genes 1 40282408
2025 PIK3R1 and G0S2 are human placenta-specific imprinted genes associated with germline-inherited maternal DNA methylation. Epigenetics 1 40568952
2023 Gastric Cancer Growth Modulated by circSNTB2/miR-6938-5p/G0S2 and PDCD4. Combinatorial chemistry & high throughput screening 1 36366842
2026 G0S2 drives lipid metabolism disorders and oxidative stress to promote M1 macrophage polarization and inflammation in polycystic ovary syndrome. Life sciences 0 41985712
2026 Novel Insights into G0S2 as a Central Regulator of Lipid Metabolism and Its Implications for Meat Quality. Animals : an open access journal from MDPI 0 42193761
2025 G0S2 modulates normal vitreous-induced proliferation in endothelial cells. Communications biology 0 40185884
2025 Metabolic profiling of glioblastoma and identification of G0S2 as a metabolic target. Frontiers in oncology 0 40519301
2024 The repression of the lipolytic inhibitor G0s2 enhancers affects lipid metabolism. Gene 0 39667714
2019 Correction to: Lipolytic inhibitor G0S2 modulates glioma stem-like cell radiation response. Journal of orthopaedic surgery and research 0 31311601

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