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Differentially Expressed Nedd4-binding Protein Ndfip1 Protects Neurons Against Methamphetamine-induced Neurotoxicity.
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January 2025
Molecular Neuropsychiatry Section, Intramural Research Program, NIH/ NIDA, 21224, Baltimore, MD, U.S.A.
To identify factors involved in methamphetamine (METH) neurotoxicity, we comprehensively searched for genes which were differentially expressed in mouse striatum after METH administration using differential display (DD) reverse transcription-PCR method and sequent single-strand conformation polymorphism analysis, and found two DD cDNA fragments later identified as mRNA of Nedd4 (neural precursor cell expressed developmentally downregulated 4) WW domain-binding protein 5 (N4WBP5), later named Nedd4 family-interacting protein 1 (Ndfip1). It is an adaptor protein for the binding between Nedd4 of ubiquitin ligase (E3) and target substrate protein for ubiquitination. Northern blot analysis confirmed drastic increases in Ndfip1 mRNA in the striatum after METH injections, and in situ hybridization histochemistry showed that the mRNA expression was increased in the hippocampus and cerebellum at 2 h-2 days, in the cerebral cortex and striatum at 18 h-2 days after single METH administration.
View Article and Find Full Text PDFProtective role of ABCC drug subfamily resistance transporters (ABCC1-7) in intestinal inflammation.
Immunol Res
January 2025
Inflammatory Bowel Disease Clinic, Department of Gastroenterology, National Institute of Medical Sciences and Nutrition Salvador Zubirán, Vasco de Quiroga #15, Col. Belisario Domínguez Sección XVI, 14080, Mexico City, CPCDMX, Mexico.
The ABCC subfamily contains thirteen members. Nine of these transporters are called multidrug resistance proteins (MRPs). The MRPs have been associated with developing ulcerative colitis (UC).
View Article and Find Full Text PDFElevated visfatin levels illuminate the inflammatory path in bronchopulmonary dysplasia.
Turk J Pediatr
December 2024
Department of Biochemistry, Faculty of Pharmacy, Ankara University, Ankara, Türkiye.
Background: Bronchopulmonary dysplasia (BPD) is a chronic lung disease in premature infants caused by an imbalance between lung injury and lung repair in the developing immature lungs of the newborn. Pulmonary inflammation is an important feature in the pathogenesis of BPD. The aim of this study was to evaluate the relationship between the inflammatory microenvironment and the levels of visfatin and nesfatin-1, which are among the new adipocytokines, in BPD patients.
View Article and Find Full Text PDFComprehensive analyses reveal the promising value of gasdermins as prognostic biomarkers and immunotherapeutic targets in head and neck squamous cell carcinoma.
Heliyon
January 2025
Department of Medical Oncology, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Guangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and Therapy, Guangdong Provincial Clinical Research Center for Cancer, Guangzhou, 510060, PR China.
Background: In several studies of head and neck squamous cell carcinoma (HNSC), the regulation of tumorigenesis and therapeutic sensitivity by pyroptosis has been observed. However, a systematic analysis of gasdermin family members (GSDMs, including GSDMA/B/C/D/E and PJVK), which are deterministic executors of pyroptosis, has not yet been reported in HNSC.
Methods: We performed comprehensive analyses of the expression profile, prognostic value, regulatory network, and immune infiltration modulation of GSDMs in HNSC on the basis of a computational approach and bioinformatic analysis of publicly available datasets.
Discovery of a potent PROTAC degrader for RNA demethylase FTO as antileukemic therapy.
Acta Pharm Sin B
December 2024
School of Pharmaceutical Science and Technology, Hangzhou Institute for Advanced Study, University of Chinese Academy of Sciences, Hangzhou 310024, China.
The fat mass and obesity-associated protein (FTO) is an RNA demethylase required for catalytic demethylation of -methyladenosine (mA); it is highly expressed and functions as an oncogene in acute myeloid leukemia (AML). Currently, the overarching objective of targeting FTO is to precisely inhibit the catalytic activity. Meanwhile, whether FTO degradation also exerts antileukemic effects remains unknown.
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