Ask about this productRelated genes to: QPRT antibody
- Gene:
- QPRT NIH gene
- Name:
- quinolinate phosphoribosyltransferase
- Previous symbol:
- -
- Synonyms:
- QPRTase
- Chromosome:
- 16p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-11-16
- Date modifiied:
- 2014-11-19
Related products to: QPRT antibody
Related articles to: QPRT antibody
- Acute kidney injury (AKI) is a frequent complication in hospitalized patients, affecting up to 50% of those in intensive care units (ICU). It is linked to high morbidity and mortality, with severity closely tied to patient outcomes. While early biomarkers like KIM1 and NGAL can detect subclinical AKI, their practical benefit is limited, as treatment must begin at suspicion rather than biomarker confirmation. Conversely, when injury exceeds serum creatinine's diagnostic capacity, a "blind spot" emerges, highlighting the need for "supra-clinical" AKI biomarkers. The KDIGO staging system, based on urine output and creatinine, lacks granularity: even in stage 3, outcomes range from full recovery to permanent dialysis. Anuric patients, despite complete loss of filtration, also show heterogeneous recovery, suggesting injury severity influences prognosis. This study aims to explore "supra-clinical" AKI and assess whether further injury occurs beyond current clinical markers using a preclinical ischemia-reperfusion model and human single-cell transcriptomic data. - Source: PubMed
Publication date: 2026/08/26
Serre JustineLegouis DavidPlacier SandrineVerney CharlesDesvarieux WionnaBuob DavidGalichon PierreHadchouel Juliette - Altered tryptophan (Trp) metabolism and disrupted nicotinamide adenine dinucleotide (NAD) synthesis are hallmarks of IBD, yet how intestinal microbiota contribute to these metabolic shifts during intestinal inflammation remains poorly understood. - Source: PubMed
Publication date: 2026/08/11
Wehkamp LinaAlsaadi Abrar IHarris Danielle M MYu MeipingMekdoud TaousBornhäuser JohannaSpringer EvaGilloteau ClaraPothakamury Anant ASmith Jaclyn DJenkins Brenita CGuggeis MartinaSommer FelixWaschina SilvioRosenstiel PhilipSchreiber StefanMcReynolds Melanie RAden Konrad - Breast cancer heterogeneity presents a significant challenge for effective diagnosis and treatment. A deeper understanding of the tumor microenvironment (TME) and its metabolic dynamics is essential for addressing this complexity. This study explored the interplay between TME components and metabolic profiles in breast cancer using RNA sequencing data from both bulk and single-cell analyses. - Source: PubMed
Publication date: 2026/06/22
Huang ZhongLin ShuhuiLiang YingKhan MuhammadChen WeiruiLi XuefengLiu XiaolanWu YunyuYe Jiacai - ELOC-mutated renal cell carcinoma (RCC) is a rare tumor with only ∼40 cases reported to date; it shares a molecular background with clear cell RCC (ccRCC) in terms of hypoxia-inducible factor-alpha (HIF-α) protein accumulation. ELOC-mutated RCC is characterized by prominent leiomyomatous stromal growth and a more indolent clinical course compared with ccRCC. In our previous study, whole-genome sequencing of 102 ccRCC cases identified 5 cases of ELOC-mutated RCC. In the present study, we conducted proteomic and immunohistochemical analyses on up to 13 Japanese ELOC-mutated RCCs, including 8 previously reported cases, to elucidate its distinct molecular mechanisms and identify biomarkers that may be useful in distinguishing ELOC-mutated RCC from ccRCC. Proteomic profiling revealed that molecules, including cytokeratin 7, scinderin (SCIN), and sortilin 1 (SORT1), were significantly overexpressed in ELOC-mutated RCC compared with ccRCC. Notably, SCIN and SORT1 emerged as novel potential diagnostic biomarkers for distinguishing ELOC-mutated RCC from ccRCC. The analysis further suggested that ELOC-mutated RCC relies more on oxidative phosphorylation and less on glycolysis than ccRCC. This metabolic shift may be linked to the relative depletion of NAD+ due to the low expression of NAPRT and QPRT. In addition, we observed geographic variation in the disease frequency among different cohorts, with a higher frequency in Japan. Our findings provide novel insights into the pathogenesis of ELOC-mutated RCC and highlight SCIN and SORT1 as potential supportive biomarkers. - Source: PubMed
Publication date: 2026/07/13
Fukagawa AkihikoArai YasuhitoMaeshima AkikoHama NatsukoTotoki YasushiNakamura HiromiSaito-Adachi MihokoHokazono YukioNakamura EijiroMatsui YoshiyukiAdachi ShungoHamamoto RyujiUshiku TetsuoYachida ShinichiShibata Tatsuhiro - Colorectal cancer (CRC) is characterized by molecular heterogeneity, with BRAF-mutated tumors being particularly aggressive and refractory to standard therapies. This study aimed to identify distinctive proteomic signatures associated with the BRAF V600E mutation through comparative tumor tissue profiling. Thirty-three tumor tissues were analyzed: 9 BRAF-mutated, 14 RAS-mutated, and 10 wild-type (WT). Proteomic profiling was performed on formalin-fixed, paraffin-embedded (FFPE) tissues using bottom-up LC-MS/MS in a data-independent acquisition mode. Protein identification and relative expression were achieved by using DIA-NN label-free analysis. Group differences were evaluated through multiparametric analyses, and Cox proportional hazard models were applied to identify proteins associated with overall survival. BRAF-mutated tumors showed distinct proteomic alterations, including overexpression of dipeptidyl peptidase 4 (DPP4) and lysophosphatidylcholine acyltransferase 1 (LPCAT1) alongside the downregulation of quinolinic phosphoribosyltransferase (QPRT) involved in NAD+ biosynthesis. Pathway analysis revealed the enrichment of protein folding associated with endoplasmic reticulum (ER) stress. Prognostic accuracy improved when tumor genotype was combined with the expression of activator of HSP90 ATPase activity 1 (AHSA1) and thioredoxin domain-containing 5 (TXNDC5), involved in ER-associated protein folding. These findings define a distinctive proteomic signature in BRAF-mutated CRC, characterized by dysregulated protein folding associated with ER stress and supporting the development of targeted therapies and more precise prognostic models. - Source: PubMed
Miolo GianmariaMarus WallyCanil GiovanniInversi AmyPuglisi FabioCorona Giuseppe