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Our results suggested that the PPARD gene is associated with dynamic balance performance of human being, and further studies to reveal its etiology is strongly suggested.
Data demonstrate that PPARD strongly potentiates multiple tumorigenic pathways to promote colorectal cancer progression and invasiveness.
We show that the PPARb/d inverse agonist PT-S264 impairs transcription initiation by decreasing recruitment of activating Mediator subunits, RNA polymerase II, and TFIIB, but not of TFIIA, to the ANGPTL4 promoter.
Dual activation of peroxisome proliferator-activated receptors alpha and delta improves the efficacy of adoptive cell therapy by reprogramming T-cell metabolism and cytokine expression.
there was no significant link between heterogeneity and expression of PPARD SNP 87 T>C in colorectal cancer
The study indicates a significant association between the G-alleles of PPARD rs3777744 and rs3798343 and a decreased coronary artery disease risk.
PPAR polymorphisms may predict intellectual outcome changes in children treated for medulloblastoma
CHI3L1 ameliorates LPS-induced atherosclerotic reactions via PPARdelta-mediated suppression of inflammation and ER stress.
this study reports two functionally validated cis-regulatory elements in PPARD gene which will aid in understanding its regulation and role in metabolic functions.
increased expression of ALDH1A1-RDH10-RARalpha- PPARbeta/delta pattern could be considered as adverse prognostic factor associated with a higher concentration of paraprotein and worst overall survival of patients with newly diagnosed multiple myeloma.
This review discusses the complex relationship between PPARD in health and disease and highlights our current knowledge regarding the different roles that PPARD plays in metabolism, inflammation, and cancer. [review]
Carriers of rs2016520 PPARD C allele exhibited a significant decrease in Chol through training with an accompanying decrease in TGL. There was also overrepresentation of PPARD rs1053049 TT homozygotes in the group with higher post-training TGL levels
This is a new finding that the PPARD rs7770619 C>T SNP is a novel candidate variant for HTN based on the association between PPARD and plasma MDA in a Korean population.
Low PPARD expression is associated with Prostate Cancer Growth.
Study demonstrates that oleanolic acid, as a natural product, can ameliorate the high glucose-triggered endothelial function by activating the nuclear receptor PPARdelta.
PPARD rs7770619 is a novel candidate variant for impaired fasting glucose and type 2 diabetes and shows association with malondialdehyde levels.
The negative responders for aerobic training are carriers of the PPARD rs2267668 G allele. The best responders to aerobic training are PPARD rs1053049 TT and rs2267668 AA.
The current results suggest that A/A carriers of PPAR-delta SNP (rs2267668) may enjoy fewer beneficial effects of exercise-centered lifestyle intervention on anthropometric indices and blood measurements.
Polymorphism of PPARD is associated with late onset of type 2 diabetes mellitus.
findings suggest that PPARdelta conditions CLL cells to survive in harsh microenvironmental conditions by reducing oxidative stress and increasing metabolic efficiency.
esides hepatoprotective and metabolic beneficial effects, current study showed that elafibranor inhibited the progression of HFD-induced chronic kidney disease (CKD) through activation of renal PPARalpha, PPARdelta, SIRT1, autophagy, reduction of oxidative stress, and apoptosis in mice with steatohepatitis.
PPARD overexpression in villin-expressing gastric progenitor cells results in inflammation, dysplasia, and tumor formation.
These findings implicate PPAR-delta as a regulator of the metabolic program during thymocyte and T cell growth.
METRNL alleviates inflammation and insulin resistance and induces fatty acid oxidation through AMPK or PPARdelta-dependent signaling in skeletal muscle.
PPARbeta/delta has a protective role in melanoma progression and metastasis.
The results confirmed that silencing miR29a induced a decrease in glucose transport and affected lipid metabolism in PAtreated C2C12 cells, and therefore may be involved in insulin resistance by targeting PPARdelta in skeletal muscle.
Deletion of intestinal PPARdelta protects against diet-induced obesity, insulin resistance and dyslipidemia.
Data suggest that interaction of Ppard with Tcptp45 blunts insulin resistance and leads to retention of Tcptp45 in nucleus of hepatocytes, myotubes, and adipocytes; alteration of such interactions may be involved in insulin resistance observed in obesity. (Ppard = peroxisome proliferator activator receptor delta; Tcptp45 = protein tyrosine phosphatase non-receptor type 2 [Ptpn2], 45kDa alternative splicing variant)
CRY1/2 seem to repress a distinct subset of PPAR delta target genes in muscle compared to the co-repressor NCOR1. In vivo, genetic disruption of Cry1 and Cry2 enhances sprint exercise performance in mice.
