NATURE CONFERENCE ON INFLAMMATORY DISEASES Presented by: Chinese Academy of Medical Sciences & Peking Union Medical College | Chinese Society for Immunology (CSI) | Nature Reviews Immunology | Nature Immunology | Nature | Nature Communications
This conference will feature sessions on microbiota, cell death, metabolism, technologies, and innate sensing and signaling as they relate to inflammatory diseases and cancer.
Science in the age of Trump p409 doi:10.1038/ncb3526 The steep cuts in science funding proposed in the 2018 US budget blueprint have raised alarm in scientific quarters, and signal the current administration's disregard for the significance of science and research in modern society.
Terminating the replication helicase pp410 - 412 Vincent Gaggioli and Philip Zegerman doi:10.1038/ncb3519 A feature of the cell cycle is that the events of one cycle must be reset before the next one begins. A study now shows that the replication machinery is removed from fully replicated DNA by a conserved ubiquitin- and CDC48 (also known as p97)-dependent pathway. This explains how eukaryotic chromosomes are returned to the unreplicated state.
SIRT2 and glycolytic enzyme acetylation in pluripotent stem cells pp412 - 414 Tong Ming Liu and Ng Shyh-Chang doi:10.1038/ncb3522 The metabolic transition from mitochondrial oxidative phosphorylation (OXPHOS) to glycolysis is critical for somatic reprogramming of induced pluripotent stem cells (iPSCs). SIRT2 has now been established as a previously unknown regulator of this metabolic transition during somatic reprogramming by controlling the acetylation status of glycolytic enzymes.
Metabolic changes promote rejection of oncogenic cells pp414 - 415 Jonathan L. Coloff and Joan S. Brugge doi:10.1038/ncb3521 Dysfunctional cells are eliminated from epithelial monolayers by a process known as cell extrusion to maintain tissue homeostasis. Normal epithelial cells are now shown to induce the extrusion of oncogene-transformed cells by inducing metabolic changes in the oncogene-expressing cells through PDK4-mediated inhibition of PDH and mitochondrial metabolism.
Context-specific roles of EMT programmes in cancer cell dissemination pp416 - 418 M. Angela Nieto doi:10.1038/ncb3520 The role of the epithelial-to-mesenchymal transition in tumour progression remains a topic of intense debate. Now, data on the role of Zeb1 in the metastatic spread of pancreatic cancer clarify apparently conflicting views by revealing context-specific, differential use of individual epithelial-to-mesenchymal transition transcription factors in cancer cell dissemination.
When cancer needs what's non-essential pp418 - 420 Mark R. Sullivan and Matthew G. Vander Heiden doi:10.1038/ncb3523 The non-essential amino acids serine and glycine are critical for proliferative metabolism. A study in Nature now finds that dietary serine and glycine deprivation inhibits growth of some tumours. Whether this dietary intervention is effective depends on both the oncogenic context and tumour tissue of origin.
This Insight explores brain ageing and possible rejuvenation and updates our understanding of Alzheimer's disease, amyotrophic lateral sclerosis and Parkinson's disease. It also discusses how knowledge from prion disease may apply to more common neurodegenerative disorders and provides a structural perspective on the properties of amyloids.
High-resolution myogenic lineage mapping by single-cell mass cytometry pp558 - 567 Ermelinda Porpiglia, Nikolay Samusik, Andrew Tri Van Ho, Benjamin D. Cosgrove, Thach Mai et al. doi:10.1038/ncb3507 Porpiglia et al. use single-cell mass cytometry to analyse surface markers and key myogenic transcription factors of skeletal muscle stem cells during homeostasis and repair, and identify previously unrecognized myogenic progenitor cell populations.
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