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anti-Human CPT1A Anticorps:
anti-Mouse (Murine) CPT1A Anticorps:
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Human Polyclonal CPT1A Primary Antibody pour IHC (p), IHC - ABIN251677
Rayner, Esau, Hussain, McDaniel, Marshall, van Gils, Ray, Sheedy, Goedeke, Liu, Khatsenko, Kaimal, Lees, Fernandez-Hernando, Fisher, Temel, Moore: Inhibition of miR-33a/b in non-human primates raises plasma HDL and lowers VLDL triglycerides. dans Nature 2011
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Cow (Bovine) Polyclonal CPT1A Primary Antibody pour IHC, WB - ABIN2782010
Roomets, Kivelä, Tyni: Carnitine palmitoyltransferase I and Acyl-CoA dehydrogenase 9 in retina: insights of retinopathy in mitochondrial trifunctional protein defects. dans Investigative ophthalmology & visual science 2008
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Human Polyclonal CPT1A Primary Antibody pour IF, WB - ABIN6678597
Yang, He, Yao, Tan, Zhu, Li, Guo, Wei: Regulation of AMPK-related glycolipid metabolism imbalances redox homeostasis and inhibits anchorage independent growth in human breast cancer cells. dans Redox biology 2018
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Human Polyclonal CPT1A Primary Antibody pour ELISA, WB - ABIN545294
Cook, Park: Expression and regulation of carnitine palmitoyltransferase-Ialpha and -Ibeta genes. dans The American journal of the medical sciences 1999
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Human Polyclonal CPT1A Primary Antibody pour IF (p), IHC (p) - ABIN677018
Fan, Wang, Ge, Wang, Li, Kong: Betaine supplementation protects against high-fructose-induced renal injury in rats. dans The Journal of nutritional biochemistry 2014
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Human Polyclonal CPT1A Primary Antibody pour IF, WB - ABIN6138976
Ni, He, Dai, Yao, Guo, Wei: Oroxylin A suppresses the development and growth of colorectal cancer through reprogram of HIF1α-modulated fatty acid metabolism. dans Cell death & disease 2018
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Human Polyclonal CPT1A Primary Antibody pour IHC (p), WB - ABIN5553254
Patsoukis, Bardhan, Chatterjee, Sari, Liu, Bell, Karoly, Freeman, Petkova, Seth, Li, Boussiotis: PD-1 alters T-cell metabolic reprogramming by inhibiting glycolysis and promoting lipolysis and fatty acid oxidation. dans Nature communications 2015
Mouse (Murine) Polyclonal CPT1A Primary Antibody pour ELISA - ABIN451728
Mazzarelli, Pucci, Bonanno, Sesti, Calvani, Spagnoli: Carnitine palmitoyltransferase I in human carcinomas: a novel role in histone deacetylation? dans Cancer biology & therapy 2008
Human Polyclonal CPT1A Primary Antibody pour IHC (p), ELISA - ABIN547754
Pocai, Lam, Obici, Gutierrez-Juarez, Muse, Arduini, Rossetti: Restoration of hypothalamic lipid sensing normalizes energy and glucose homeostasis in overfed rats. dans The Journal of clinical investigation 2006
A reversible carnitine palmitoyltransferase (CPT1) inhibitor offsets the proliferation of chronic lymphocytic leukemia cells.
Data show that PPAR coactivator-1alpha (PGC1alpha) and CCAAT/enhancer binding protein beta (CEBPB) form a complex and bind to the promoter of carnitine palmitoyl transferase 1 A (CPT1A).
CPT1A methylation level is associated with body mass index in late gestation.
Targeting CPT1A could be a beneficial regimen to improve the therapeutic effects of radiotherapy in NPC patients.
CPT1 is associated with anabolic processes that support healthy mitochondrial function and cancer cell proliferation independent of fatty acid oxidation.
CPT1A-mediated FAO activation induces CRC cells to resist anoikis.
Targeted analysis of DNA methylation array revealed the mesenchymal stem cells in infants born to obese mothers had hypermethylation in genes regulating Fatty Acid Oxidation (PRKAG2, ACC2, CPT1A, SDHC) and corresponding lower mRNA content of these genes. Moreover, mesenchymal stem cells methylation was positively correlated with infant adiposity.
CPT1A1A contributes to breast cancer-induced invasion and lymphangiogenesis of lymphatic endothelia cells via VEGF-C/VEGF-D/VEGFR-3 signaling.
We demonstrated that inhibition of CPT1 by systemic application of Etomoxir has beneficial effects in the treatment of depression in a highly validated CMS depression model.
These deleterious effects could be partially prevented by MCT-therapy and totally corrected by ETX. Inhibition of CPT1 may be view as a new therapeutic target for patients with a severe form of Mitochondrial Trifunctional Protein deficiency.
the expression of CPT1A was higher in oestrogen receptor (ER)-positive, compared to ER-negative tumours and cell lines. Importantly, overexpression of CPT1A significantly decreased the proliferation and wound healing migration rates of MDA-MB231 breast cancer cells, compared to basal expression control
We review here what is known and not known about the P479L variant and argue that public health action is premature. [review]
High expression level of CPT1A is associated with breast cancer.
The rs80356779, a p.Pro479Leu variant in CPT1A, was highly significantly associated with a range of fatty acid metabolism measures in a population-based sample from Greenland.
associations between methylation in CPT1A and lipoprotein measures highlight the epigenetic role of this gene in metabolic dysfunction.