CD36 is essential for endurance improvement, changes in whole-body metabolism, and efficient peroxisome-proliferator activated receptors (PPAR)-related transcriptional responses in the muscle with exercise training.
Exhaustion of systemic glucose limits endurance exercise. PPARdelta regulates substrate utilization without mitochondrial biogenesis. PPARdelta represses glycolytic genes in muscle to slow glucose consumption. Glucose sparing by PPARdelta dramatically extends running time.
The HFHC diet polarized the liver toward a proinflammatory M1 state, which was reversed by GW1516 intervention. Thus, PPARdelta agonist treatment inhibits the progression of preestablished hepatic steatosis.
data suggested that PPARbeta-regulated PDK1/Akt and E2f signaling that controls metabolism and proliferation is involved in the normal progression of liver regeneration
Since the R6/2 mice represent a 'truncated' huntingtin (Htt) mouse model of Huntington's disease (HD), we tested the efficacy of bezafibrate in a 'full-length' Htt mouse model, the BACHD mice. Bezafibrate treatment restored the impaired PPARg, PPARd, PGC-1a signaling pathway, enhanced mitochondrial biogenesis and improved antioxidant defense in the striatum of BACHD mice
we demonstrated that by modulating mitochondrial energy metabolism through Mfn2 and mitochondrial Ca2+, PPAR-b took an important role in neuronal differentiation induced by flavonoid compound 4a
the metabolic events, controlled by PPARs, occurring during neuronal precursor differentiation, the glucose and lipid metabolism was investigated.
PPAR-delta activation prevents in-stent restenosis and stent thrombosis.
The results demonstrate that PPARdelta-mediated inhibition of ER stress contributes to the vascular benefits of exercise.
this study shows that PPARbeta/delta is an important regulator of mast cell phenotype
Gene expression of the carnitine transporter OCTN2 and carnitine transport are regulated by PPARbeta/delta in bovine cells.
Our results provide novel insights into regulation of PPAR expression in ovarian follicles. We observed that FSH increased mRNA and protein expression of all PPARs isoforms, while LH only increased PPAR alpha and gamma. Steroids like progesterone and estradiol increased expression of PPAR alpha and gamma without affecting the beta isoform, while testosterone had no effect on all PPARs expression.
provide evidence that PPARD G32E is the variation underlying the ear size QTL
study provides evidence for an association between PPARD and backfat thickness.
PPAR profiles in bladder smooth muscle (BSM) may contribute to the susceptibility of BSM to lipotoxicity in the metabolic syndrome.
Overexpression of PPARdelta inhibits myotube formation and also enhances adipocyte differentiation in cultured mouse myoblasts.
Hypothyroidism increased total cholesterol and glycogen content, but reduced triacylglycerol content in the ovary. This was accompanied by a reduction in the expression of PLIN-A, changes in the presence of granules containing oxidative lipids and low PPARdelta expression. The results suggest that hypothyroidism modifies the content and signalling of lipids in the ovary, possibly affecting follicle maturation.
This gene encodes a member of the peroxisome proliferator-activated receptor (PPAR) family. PPARs are nuclear hormone receptors that bind peroxisome proliferators and control the size and number of peroxisomes produced by cells. PPARs mediate a variety of biological processes, and may be involved in the development of several chronic diseases, including diabetes, obesity, atherosclerosis, and cancer. This protein is a potent inhibitor of ligand-induced transcription activity of PPAR alpha and PPAR gamma. It may function as an integrator of transcription repression and nuclear receptor signaling. The expression of this gene is found to be elevated in colorectal cancer cells. The elevated expression can be repressed by adenomatosis polyposis coli (APC), a tumor suppressor protein related to APC/beta-catenin signaling pathway. Knockout studies in mice suggested the role of this protein in myelination of the corpus callosum, lipid metabolism, and epidermal cell proliferation. Alternate splicing results in multiple transcript variants.
, nuclear hormone receptor 1
, nuclear receptor subfamily 1 group C member 2
, peroxisome proliferator-activated nuclear receptor beta/delta variant 2
, peroxisome proliferator-activated receptor beta
, Peroxisome proliferator-activated receptor beta
, peroxisome proliferator-activated receptor delta
, peroxisome proliferative activated receptor, delta
, peroxisome proliferator-activated receptor delta-like
, peroxisome proliferator activated receptor delta
, peroxisome proliferator activator receptor beta
, peroxisome proliferator activator receptor, delta
, peroxisome proliferator activator receptor delta
, peroxisome proliferator activated receptor delta/beta