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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 increases the expression of mTOR and p-mTOR at the site of Ser2448, and the stimulation of Abeta is likely to depend on sirtuin 1, PPARgamma, and PGC-1beta pathway in regulating mTOR expression.
MyoD regulates the oxidative metabolic capacity of adult skeletal muscle;ChIP-seq analysis identified MyoD binding on the PGC-1b, but not PGC-1a, gene locus;MyoD cooperates with alternative NF-kappaB to regulate PGC-1b transcription; MyoD and RelB 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-1b inhibited downstream inflammatory signals via binding with TAB1 and thus preventing TAB1/TAK1 binding and TAK1 activation.
the anti-inflammatory environment in muscle promoted by the PGC-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
PGC1beta represses proangiogenic genes and stimulates antiangiogenic genes in muscle ischemia. PGC1beta inhibits neoangiogenesis and blocks ischemic revascularization.
The data indicate a novel detrimental age-dependent role of PPAR beta/delta in Alzheimer disease by increasing pro-BDNF and decreasing BDNF/TrkB survival pathways.
The results highlight a novel function for SYVN1 in the control of body weight and mitochondrial biogenesis through negative regulation of PGC-1b.
PGC-1beta in the gut acts as an adaptive self-point regulator, capable of providing a balance between enhanced mitochondrial activity and protection from increased ROS production
Fisetin regulates the expression of hepatic lipid metabolism genes by downregulating miR-378 and the host gene PGC-1beta.
Our aim was to assess the role of PGC-1 coactivators during postnatal cardiac development and in adult hearts in mice.
Gene expression profiling of PGC-1alphabeta(-/-) hearts revealed reduced expression of the gene encoding CDP-diacylglycerol synthase 1 (Cds1), an enzyme that catalyzes the proximal step in CL biosynthesis.
PGC-1 beta is Critical for electron transport chain Capacity
Hepatic-specific action of PGC-1beta regulates lipid synthesis and secretion, as well as mitochondrial biogenesis and function.
PGC-1beta plays dual roles in regulating hepatic fatty acid metabolism by controlling the expression of programs of genes involved in both fatty acid oxidation and de novo fatty acid synthesis.
the KAT4 promoter was significantly activated by the transcriptional factors, NFE2related factor 2 and peroxisome proliferatoractivated receptor coactivator 1beta, which are targets of Syvn1induced degradation
Incrementally paced murine Pgc1beta(-/-) hearts show pro-arrhythmic atrial phenotypes that are age dependent.
Insulin-like growth factor 1 receptor, associate of Myc 1, and peroxisome proliferator-activated receptor gamma coactivator 1beta are direct targets of miR-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 and IL-1beta expression
the forkhead box O3 (FOXO3)/liver kinase B1 (LKB1)/AMP-activated protein kinase/peroxisome proliferator-activated receptor-gamma co-activator-1beta (PGC-1beta)/pyruvate dehydrogenase-A1 pathway is essential for CD44 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-overexpression and PGC-1beta. PGC-1beta knockdown impairs HER2-overexpressing cells proliferation acting on ERRalpha 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-tagged PPARGC1B coprecipitated more intensely with ERalpha in the +102525A than the +102525G construct after 17beta estradiol treatment
Data suggest that PGC-1alpha and PGC-1beta could play a role in regulating retina cell survival, and may be therapeutic targets to prevent retinal degeneration.
PGC-1(beta) and estrogen-related receptor alpha are aberrantly expressed in human colon cell lines and tumors.
RUNX3 is related to both the severity of AS and the function of daily life. PPARGC1B is related to the function of daily life.
Data show that PGC-1beta protein mediated the expression of proinflammatory cytokines and apoptosis through extracellular signal-regulated kinase (ERK), p38 and NF-kappaB in rheumatoid arthritis fibroblast-like synoviocytes.
Variation in the PPARGC1B gene may be associated with type 2 diabetes among middle-aged Chinese men and women.
cell apoptosis is orchestrated by the balance between several signaling pathways, and PGC-1beta takes part in these events in breast cancer cells mediated by the mTOR signaling pathway.
PPARgamma and PPARGC1B polymorphisms modulate the association between phthalate exposure and BC risk
DNA polymorphisms of PPARGC1B, coding a bona fide ER co-activator, are associated with ER-positive breast cancer risk.
PGC-1b, a coactivator of both LXR-alpha and SREBP-1, was markedly down-regulated by OEPAs compared with EPA.
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