Ask about this productRelated genes to: GART antibody
- Gene:
- GART NIH gene
- Name:
- phosphoribosylglycinamide formyltransferase, phosphoribosylglycinamide synthetase, phosphoribosylaminoimidazole synthetase
- Previous symbol:
- PRGS, PGFT
- Synonyms:
- GARS-AIRS-GART
- Chromosome:
- 21q22.11
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2017-11-24
Related products to: GART antibody
Related articles to: GART antibody
- Nanoplastic pollution is a serious global concern, which has caused great threat to the human health. However, the relationship between nanoplastic exposure and the development and progression of ulcerative colitis (UC) is still unknown. We established a chronic dextran sulfate sodium (DSS)-induced colitis model with exposure to polystyrene nanoplastics (PS-NPs) and evaluated disease severity, gut inflammation, and intestinal barrier function. The immune microenvironment was assessed using fluorescence multiplex immunohistochemistry (mIHC), while histone lactylation modification was analyzed via western blot and Cleavage Under Targets and Tagmentation (CUT&Tag). Additionally, lipopolysaccharide (LPS)-treated RAW264.7 cells were cultured and intervened to further investigate the molecular mechanism of PS-NPs in colitis. Continuous exposure to PS-NPs exacerbated gut inflammation and damage intestinal barrier function in DSS-induced colitis. PS-NPs exposure is closely correlated with increased macrophage infiltration, enhanced the glycolysis and up-regulated the histone H3 lactylation in macrophages. CUT&Tag analysis showed that PS-NPs influenced the expression of GART via histone H3K18la lactylation. Intervention in histone H3K18la lactylation significantly altered the expression of GART and levels of inflammatory factors in LPS-treated RAW264.7 cells. Downregulating GART expression reduced inflammatory factor levels in RAW264.7 cells treated with LPS plus PS-NPs. PS-NPs exposure exacerbates colitis by upregulating histone H3 lactylation. This study reveals a novel mechanism underlying nanoplastic-exacerbated intestinal injury and provides a direction for future risk assessment of nanoplastics. - Source: PubMed
Publication date: 2026/08/20
Tian ShanHu YugangZou JinhuiHao NanLiu JianLi RuixueLi Jiao - Down syndrome (DS), the most frequent human genetic disorder marked by an extra copy of chromosome 21 (Hsa21) or a portion thereof, leads to physical and cognitive impairments. Following the Lejeune work, researchers focused on a potential anomaly within the folate-mediated one-carbon metabolism (FOCM). Here, we present a FOCM model modified from a previous work with the incorporation of the enzyme cystathionine beta-synthase (CBS), whose encoding gene is located on Hsa21, coupled with the methionine input rate. Systematic perturbation of FOCM enzyme activity rates has been performed to explore possible in silico configurations to simulate the DS condition. The perturbed vs. unperturbed model-derived ratio concentrations of tetrahydrofolate, 5-formyl-tetrahydrofolate, 5-methyl-tetrahydrofolate, S-adenosyl-homocysteine, and S-adenosyl-methionine were compared with the known literature through various statistical approaches. After investigating public transcriptomic databases, the FTS (formate-tetrahydrofolate ligase) perturbation achieved the best overall score. Although the FTS encoding gene (MTHFD1) is not located on Hsa21, it was found to be overexpressed in the DS condition. In addition, an interesting correlation emerged with the PTG (phosphoribosylglycinamide formyltransferase) perturbation and the corresponding encoding gene (GART), located on Hsa21 and notably over-expressed in the DS condition. The model thus identifies key enzyme activities that warrant further investigation. - Source: PubMed
Publication date: 2026/06/26
Piovesan AllisonPoluzzi DilettaRamacieri GiuseppeLocatelli ChiaraAntonaros FrancescaVione BeatriceCaracausi MariaPelleri Maria ChiaraMarchetti Luca - Epigenetic alterations play an increasingly recognized role in carcinogenesis and in the development of resistance to anticancer therapies. Epigenetic enzymes (writers and erasers) and effectors (readers) are largely influenced by the availability of metabolites generated through one-carbon metabolism (OCM), the tricarboxylic acid (TCA) cycle, and acetyl-CoA synthesis (ACS). In this study we examined the expression of epigenetic and metabolic genes to investigate their interplay in cholangiocarcinoma (CCA). - Source: PubMed
Publication date: 2026/06/04
Lopez-Pascual AmayaElurbide JasminValbuena-Goiricelaya EmilianaLatasa M UjueAnaya ElenaAdan-Villaescusa ElenaCastelló-Uribe BorjaMartínez-Pérez Luz AUriarte IkerArechederra MariaCiordia SergioCorrales Fernando JStrnad PavelFrankova SonaSticova EvaFabian OndrejColyn LeticiaInacio PatriciaBayo JuanHuch MeritxellBerasain CarmenFernández-Barrena Maite GAvila Matías A - This study introduces a non-inferiority test, which is based on the method of variance estimates recovery (MOVER), for the odds ratio in two independent binomial populations. In order to address the limitations of existing methods for single binomial proportions, we propose modified asymptotic confidence intervals within the MOVER framework, incorporating asymmetric parameters. We systematically evaluate the type I error control and statistical power of seven MOVER variants (M1-M7) and the Gart adjusted logit test (GAL) in non-inferiority settings. Comprehensive evaluations demonstrate that the M6 achieves optimal performance, maintaining the highest proportion of type I error rates below the significance level while retaining competitive power. When stricter type I error control is prioritized, M5 or M4 provides viable alternatives. Although M7 yields the highest power, its type I error is significantly inflated. The M1-M3 exhibit adequate error control but critically low power, while GAL shows moderate performance. The MOVER-based approach offers enhanced flexibility to accommodate diverse research requirements, with empirical results supporting its practical utility in non-inferiority testing. The proposed tests were illustrated with a real-world example. - Source: PubMed
Publication date: 2026/06/05
Chen HuidaWang DongshengWu YutongHuang ShifuHuang JieLiu HongwenChen YantingChen Chao - Energy homeostasis requires precise coordination between brain-derived appetitive signals and peripheral nutrient-handling mechanisms. Although Neuropeptide F (NPF) and its mammalian homolog NPY are well-established central stimulators of feeding, whether and how they regulate nutrient assimilation in the gut remains unknown. Here, using , we identify a previously unrecognized transcriptional circuit between NPF and the purine synthesis enzyme GART trifunctional enzyme () that governs feeding by controlling gut absorptive efficiency. We show that NPF signaling acts via its receptor NPFR to positively regulate expression specifically within the intestine. Conversely, activity exerts negative feedback on NPF expression, forming a reciprocal regulatory loop. Functionally, gut-specific, but not glial or fat body-specific, is necessary and sufficient for promoting food absorption and consumption. Genetic epistasis experiments demonstrate that acts downstream of NPF to execute its function. Strikingly, peripheral NPF from the fat body and gut, rather than brain-derived NPF, serves as the primary systemic signal driving this loop. Our findings reveal a gut-centered homeostatic module where NPF activates to boost nutrient absorption, while the resultant feeding activity in turn curbs the signal, ensuring calibrated energy intake. This work redefines a canonical neuropeptide's role from a pure behavioral driver to a key regulator of peripheral metabolic efficiency, and establishes a novel framework for understanding gut-brain communication in energy balance. - Source: PubMed
Publication date: 2026/05/21
He LeiWei QinGuo YifeiLi QingqingZhao Zhangwu