CPT1A
- Known as:
- CPT1A
- Catalog number:
- Y213587
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- CPT1A
Related genes to: CPT1A
- Gene:
- CPT1A NIH gene
- Name:
- carnitine palmitoyltransferase 1A
- Previous symbol:
- CPT1
- Synonyms:
- CPT1-L, L-CPT1
- Chromosome:
- 11q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1995-05-30
- Date modifiied:
- 2016-10-05
Related products to: CPT1A
Related articles to: CPT1A
- To determine the impact of low versus atmospheric oxygen tension during only the pre-maturation phase of biphasic capacitation in vitro maturation. - Source: PubMed
Publication date: 2026/04/30
Huynh Kha TNguyen Dung T PLe Anh HKhong Nhu T MPham Toan DNguyen Diem T NNguyen Minh H NLe Ho LLe Tien KHuynh Bao GTruong Nhung HAnckaert EllenSmitz Johan E JGilchrist Robert BHo Tuong MAkin NazliVuong Lan N - Idiopathic pulmonary fibrosis (IPF) is a progressive lung disorder with few effective treatments. This study examines how Krüppel-like factor 14 (KLF14) influences fatty acid oxidation (FAO) and fibroblast senescence in IPF. - Source: PubMed
Publication date: 2026/04/30
Ren JingruiWan RuijieZhou ShuaiMa XinranZhu ChenxiMa JinxinChen JianqiaoZhao LiminWu Wenjuan - Accumulating evidence suggests that the intestinal microbiota participates in the progression of metabolic dysfunction-associated steatotic liver disease (MASLD) through microbiota-host interaction. However, the beneficial role of commensal mycobiota in MASLD progression remains poorly understood. By comparing the gut microbiome differences, we demonstrated that the deficiency of Caspase Recruitment Domain-containing protein 9 (CARD9), an adaptor protein for a microbiota recognition receptor, exacerbated high-fat diet (HFD)-induced MASLD in a gut fungi-dependent manner. CARD9 deficiency reduced the abundance of Saccharomyces cerevisiae (S. cerevisiae), which was a probiotic alleviating MASLD progression. S. cerevisiae promoted a significantly greater abundance of 5-hydroxyindoleacetic acid (5-HIAA) in the intestine through Toll-like receptor 1 (TLR1), which reduced body weight in mice and alleviated MASLD phenotypes via the "gut-liver" axis. Particularly, 5-HIAA directly binds to aryl-hydrocarbon receptor (AhR) and stimulates its nuclear translocation, subsequently inducing fatty acid oxidation via carnitine palmitoyltransferase 1A (CPT1A) and acyl-CoA oxidase 1 (ACOX1) transactivation. MASLD patients exhibited decreased levels of S. cerevisiae and 5-HIAA, and S. cerevisiae effectively reduced hepatic steatosis and improved glucose homeostasis in patients with MASLD. In summary, our findings identified a novel pathway of fungi-S. cerevisiae stimulating intestinal 5-HIAA production and indicated that S. cerevisiae and 5-HIAA might alleviate MASLD progression, highlighting that the mycobiota-dependent gut-liver axis was a promising target for the prevention of MASLD. - Source: PubMed
Publication date: 2026/04/29
Qiao ShupingFan ShuangyaXu JuanXu ZhenPeng ChenQu JunxingBing ZiqianZhou ShizhenShen SunanXu GuifangZhao YueWang Tingting - Papillary thyroid carcinoma (PTC), the most prevalent thyroid malignancy, exhibits aggressive behavior in subsets with metastasis. Despite advances in risk stratification, biomarkers predicting metastatic potential remain limited. Here, we identify lactate as a critical driver of PTC metastasis through lactylation of carnitine palmitoyltransferase 1 A (CPT1A), the rate-limiting enzyme in fatty acid β-oxidation (FAO). Multi-omics profiling of 27 paired PTC tissues revealed elevated lactate levels and FAO activation, corroborated by TCGA data. Functional assays demonstrated that exogenous lactate enhances PTC cell migration via CPT1A-dependent FAO. Mechanistically, lactate upregulated CPT1A transcription by promoting histone H3K18 lactylation (H3K18la), simultaneously stabilized CPT1A protein via lactylation of CPT1A at K180/K285 to suppress its ubiquitin-proteasomal degradation. Genetic or pharmacological inhibition of CPT1A abolished lactate-driven migration and FAO activity. In vivo, lactylation-deficient CPT1A mutants (K180R/K285R) attenuated lung metastasis and subcutaneous tumor growth in nude mice. This study reveals that lactate-CPT1A axis synergistically amplifies FAO to fuel PTC progression, suggesting CPT1A lactylation as a therapeutic vulnerability for metabolic intervention. - Source: PubMed
Publication date: 2026/04/27
Zhao MingjianHan HaifengSun MinLi RuowenChen HuiminLiu FangyuMiao ChengxuWu YongkangShi XiaojiaWu MengtingMaterazzi GabrieleMiccoli PaoloLu JinghuiYue Xuetian - Natural killer (NK) cells are critical for early antiviral immunity, yet their metabolic regulation during acute human viral infection remains incompletely understood. We analyzed NK cell activation and metabolic reprogramming in 47 vaccinated individuals with mild breakthrough SARS-CoV-2 infection and 20 matched healthy control subjects. COVID-19 patients exhibited elevated plasma interferon α and NK cell activation markers (CD69, CD38), alongside increased basal STAT5 phosphorylation, consistent with IL-15-mediated signaling. Functionally, NK cells from infected subjects displayed heightened cytotoxicity. Metabolic profiling at the single-cell level revealed increased cell size, translational activity, amino acid and glucose uptake, and mitochondrial membrane potential, indicating a globally activated metabolic state specific to NK cells. Using newly developed spectral cytometry panels targeting metabolic regulators, we identified CPT1a as the most discriminative marker between patient and control NK cells, with elevated expression in both CD56bright and CD56dim subsets. CPT1a levels correlated with CD38 expression and with uptake of the fluorescent palmitate analog BODIPY-FL C16, reflecting enhanced long-chain fatty acid oxidation. These changes were absent in B and T lymphocytes. Our findings support that during SARS-CoV-2 infection, human NK cells undergo coordinated cytokine-driven activation and metabolic remodeling, integrating glycolysis and lipid oxidation to support amplified effector function. - Source: PubMed
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