Homozygosity for the arctic variant is associated with increased risk of infant mortality, which may be mediated in part by an increase in infectious disease risk. Further studies are needed to determine whether the association we report represents a causal association between the CPT1A arctic variant and infectious disease-specific mortality
We provide evidence that the downregulation of hsa-miR-124-3p, hsa-miR-129-5p and hsa-miR-378 induced an increase in both expression and activity of CPT1A, CACT and CrAT in malignant prostate cells.
The recent findings and the current understanding of fatty acid oxidation and CPT1A in cancer have been summarized thus providing theoretical basis for this enzyme as an emerging potential molecular target in cancer therapeutic intervention. (Review)
Methylation of a CpG site in CPT1A is associated with circulating adiponectin levels, likely in an obesity-dependent manner, in three population-based adult cohorts of European descent.
Furthermore, given the already low abundance of Cpt1b in white adipose tissue, it is unlikely that decreases in its expression can quantitatively decrease whole body energy expenditure enough to contribute to an obese phenotype.
acetate is the primary product of hepatic mitochondrial beta-oxidation in Sus scrofa and that regulation during early development is mediated primarily via kinetic modulation of CPT I
This study evaluated the effects of nonesterified fatty acids and glucose on carnitine palmitoyltransferase-I (CPT-I) mRNA expression in cultured bovine hepatocytes using real-time reverse transcription polymerase chain reaction and ELISA methods.
It was conclude that suppression of CPT activity by positive energy balance appears to be specific for the liver in mid-lactating dairy cows.
these data demonstrate that while exercise-induced mitochondrial-derived ROS does not influence CPT-I substrate sensitivity, it inhibits ADP sensitivity independent of P-CoA. These data implicate mitochondrial redox signaling as a regulator of oxidative phosphorylation.
Concurrent exercise improves insulin resistance and nonalcoholic fatty liver disease by upregulating PPAR-gamma, CPT-1A and Mcad activities.
Alogliptin increased hepatic mRNA expression levels associated with fatty acid oxidation. In addition, the results of the present study suggested that ALO promotes CPT1a expression via Thr172 phosphorylation of AMPKalpha.
beneficial effects of muscle CPT1mt expression suggest that a direct modulation of the malonyl-CoA/CPT1 partnership in skeletal muscle could represent a potential strategy to prevent obesity-induced insulin resistance
The data suggest that AMPK is not required for the regulation of the intermediate filament interaction with CPT-I during exercise.
These results suggest that n-3 polyunsaturated fatty acids could improve lipid oxidation-related enzymes in liver subjected to hemorrhagic shock/resuscitation.
these results demonstrated that L-carnitine ameliorated liver inflammation and serum pro-inflammatory markers in cancer cachexia through regulating CPT I-dependent PPARg signaling
-Carnitine exerts its ameliorative effects in cancer cachexia in association with the PPAR-gamma signaling pathway.
Data show that peroxisome-proliferator-activated receptor beta/delta (PPARbeta/delta) activation restored the lipid-induced endothelial dysfunction by up-regulation of carnitine palmitoyltransferase)-1 (CPT-1).
Our results indicated that exercise-induced CPT1b expression was at least in part mediated by HDAC5/MEF2A interaction.
Data indicate that muscle mutated carnitine palmitoyltransferase 1 (CPT1mt) expression enhanced mitochondrial fatty acid oxidation (mFAO) capacity.
Potential epigenetic mechanisms underlying transcriptional regulation of Cpt1alpha in hepatic steatosis occur in response to binge ethanol administration.
an environment-dependent structural switch underlies the regulation of carnitine palmitoyltransferase 1A
miR-370 acting via miR-122 may have a causative role in the accumulation of hepatic triglycerides by modulating initially the expression of SREBP-1c, DGAT2, and Cpt1alpha.
Results show that CREB and HNF4alpha bind the CPT promoter, that PGC-1 is involved in liver carnitine palmitoyltransferase I (CPT) gene activation by cylic AMP, and that PGC-1 acts to coordinate the process of metabolic adaptation in the liver.
role of thyroid hormone response unit formed between the promoter and first intron in mediating liver-specific induction by thyroid hormone
Malonyl-CoA/CPTI interaction is a component of a metabolic signaling network that controls insulin secretion.
modulation of CPT1A expression by PI3K-dependent signaling is the major mechanism by which cells suppress beta-oxidation during anabolic growth
These results suggested that astaxanthin promoted lipid metabolism rather than glucose utilization during exercise via CPT I activation, which led to improvement of endurance and efficient reduction of adipose tissue with training.
The mitochondrial oxidation of long-chain fatty acids is initiated by the sequential action of carnitine palmitoyltransferase I (which is located in the outer membrane and is detergent-labile) and carnitine palmitoyltransferase II (which is located in the inner membrane and is detergent-stable), together with a carnitine-acylcarnitine translocase. CPT I is the key enzyme in the carnitine-dependent transport across the mitochondrial inner membrane and its deficiency results in a decreased rate of fatty acid beta-oxidation. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.
carnitine palmitoyltransferase 1A (liver)
, carnitine O-palmitoyltransferase 1, liver isoform-like
, CPT I
, carnitine O-palmitoyltransferase 1, liver isoform
, carnitine O-palmitoyltransferase I, liver isoform
, carnitine palmitoyltransferase I, liver
, carnitine palmitoyl transferase I liver isoform
, liver type carnitine palmitoyltransferase I
, mitochondrial carnitine palmitoyltransferase 1A
, carnitine palmitoyltransferase 1A
, carnitine palmitoyltransferase I
, carnitine palmitoyl transferase I isoform
, L-CPT I
, carnitine palmitoyltransferase 1, liver
, Carnitine palmitoyltransferase 1 alpha, liver isoform