HPRT1 (Hypoxanthine Phosphoribosyltransferase 1)

Our findings suggest that MBZ modulates nucleotide synthesis pathways, contributing to its selective antiproliferative effects in GC cells. This study highlights potential new pharmacological targets for drug repurposing and further investigation into the broader therapeutic applications of MBZ.

Our study established a NM-related gene signature closely linked to immune microenvironment and drug sensitivity, highlighting potential biomarkers and therapeutic targets for prognosis and personalized therapy in HNSCC.

This study highlights the potential of 3D culture systems to elucidate context-specific mechanisms of metabolic regulation, such as the suppressive effect of HPRT1 on carnosine production. Our findings demonstrate that metabolic phenotypes observed in 2D cultures may not fully capture the complexity of in vivo metabolism, whereas 3D models can reveal regulatory pathways that are otherwise overlooked, including context-dependent regulation of carnosine metabolism by HPRT1.

MiR-193b-3p targets and downregulates HPRT1. Overexpression of HPRT1 reverses the suppressive effects caused by JHDM1D-AS1 depletion on CRC cell malignancy. In conclusion, JHDM1D-AS1 promotes CRC cell proliferation, metastasis, invasion and tumor development by upregulating HPRT1 expression via miR-193b-3p.

Furthermore, IGFBP3 exerts neuroprotective effects against MPP+ toxicity, likely mediated through the activation of PI3K/Akt/GSK3β pathway and inhibition of apoptosis. IGFBP3 warrants further investigation as a diagnostic biomarker and therapeutic target for PDD, necessitating future validation in larger cohorts and in vivo models.

qPCR of cfDNA from patients with neuroblastoma revealed differences in the stability of various reference genes. Prioritizing reference genes with better stability may facilitate more accurate detection of intergroup differences in the samples.

Instead, we recommend the use of GUSB and HMBS as a stable reference gene pair. These are expressed at a suitable level for accurate normalisation of biomarker expression using dPCR.

Myositis following BV therapy has not been reported. Findings suggest an immune-mediated mechanism with B-cell involvement. Given the response to IVIG, B-cell-directed therapies may be beneficial. This case identifies BV-induced myositis as a novel irAE.

This study successfully identified seven signature MRDEGs as significant diagnostic biomarkers for MASH. The findings not only offer novel strategies for non-invasive diagnosis of MASH but also highlight the substantial role of immune cell infiltration in the progression of MASH.

Furthermore, in vitro human HPRT inhibition assay confirmed and revealed inhibitory potential for Gibberellin A34 (Ki 0.121 µM) and Chasmanthin (Ki 0.368 µM), as compared to standard inhibitor, HGPRT/TBrHGPRT1-IN-1 (Ki 0.032 µM). Overall, these results strongly recommend further experimental work concerning these plant-based molecules as human HPRT inhibitors for anticancer drug development.

Analysis of RNA expression over time showed that PPIB, which has the highest signal, was the most degraded in both adjusted transcript and H-score quantification methods (R2 = 0.35 and R2 = 0.33, respectively). This proves that although the RNAscope probes are designed to detect fragmented RNA, performing a sample quality check using HKGs is strongly recommended to ensure accurate results.

Cisplatinum nephrotoxicity was conducted in rat model via an oral dose of (2 mg/kg BW) for one month furthermore a comparative study was conducted among TiNPs-loaded Cisplatinum and Lactoferrin loaded Cisplatinum. Loaded drug delivery system counteracted Cisplatinum triggered nephrotoxicity via controlling autophagy and apoptotic XBP, CHOP, HPRT, FKBP, C-myc, P53 and TNF-α signaling pathway.