Protein phosphorylation plays a fundamental role in most of the cellular regulatory pathways. Experimental detection of protein phosphorylation sites is labour intensive and often limited by the availability and optimisation of enzymatic reactions. The in silico prediction of phosphorylation sites using protein's primary sequences may provide guidelines for further experimental consideration and interpretation of phosphoproteomic data. An array of such tools exists over the internet and provides the prediction for protein kinase families. We developed an independent dataset to compare the performances of these methods to provide scientists with a better understanding of which method to use for their research.
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http://dx.doi.org/10.1504/IJBRA.2009.022461 | DOI Listing |
J Vis Exp
January 2025
Institute of Biochemistry and Molecular Biology, Hengyang Medical School, University of South China; National Health Commission Key Laboratory of Birth Defect Research and Preventio, Hunan Provincial Maternal and Child Health Care Hospital;
Both DNA replication and RNA transcription utilize genomic DNA as their template, necessitating spatial and temporal separation of these processes. Conflicts between the replication and transcription machinery, termed transcription-replication conflicts (TRCs), pose a considerable risk to genome stability, a critical factor in cancer development. While several factors regulating these collisions have been identified, pinpointing primary causes remains difficult due to limited tools for direct visualization and clear interpretation.
View Article and Find Full Text PDFJ Cancer Res Clin Oncol
January 2025
Key Laboratory of Laboratory Medicine, Ministry of Education of China, School of Laboratory Medicine and Life Sciences, Wenzhou Medical University, Wenzhou, 325035, Zhejiang, China.
Purpose: Growing evidence suggests that the tyrosine phosphatase SHP2 is pivotal for tumor progression. Triple-negative breast cancer (TNBC) is the most lethal subtype of breast cancer, characterized by its high recurrence rate, aggressive metastasis, and resistance to chemotherapy. Understanding the mechanisms of tumorigenesis and the underlying molecular pathways in TNBC could aid in identifying new therapeutic targets.
View Article and Find Full Text PDFMol Biol Cell
January 2025
Department of Cell Biology, Emory University, 615 Michael St, Atlanta, GA, USA, 30322.
Rare inherited diseases caused by mutations in the copper transporters (CTR1) or induce copper deficiency in the brain, causing seizures and neurodegeneration in infancy through poorly understood mechanisms. Here, we used multiple model systems to characterize the molecular mechanisms by which neuronal cells respond to copper deficiency. Targeted deletion of CTR1 in neuroblastoma cells produced copper deficiency that produced a metabolic shift favoring glycolysis over oxidative phosphorylation.
View Article and Find Full Text PDFAppl Environ Microbiol
January 2025
Joint Degree Program of Kasetsart University and Yamaguchi University, Graduate School of Science and Technology for Innovation, Yamaguchi University, Yamaguchi, Japan.
Unlabelled: Incomplete oxidation of glucose by sp. strain CHM43 produces gluconic acid and then 2- or 5-ketogluconic acid. Although 2-keto-D-gluconate (2KG) is a valuable compound, it is sometimes consumed by itself via an unknown metabolic pathway.
View Article and Find Full Text PDFElife
January 2025
Centre for Cellular Biology and Signalling, Zhejiang University-University of Edinburgh (ZJU-UoE) Institute, Haining, China.
Mitochondrial dysfunction is involved in numerous diseases and the aging process. The integrated stress response (ISR) serves as a critical adaptation mechanism to a variety of stresses, including those originating from mitochondria. By utilizing mass spectrometry-based cellular thermal shift assay (MS-CETSA), we uncovered that phosphatidylethanolamine-binding protein 1 (PEBP1), also known as Raf kinase inhibitory protein (RKIP), is thermally stabilized by stresses which induce mitochondrial ISR.
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