Ask about this productRelated genes to: ASAHL antibody
- Gene:
- NAAA NIH gene
- Name:
- N-acylethanolamine acid amidase
- Previous symbol:
- ASAHL
- Synonyms:
- -
- Chromosome:
- 4q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-04-13
- Date modifiied:
- 2014-11-19
Related products to: ASAHL antibody
Related articles to: ASAHL antibody
- Long COVID is a complex condition where symptoms persist for more than 3 months after SARS-CoV-2 infection and affects an estimated 5-30% of individuals. While persistent inflammation has emerged as an important feature of this condition, it is unclear if immune responses from COVID-19 vaccination or SARS-CoV-2 re-infection exacerbate or mirror the initial inflammatory responses. - Source: PubMed
Publication date: 2026/04/13
Bansal AmitOlechnowicz Sam W ZKiernan-Walker NicholasCumming JacobAbdul Azeez ImadhMazhari Ramin Cox Rebecca JMueller IvoBowden RoryEriksson Emily M - Fabry disease (FD) is an X-linked lysosomal disorder caused by a deficiency in α-galactosidase A, leading to the accumulation of globotriaosylceramide (Gb3) and lysoGb3. While this accumulation was long seen as the leading cause of symptoms, FD pathogenesis now involves complex mechanisms like autophagy dysregulation, inflammation, oxidative stress, and inter-organelle communication. Cardiovascular diseases (CVD) remain a significant reason for premature death in FD. Gaining a better understanding of cardiac pathophysiology and developing new biomarkers for early detection and monitoring in FD are still essential. In this study, we proposed an FD-CVD protein signature by analyzing the plasma proteome of 55 FD patients, including 18 with CVD and 37 without (woCVD), and 30 non-FD controls. We found 141 altered proteins in FD-CVD compared to FD-woCVD. Among them, 38 differential proteins are related to cardiometabolism. Moreover, ten proteins were identified as potential biomarkers for differentiating FD-CVD from FD-woCVD. The 10-protein signature performed well in RF and partial least squares discriminant analysis models but had limited predictive ability in support vector machine and logistic regression. Importantly, this biosignature demonstrated an ability to classify FD and non-FD controls, regardless of CVD complications, with AUCs greater than 0.90. Using a local interpretable model-agnostic explanation, the RF model interpretation revealed the classification rule for FD-woCVD and highlighted the significance of GDF15, NOS1, CCN5, CTSF, and NAAA. Our findings suggest an early indication of combined cardiac involvement in FD, paving the way for future validation studies that may ultimately inform personalized treatment before irreversible heart damage develops. KEY MESSAGES: Cardiovascular diseases (CVD) remain the leading cause of premature death in Fabry. A ten-protein signature was identified to differentiate Fabry with and without CVD. The protein signature could classify Fabry with controls regardless of CVD status. - Source: PubMed
Publication date: 2026/03/29
Nguyen Thi Hai YenNguyen Quang ThuDucatez FranklinTebani AbdellahNguyen Phuoc LongBekri Soumeya - In East Asia, the root of Glehnia littoralis (J.G.Cooper) F.Schmidt ex Miq. is traditionally used to relieve "yin-deficiency lung dryness," nourishing yin, moistening the lungs, and promoting the generation of body fluids. It is commonly incorporated into decoctions to relieve chronic inflammatory symptoms. However, the primary active constituents and the molecular mechanisms responsible responsible for its anti-inflammatory effects remain insufficiently defined. - Source: PubMed
Publication date: 2026/03/25
Lu LiliXu HaochenZhang GangHe XiwenZhang FangHu FanYang Longhe - Palmitoylethanolamide (PEA) is an endogenous lipid mediator with immunomodulatory actions, yet its effects in skeletal muscle remain poorly defined. We examined whether PEA influences myogenesis and profiled the acute transcriptomic response of differentiated C2C12 myotubes to 10 μM PEA. PEA decreased myotube number (90.3 ± 10.6 vs. 112.6 ± 10.1 control) while increasing nuclear fusion index (37.8 ± 5.7% vs. 30.7 ± 3.2%); myotube area was unchanged. In myoblasts, 24 h PEA increased G/G (48.2 ± 1.2% vs. 42.3 ± 1.9%) and reduced S-phase (21.7 ± 1.2% vs. 25.5 ± 1.2%), consistent with G arrest. RNA sequencing identified 1952 differentially expressed genes enriched for cytokine-receptor interactions and inflammatory signaling. PEA downregulated NF-κB target cytokines while upregulating interferon-related and chemokine genes, indicating an anti-inflammatory/immune-priming profile. N-acylethanolamine acid amidase was highly expressed and induced, whereas fatty acid amide hydrolase remained low and unchanged, suggesting muscle-specific reliance on NAAA metabolism. These data show that PEA biases skeletal muscle toward a less proliferative but more fused and inflammation-resolving phenotype, with transcriptional reprogramming of immune pathways and preferential NAAA engagement. These findings motivate in vivo studies to test whether such actions benefit muscle regeneration, adaptation, or anti-atrophy interventions. - Source: PubMed
Cole Paige LGillham Scott HViggars Mark RClose Graeme LOwens Daniel J - Peripheral injury reprograms metabolism in spinal cord oligodendrocytes, initiating a molecular cascade that drives chronic pain via neuronal β-amyloid (Aβ) release. After injury, mouse spinal oligodendrocytes downregulate myelin protein synthesis and upregulate lipid biosynthesis-but reroute lipids toward neuroplastic remodeling and away from myelin maintenance. This metabolic reallocation disrupts myelin integrity and axonal function, causing neuronal accumulation of amyloid precursor protein, enhanced expression of its processing β-secretase BACE1, and local release of Aβ peptides. Blocking Aβ production or clearing Aβ deposits stops the transition to pain chronicity. Deleting the lysosomal lipid hydrolase NAAA in oligodendrocytes prevents both injury-induced Aβ production and chronic pain development. The findings identify an unexpected mechanistic link between chronic pain and Alzheimer's-like neurodegeneration, positioning Aβ as a target for therapeutic intervention. - Source: PubMed
Publication date: 2026/01/25
Fotio YannickAl Masri SaeedShi ZechuanLe JohnnyDas SudeshnaRubtsova Varvara IMabou Tagne AlexJang CholsoonSwarup VivekPiomelli Daniele