Ask about this productRelated genes to: LYCAT antibody
- Gene:
- LCLAT1 NIH gene
- Name:
- lysocardiolipin acyltransferase 1
- Previous symbol:
- LYCAT
- Synonyms:
- FLJ37965, ALCAT1, AGPAT8
- Chromosome:
- 2p23.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-10-28
- Date modifiied:
- 2014-11-19
Related products to: LYCAT antibody
Related articles to: LYCAT antibody
- This study confirmed that low-temperature, high-salinity depuration mitigates apoptosis and preserves quality in anhydrously stored Pacific oysters through targeted suppression of cardiolipin oxidation. We compared standard depuration (20 °C, 31‰) with low-temperature, high-salinity depuration (12 °C, 38‰). After five days, the latter maintained 30% higher survival, preserved glycogen and ATP equivalents, and sustained texture through suppressed serine protease activity. Integrated lipids and molecular index revealed that low-temperature, high-salinity depuration stabilized 23 cardiolipin (CL) molecular species, inhibited polyunsaturated fatty acid oxidation, and limited oxidized cardiolipin (oxCL) formation. These effects coincided with the down-regulation of pro-apoptotic genes (Bcl-2-associated X protein (Bax), Cytochrome c (Cyt-c), Caspase-3 (Casp3)) and the up-regulation of anti-apoptotic (B-cell Lymphoma 2 (Bcl-2), Heat shock protein 70 (Hsp70)) and cardiolipin synthase (Cls), Lysocardiolipin acyltransferase 1 (Lclat1)) genes, reducing mitochondrial reactive oxygen species, swelling, and mitochondrial permeability transition pore opening. Combined with time-lag correlation analysis and mediation effect analysis confirmed an oxCL-apoptosis-quality axis. Thus, low-temperature, high-salinity depuration safeguards mitochondrial integrity, delays apoptosis, and prolongs shelf life, offering a practical strategy for live oyster transport. - Source: PubMed
Publication date: 2026/07/30
Meng NanCao XinyuSong YuCong PeixuLiu YanjunLiu YiXue ChanghuXu Jie - To preliminarily elucidates the role of EBNA1 in epigenetically regulating miR-127-5p and influencing the proliferation, apoptosis, and metabolism of Burkitt's lymphoma (BL) cells. - Source: PubMed
Wang Shun-YongWang YanLi Han-JingCao Huo-LiangZheng Qiang-QiangHuang Bing-YuQiu Chen-XiChen Ning-NingFu Hai-Ying - BackgroundEmbryonal tumor with multilayered rosettes (ETMR) is an aggressive pediatric brain tumor that carries a poor prognosis, and there is currently no standard of care. Dysregulated mitochondrial bioenergetics and dynamics have been associated with the progression of diverse cancers. Cardiolipins are mitochondrial-specific lipids, and their fatty acid composition has been shown to regulate mitochondrial structure and function. Despite the known functional significance of cardiolipins, their structure-specific accumulation in relation to mitochondrial phenotypes in ETMR remains ill-defined. - Source: PubMed
Publication date: 2025/10/21
Liapis EvangelosMaas AllisonO'Neill Kelly CPonzoni AdeleLozy TaraPamreddy AnnapurnaCozzi Francesca MHarris Brent THanson DerekCarter Claire L - Cardiometabolic phenotypes such as obesity and impaired insulin action are key determinants of type 2 diabetes (T2D). Growing evidence highlights the postprandial state as a critical window in metabolic regulation, where epigenetic mechanisms, particularly DNA methylation in insulin-sensitive tissues, may play pivotal roles. However, their dynamics across prandial states in subcutaneous adipose tissue (SAT) remain unclear. We analyzed genome-wide DNA methylation in paired fasting and postprandial SAT biopsies from 29 asymptomatic, drug-naïve individuals classified as controls ( = 8), prediabetes = 9), or T2D ( = 12). Postprandial samples followed a standardized mixed-meal test. DNA methylation was quantified using the Illumina MethylationEPIC array and analyzed through the Chip Analysis Methylation Pipeline (ChAMP) pipeline. Differential methylation was more pronounced postprandially, especially in the T2D group. After adjusting for age and sex, 4599 differentially methylated CpG sites (DMCs) were identified, with increased hypermethylation in T2D. A total of 130 DMCs across 99 genes, including , , , and , were shared by prediabetes and T2D groups. Over-representation analysis revealed 202 enriched pathways related to insulin resistance, AMPK signaling, and immune responses. Additionally, 110 Differentially Methylated Regions (DMRs), including and , were detected. These findings reveal early, prandial-dependent epigenetic alterations in SAT that precede overt dysglycemia, offering insights into personalized prevention in T2D. - Source: PubMed
Publication date: 2025/11/22
Escalante-Araiza FabiolaMartínez-Hernández AngélicaGarcía-Ortiz HumbertoHuerta-Ávila EiraVillafan-Bernal José RafaelContreras-Cubas CeciliaCenteno-Cruz FedericoGemm Family Study Nava-González Edna JCarrillo-Ruiz José DamiánRodriguez-Ayala ErnestoBastarrachea Raúl ABarajas-Olmos FranciscoOrozco Lorena - Congenital heart defects (CHDs) occur in 50-75% of patients with 22q11.2 deletion syndrome (22q11.2DS), ranging from mild to severe manifestations. The genetic and environmental factors contributing to variable CHD phenotypes in 22q11.2DS are largely unknown. In this study, we used a mouse model of 22q11.2DS, termed Df1/+, to evaluate the effect of maternal vitamin A (VitA) dietary imbalance (supplementation or deficiency) on the incidence of aortic arch defects (AADs), which is a common type of CHD observed in both 22q11.2DS patients and Df1/+ mouse embryos. While most groups showed a previously observed 30% AAD incidence, two groups exhibited significantly higher rates: (1) Df1/+ embryos from WT mothers on a VitA-Supl diet (51% AADs) and (2) Df1/+ embryos from Df1/+ mothers on a VitA-Def diet (45% AADs). Thus, a low or high maternal VitA diet can increase the frequency of AADs in embryos depending on the maternal genotype. Transcriptomic analysis of the hearts of these high-risk embryos at embryonic day (E)18.5 revealed downregulation of key genes (, , , and ) associated with energy metabolism pathways, such as oxidative phosphorylation and glycolysis, suggesting impaired cardiac recovery mechanisms. In conclusion, our findings demonstrate that altered VitA exposure can exacerbate AAD incidence in a maternal-genotype-dependent manner, highlighting the complex interplay between embryonic and maternal genetic background and environmental factors in CHDs associated with 22q11.2DS. - Source: PubMed
Publication date: 2025/10/30
Amengual-Cladera EmiliaLlull-Alberti Maria VictòriaVentayol-Guirado MarcJimenez-Barcelo Juan AntonioRocha Jairo EnriqueMuncunill JosepHernandez-Rodriguez JessicaMedina-Chávez DanielaLynton-Pons ElionorSureda-Horrach PaulaAsensio Victor JoseRuiz-Guerra LauraTubau AlbertJuan-Clar MiguelBilio MarchesaMorrow BerniceVives-Bauzà CristófolLania GabriellaIllingworth ElizabethBaldini AntonioHeine-Suñer Alexander Damian