Dynamic interplay between O-glycosylation and O-phosphorylation of nucleocytoplasmic proteins: alternative glycosylation/phosphorylation of THR-58, a known mutational hot spot of c-Myc in lymphomas, is regulated by mitogens.

TL;DR: This paper describes a mass spectrometry-based method for the identification of sites modified by O-GlcNAc that relies on mild β-elimination followed by Michael addition with dithiothreitol (BEMAD), and provides a strategy that uses modification-specific antibodies and enzymes to discriminate between the two post-translational modifications.

TL;DR: Findings indicate that therapeutic strategies targeting N-myc and the IGF pathway might be effective against medulloblastoma.

TL;DR: For the first time, mass spectrometry and immunological methods are combined to perform global exploration of O-GlcNAcylated proteins specific in mitochondria of rat liver and identify some mitochondrial proteins in rat liver that have a role in mitochondrial function.

TL;DR: Relationship between the mRNA expressions of genes coding O-GlcNAc cycling enzymes in breast ductal carcinomas and clinicopathological parameters were analyzed and showed that poorly differentiated tumors had significantly higher OGT expression than grade I tumors, suggesting that elevation in O- GlcNAC modification of proteins may be implicated in breast tumor progression and metastasis.

TL;DR: It is shown that complete inhibition of IMPase has no effect on the morphogenesis of Xenopus embryos and a different hypothesis to explain the broad action of lithium is presented, which suggests that lithium acts through inhibition of glycogen synthase kinase-3 beta (GSK-3beta), which regulates cell fate determination in diverse organisms including Dictyostelium, Drosophila, and Xenopus.

TL;DR: In eukaryotic cells, most proteins in the cytosol and nucleus are degraded via the ubiquitin-proteasome pathway, and the 26S proteasome is a 2-MDa molecular machine built from approximately 31 different subunits, which catalyzes protein degradation.

TL;DR: The c-myc gene was discovered as the cellular homolog of the retroviral v- myc oncogene 20 years ago and found to be activated in various animal and human tumors, suggesting that it is critical for development.