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Home: Cell Press Publisher of over 50 scientific journals across the life, physical, earth, and health sciences, both independently and in partnership with scientific societies including Cell, Neuron, Immunity, Current Biology, AJHG, and the Trends Journals
Meningeal lymphatics-microglia axis regulates synaptic physiology: Cell Gene Ontology (GO) analysis of significantly upregulated genes in microglia (adj p value < 0 05, log 2 FC > 0 2; Figure S3D) revealed GO terms for “antigen processing and presentation of exogenous peptide,” “response to type II interferon,” and “positive regulation of leukocyte cell-cell interaction ”
The recency and geographical origins of the bat viruses . . . - Cell Press Recombination-aware evolutionary analyses of the entire genomes of SARS-CoV-1-like and SARS-CoV-2-like viruses indicate that SARS-CoV-1 and SARS-CoV-2 descend from bat coronaviruses that circulated as recently as one to six years before their respective dates of human emergence These inferred virus ancestors likely needed to travel faster than closely related bat viruses in order to reach
The structure of human sweetness - Cell Press Human sweet TRCs express on their cell surface a sweet receptor that initiates the cascade of signaling events responsible for our strong attraction to sweet stimuli Here, we describe the cryo-electron microscopy (cryo-EM) structure of the human sweet receptor bound to two of the most widely used artificial sweeteners—sucralose and aspartame
CD36-mediated endocytosis of proteolysis-targeting chimeras - Cell Press In our studies, pull-down of potential interacting proteins from cell membrane lysates with biotinylated probes and sequential mass spectrometry analyses identified key clathrin endocytic cascade-associated proteins, including clathrin heavy-chain-1, clathrin adaptor protein 2 complex (AP-2), and Rab5 20 Rab-5 KD decreased protein degradation
Issue: Cell - Cell Press CAR T cell therapy can cause cognitive impairment in mouse models with central nervous system (CNS) and non-CNS cancers by inducing persistent neuroinflammation, thereby disrupting oligodendroglial homeostasis and hippocampal neurogenesis, which can be rescued by microglial depletion or CCR3 blockade