| protein
| ARA70  |
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9-cis-retinoic acid receptor (RXR) heterodimers |
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RXRalpha |
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NF-E2-related factor 2, NRF2 |
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SRC-1, TIF2, AIB-1, p300, TRAP220/DRIP205 |
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DRIP205 and p160 |
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liver fatty acid binding protein, L-FABP |
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Multiprotein bridging factor, MBF-1 |
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FKHR |
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centrosome-associated protein CAP350 |
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Breast cancer amplified sequence 2, BCAS2 |
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PPARgamma-DBD-interacting protein 1, PDIP1-alpha |
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HIV-1 Tat-interacting protein 60, Tip60 |
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SFRS1 |
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CDX1 and CEBPA |
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FGF21 |
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insulin receptor, IR |
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Sp1 |
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regulatory functions of AEBP1 on PPARG1 and NR1H3 transcriptional activity in the context of macrophage cholesterol homeostasis and inflammation |
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APMAP |
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histone deacetylase 4, HDAC4 |
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LPIN1 phosphatidic acid phosphatase activity, but not its coactivator activity, is required for induction of PPARG |
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DICER1 might have important roles in the expression of adipogenic genes including PPARG and CEBPA via regulation of the expression of miRNAs at the early, but not the late, stage of adipocyte differentiation |
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STK3/STK4 timulated the binding of SAV1 to PPARG, a transcription factor that plays a key role in adipogenesis |
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inhibits airway epithelial cell inflammatory response through a MUC1-dependent mechanism |
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PPARG may be an important TBX20 co-factor activating energy metabolism genes in the adult heart while REST, a known transcriptional repressor, may act with TBX20 to silence genes controlling genetic programs unrelated to adult heart function |
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metabolic role for FGF1 as a critical transducer of PPARG signalling that mediates the proper coupling of nutrient storage to adaptive remodelling of adipose tissue |
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blocks likely adipogenesis by reinforcing HDAC1 recruitment to the PPARG promoter, and is one of the mediators that reset the pattern of PPARG expression in response to hypoxia |
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PPARG activation contributes to the regulation of ceramide metabolism during adipogenesis via FAM57B |
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regulatory cascade containing PPARG and TWIST1 that controlled the expression of GPS2 and NCOR2 in human adipocytes |
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PPARG may contribute to the constitutive expression of LPIN1 in adipocyte, and activation of PPARG can alleviate the suppression of LPIN1 expression by ER stress |
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TAF7L is required for activating adipocyte-specific genes via a dual mechanism wherein it interacts with PPARG at enhancers and TBP/Pol II at core promoters |
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is a novel target gene of PPARG (upregulation of FAM3A by PPARG activation is correlated with increased AKT1 level in liver cells) |
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LPIN1 functions as a key regulator of PPARG activity through its ability to release co-repressors and recruit co-activators via a mechanism other than PPARA activation |
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coordinate interaction between PTGES and PPARG is required for white-to-brown fat conversion |
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is required for transcriptional activation of the MRAP gene during adipogenesis, which contributes to understanding of the molecular mechanism of lipolysis in adipocytes |
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transcription of LIPE is regulated by the PPARG/MRAP-mediated signaling pathway |
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PPARG, an E3 ubiquitin ligase, is an inhibitor of MUC1-mediated cell proliferation |
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suppression of PPARG by FABP4 in visceral fat may explain the reported role of FABP4 in the development of obesity-related morbidities, including insulin resistance, diabetes, and atherosclerosis |
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GATA2 mediated leptin inhibition of PPARG expression by its binding site in PPARG promoter in Hepatic stellate cell (HSC) and GATA2 promoted HSC activation |
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ATF3-mediated inhibition of PPARG expression may contribute to inhibition of adipocyte differentiation during cellular stress including ER stress |
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FLII binds directly to and suppresses the transcriptional activity of PPARG |
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PPARG could inhibit Hepatocellular carcinoma (HCC) cell growth via regulating the expression and blocking the oncogenic function of SEPT2 |
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activation of PPARG increases, in a PPARG-dependent manner, the expression of ADTRP in human macrophages and atherosclerotic lesions |
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WNT1 regulates the expression of CD36 through TCF4 and PPARG |
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TRIM23, stabilizes PPARG protein and mediates atypical polyubiquitin conjugation |
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AJUBA recruits CREBBP via its LIM domain and facilitates CREBBP binding to PPARG |
