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
- This study assessed virological outcomes following genotype-guided antiretroviral therapy (GART). We conducted a retrospective cohort of 235 PLHIV (2021-2023) post-GART after virological failure, analyzing baseline characteristics, 6- and 12-month viral load outcomes, and suppression factors using descriptive statistics, chi-square, Z-test, and ordinal logistic regression. The mean age of participants was 28.0 years, with an average ART duration of 11.2 years. Most (80.4%) were failing on second-line ART, while over half had NRTI (50.2%) or NNRTI (52.8%) mutations; INSTI resistance was rare (1.3%). Following GART initiation, viral suppression (≤200 copies/mL) increased significantly ( < 0.001), reaching 53.3% at 6 months and 62.7% at 12 months. High-level viremia (≥1000 copies/mL) declined from 42.1% to 31.1%, alongside substantial viral load reduction post GART. Multivariable analysis revealed higher odds of high-level viremia among those with two prior regimens (aOR = 13.27, 95% CI: 2.913-80.247, = 0.005), while failing second-line ART significantly reduced odds (aOR = 0.064, 95% CI: 0.005-0.878, = 0.040).The observed modest improvement in viral load suppression at 12-month post GART remained below the 95% UNAIDS target. Expanding GART access, resistance monitoring, adherence support, differentiated care, and affordable testing is essential to strengthen long-term virological control and patient outcomes. - Source: PubMed
Publication date: 2026/09/15
Ankunda CollinsEmunyu JudeNamasambi SharonSserunjogi ConradKyomuhangi BrendahMumbere IvingNakawesi Jane - Spermatogenesis is a tightly regulated process that involves an orchestrated transcriptional and translational event across the seminiferous epithelium. While individual regulators of this process have been studied, the network-level dynamics underlying the transition from spermatogonial stem cells (SSCs) to round spermatids (RSs) remain poorly understood. The dynamic molecular transitions between SSCs and RSs have not been fully characterised, particularly at the network level. Therefore, this study aimed to characterise the molecular and network-level dynamics underlying the transition from SSCs to RSs by integrating transcriptomic profiling, protein-protein interaction network analysis, functional enrichment, and immunohistochemical validation. - Source: PubMed
Publication date: 2026/08/08
Qorbanee AliAzizi HosseinFadhil Alsaffar MarwaSkutella Thomas - 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