GART Mouse Monoclonal Antibody
- Known as:
- GART Mouse Monoclonal Antibody
- Catalog number:
- BIN-002618-M01
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- GART Mouse Monoclonal Antibody
Related genes to: GART Mouse Monoclonal 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 Mouse Monoclonal Antibody
Related articles to: GART Mouse Monoclonal Antibody
- 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 - This study evaluates the time efficiency and safety of Wide Awake Local Anesthesia No Tourniquet (WALANT) compared to general/plexus anesthesia in emergency hand surgery. This single-center, retrospective study analyzed 812 emergency category 2b hand surgeries performed between 2018 and 2024. Patients were divided into 2 groups: local anesthesia (LA), including WALANT, and general/plexus anesthesia. In collaboration with the Institute for Medical Statistics and Biometry, "time to intervention" and postoperative surgical complications were prospectively defined as co-primary endpoints. In addition, a descriptive analysis of the study population was conducted, and a matched-pair analysis was performed to account for injury complexity. Statistical analysis included -tests, Cohen's d, and Gart and Nam's method for risk difference. The mean "time to intervention" was significantly shorter in the LA group (2.2 hours) compared to that in the general/plexus anesthesia group (4.1 hours). Postoperative surgical complication rates were comparable between the LA (8.5%) and general/plexus anesthesia (8.2%) groups, with no significant difference observed. WALANT showed a lower complication rate (5.7%) than LA without epinephrine (9.8%). A matched-pair analysis confirmed these findings. Among the general/plexus anesthesia cases, 16.2% exceeded the recommended 6-hour treatment window, compared to 6.6% in the LA group. Wide Awake Local Anesthesia No Tourniquet facilitates faster treatment of emergency hand surgery cases while maintaining equivalent quality of care compared to general/plexus anesthesia. This study highlights the time efficiency and safety of WALANT in emergency settings, supporting its broader application. - Source: PubMed
Publication date: 2026/04/30
Hohenstein Ayla AMatros RomanNguyen Cam TuFricke MarkEisenhardt Steffen ULeibig Nico - Asthma is a heterogeneous disease characterized by chronic airway inflammation and airway hyperresponsiveness. It represents the most common chronic respiratory condition in children and remains a highly prevalent disorder worldwide. - Source: PubMed
Publication date: 2026/04/11
Dai YunyunYao HefengYang ZihanWang JunyangYin LeyiMao Wei - Leishmaniasis is a vector-borne disease caused by a protozoan parasite of the genus . The infection is transmitted by the bite of infected female sandflies of the genus in the Old World or in the New World. The diagnosis is made by stained smear microscopy, in vitro culture, and DNA-based detection methods. - Source: PubMed
Publication date: 2026/03/18
Al-Jawabreh HananEreqat SuheirAl-Jawabreh AmerDana LinaNasereddin Abedelmajeed - Precision oncology workflows rely heavily on genomic identification of oncogenic driver mutations or the functional loss of tumor suppressors. These pipelines can identify single-agent treatments for patients, but monotherapy is often insufficient and can drive resistance. Recently, functional drug screening has been employed to evaluate tumor-specific drug sensitivities that complement molecular testing. We describe a resistance evaluation after first line exposure (REFLEX) multi-omic paradigm using drug-induced molecular changes to prioritize effective hits from combination screening. In KRAS-mutant cancer models, trametinib treatment caused dysregulation of the purine biosynthetic pathway driven by reductions in enzyme GART. This induced vulnerability nominated purine analog 6-thioguanine as a synergistic partner. Across diverse KRAS-mutant lineages, trametinib-induced GART loss predicts sensitivity to the combination. , the treatment significantly increases overall survival without systemic toxicity. Integrating drug-induced multi-omic changes with functional screening identifies therapeutic strategies, supporting the use of purine analogs with MEK inhibitors for KRAS-mutant tumors. - Source: PubMed
Publication date: 2026/02/07
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