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dual roles for JMJD6 in promoting adipogenic gene expression program by post-transcriptional regulation of CEBPB and CEBPD and direct transcriptional activation of PPARG2 and CEBPA during adipocyte differentiation |
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SOX6 regulates adipogenesis in vertebrate species by activating adipogenic regulators including PPARG, CEBPA and MEST |
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ZFP36L1 overexpression might repress adipogenesis at least by down-regulating PPARG expression through post-transcriptional mechanisms |
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PPARG binds to the promoter of DLC1 gene to regulate its expression during both white and brown adipocyte differentiation |
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CACUL1 tightly regulates PPARG signaling through the mutual opposition between SIRT1 and KDM1A, providing insight into its potential use for anti-obesity treatment |
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HES6 prevents hepatic lipid accumulation through inhibition of PPARG expression |
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MAGED1 bound to PPARG and suppressed the stability and transcriptional activity of PPARG |
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PIAS1 is a specific E3 ligase for PPARG SUMOylation |
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likely FGF11 indirectly controls the expression of PPARG through modifying the expression of multiple PPARG regulators, thereby mediating adipogenesis |
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NOVA2 integrated splicing decisions in order to regulate PPPARG and E2F1 activities |
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| mouse PPAR gamma gene knockout leads to severe myocardial thinning and death by E10.0 | |
Homozygous PPAR gamma-deficient embryos died at 10.5-11.5 dpc due to placental dysfunction |
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Heterozygous PPAR gamma-deficient mice showed overexpression and hypersecretion of leptin despite the smaller size of adipocytes and decreased fat mass |
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mice chimeric for wild-type and PPAR gamma null cells show little or no contribution of null cells to adipose tissue |
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PPAR-gamma(+/-) mice display no statistically significant differences in body weight, basal glucose, insulin, or FFA levels compared to wild-type |
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insulin-induced increase in glucose disposal rate was significantly increased and insulin-induced suppression of hepatic glucose production was significantly greater in the PPAR-gamma(+/-) mice |
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Pparg mutant mice exhibit impaired skin wound healing |
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deletion of the PPARgamma gene in mouse mammary epithelium and epithelial cells, B- and T-cells, and ovary does not affect mammary development and propensity for tumor formation but leads to reduced fertility |
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neither hemizygous deletion of Pparg nor complete ablation of Ppara influenced the development of prostate cancer in mouse model |
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elimination of expression of the PPARG gene in mouse beta cells leads to significant islet hyperplasia |
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knock out of Pparg in mouse skeletal muscle causes glucose intolerance and progressive insulin resistance |
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Targeted deletion of PPARgamma in adipose tissue results in marked adipocyte hypocellularity and hypertrophy, elevated levels of plasma free fatty acids and triglyceride, decreased levels of plasma leptin and ACRP30, increased hepatic glucogenesis and insulin resistance |
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in contrast to the embryonic lethality of PPARgamma1-deficient mice, PPARgamma2(-/-) mice survived but exhibited an overall reduction in white adipose tissue, less lipid accumulation, and decreased expression of adipogenic genes in adipose tissue, and impairment of insulin sensitivity |
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homozygous mice with the equivalent P465L mutation die in utero while heterozygous mice grow normally with normal total adipose tissue weight but a reduced interscapular brown adipose tissue, intra-abdominal fat mass, increased extra-abdominal subcutaneous fat, and are hypertensive |
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disruption of PPARgamma in mouse myeloid cells impairs alternative macrophage activation, and predisposes to development of diet-induced obesity, insulin resistance, and glucose intolerance |
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targeted deletion of PPAR gamma in mice results in the production of "toxic milk" containing elevated levels of inflammatory lipids |
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Tie2Cre/flox mouse model in which PPAR-gamma is deleted in osteoclasts but not in osteoblasts develop osteopetrosis characterized by increased bone mass, reduced medullary cavity space and extramedullary hematopoiesis in the spleen |
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blocking the endogenous activation of central nervous system PPARG with pharmacological antagonists or reducing its expression with shRNA leads to negative energy balance, restored leptin sensitivity in high-fat-diet rats and blocked the hyperphagic response to oral thiazolidinedione treatment |
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food intake was reduced and energy expenditure increased |
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C3H mice do not express Pparg and Mgat1 in the liver and are protected against hepatic steatosis while being fed a HFD during high-fat diet in mice with neuron-specific Pparg knockout |
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over-expression of PPARG in cultured cortical neurons protects neurons from either HDAC4 over-expression- or H(2) O(2) -induced damage |
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C3H mice do not express Pparg and Mgat1 in the liver and are protected against hepatic steatosis while being fed a high-fat diet (HFD) |
