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anti-Mouse (Murine) PPARGC1B Antibodies:
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These findings directly demonstrate and implicate reduced Na(+) in contrast to unchanged K(+) current, as a mechanism for slowed conduction causing atrial arrhythmogenicity in Pgc-1beta(-/-) hearts.
Mitochondrial dysfunction thus causes pro-arrhythmic Pgc-1beta(-/-) phenotypes by altering action potential conduction through reducing (dV/dt)max and causing age-dependent fibrotic change.
Hepatic PGC-1beta is a transcriptional gatekeeper of mitochondrial function and redox status in hepatocellular carcinoma, orchestrating different metabolic programs that allow tumor progression.
Pgc-1beta deficient murine hearts show atrial arrhythmic phenotype secondary to mitochondrial dysfunction that is dependent on age
Abeta (show APP Antibodies) increases the expression of mTOR (show FRAP1 Antibodies) and p-mTOR (show FRAP1 Antibodies) at the site of Ser2448, and the stimulation of Abeta (show APP Antibodies) is likely to depend on sirtuin 1 (show SIRT1 Antibodies), PPARgamma (show PPARG Antibodies), and PGC-1beta pathway in regulating mTOR (show FRAP1 Antibodies) expression.
MyoD (show MYOD1 Antibodies) regulates the oxidative metabolic capacity of adult skeletal muscle;ChIP-seq analysis identified MyoD (show MYOD1 Antibodies) binding on the PGC (show PGC Antibodies)-1b, but not PGC (show PGC Antibodies)-1a, gene locus;MyoD (show MYOD1 Antibodies) cooperates with alternative NF-kappaB (show NFKB1 Antibodies) to regulate PGC (show PGC Antibodies)-1b transcription; MyoD (show MYOD1 Antibodies) and RelB (show RELB Antibodies) co-occupy many other genes involved in aerobic respiration
We conclude that while activation of muscle PGC-1beta is sufficient to drive the complete endurance phenotype in sedentary mice, it only partially prevents the detraining response following exercise training, suggesting that the process of endurance detraining involves mechanisms beyond the reversal of muscle autonomous mechanisms involved in endurance fitness.
Data suggest that PGC-1alpha and -1beta expression are not required for training-induced exercise performance, highlighting the contribution of PGC-1-independent mechanisms.
We confirmed that PGC (show PGC Antibodies)-1b inhibited downstream inflammatory signals via binding with TAB1 (show TAB1 Antibodies) and thus preventing TAB1 (show TAB1 Antibodies)/TAK1 (show NR2C2 Antibodies) binding and TAK1 (show NR2C2 Antibodies) activation.
the anti-inflammatory environment in muscle promoted by the PGC (show PGC Antibodies)-1s might contribute to the beneficial effects of these coactivators on muscle function and provides a molecular link underlying the tight mutual regulation of metabolism and inflammation
Incrementally paced murine Pgc1beta(-/-) hearts show pro-arrhythmic atrial phenotypes that are age dependent.
Insulin-like growth factor 1 receptor (show IGF1R Antibodies), associate of Myc 1 (show MYCBP Antibodies), and peroxisome proliferator-activated receptor gamma (show PPARG Antibodies) coactivator 1beta are direct targets of miR (show MLXIP Antibodies)-139
Study provides evidence that PGC1beta rs32579 was associated with nevus count, and both melanoma risk and mortality, which further emphasizes the critical role of PGC1s in multiple steps of melanocyte formation and melanoma development.
The presence of the PPARGC1B (Ala203Pro) SNP did not modify the association between inorganic arsenic methylation capacity and breast cancer.
Genetic variants of PPARGC1B are significantly associated with gout, and a missense single nucleotide polymorphism, rs45520937, augments NLRP3 (show NLRP3 Antibodies) and IL-1beta (show IL1B Antibodies) expression
the forkhead box O3 (FOXO3 (show FOXO3 Antibodies))/liver kinase B1 (LKB1 (show STK11 Antibodies))/AMP-activated protein kinase (show PRKAA2 Antibodies)/peroxisome proliferator-activated receptor-gamma (show PPARG Antibodies) co-activator-1beta (PGC-1beta)/pyruvate dehydrogenase (show PDP Antibodies)-A1 pathway is essential for CD44 (show CD44 Antibodies) expression and cancer stem cells properties.
We also suggest a novel hepatic protective role of PGC1B as a modulator of E2 effects on mitochondrial biogenesis
we show an association of HER2 (show ERBB2 Antibodies)-overexpression and PGC-1beta. PGC-1beta knockdown impairs HER2 (show ERBB2 Antibodies)-overexpressing cells proliferation acting on ERRalpha (show ESRRA Antibodies) signaling, metabolism, and redox balance.
Further replication study confirmed the association signals of rs4705372 (P = 0.0026) and rs11743128 (P = 0.0387) in the independent validation sample. Our study results suggest that PPARGC1B is a novel susceptibility gene of Kashin-Beck disease .
Human influenza hemagglutinin (show HA Antibodies)-tagged PPARGC1B coprecipitated more intensely with ERalpha (show ESR1 Antibodies) in the +102525A than the +102525G construct after 17beta estradiol treatment
The protein encoded by this gene stimulates the activity of several transcription factors and nuclear receptors, including estrogen receptor alpha, nuclear respiratory factor 1, and glucocorticoid receptor. The encoded protein may be involved in fat oxidation, non-oxidative glucose metabolism, and the regulation of energy expenditure. This protein is downregulated in prediabetic and type 2 diabetes mellitus patients. Certain allelic variations in this gene increase the risk of the development of obesity. Three transcript variants encoding different isoforms have been found for this gene.
peroxisome proliferator-activated receptor gamma, coactivator 1 beta
, peroxisome proliferator-activated receptor gamma coactivator 1-beta-like
, ERR ligand 1
, PPAR gamma coactivator-1beta protein
, PPAR-gamma coactivator 1-beta
, peroxisome proliferator-activated receptor gamma coactivator 1 beta
, peroxisome proliferator-activated receptor gamma coactivator 1-beta
, peroxisome proliferative activated receptor, gamma, coactivator 1 beta
, peroxisome proliferator-activated receptor gamma coactivator 1beta-2a
, PGC-1-related estrogen receptor alpha coactivator