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Administration of cryopreserved as compared freshly cultured MSCs do not appear to negatively impact measures of in vivo efficacy or in vitro potency in animal models of inflammation.

Genomic analysis of initial SARS-CoV-2 waves in Kenya revealed Mombasa City as a key gateway for variants entering Coastal Kenya with onward inter-county transmission highlighting significance of surveillance in major cities for early warning of lineages entering local populations.

Arrestin-related trafficking adaptors (ARTs) undergo a K63 linked di-ubiquitin modification to promote Rsp5 E3 ligase recruitment and enhance cargo protein ubiquitination.

Genetic complementation approaches in a mouse model of anemia reveals new protein interactions which aid cell survival and promote sensing of environmental cues.

Biochemical studies in combination with computational modeling and molecular dynamics simulations reveal that the lipid bilayer promotes intramembrane proteolysis by stabilizing the enzyme-substrate complex and the protease active site.

Mg²⁺-dependent JAK1-mediated phosphorylation sensitizes TRPV2 activity and thermo-threshold, which is counterbalanced by PTPN1-mediated dephosphorylation, highlighting a role of phosphorylation homeostasis in setting the basal activity of TRPV2.

Combined experimental and theoretical analysis identifies a molecular mechanism akin to working memory that enables single cells to perform complex navigation tasks in changing growth factor fields, beyond simple stimulus-response associations.

A model-based approach for modelling the immune control of viral dynamics is applied to quantify the effect of several SARS-CoV-2 vaccine platforms and to define mechanistic correlates of protection.

The brain’s projection of linguistic knowledge onto speech is reflected by the automatic, reflexive neural tracking of phrases, while the distribution of phrasal-rate tracking and connectivity, particularly the involvement of inferior frontal cortex, is subject to task demands.

Electrophysiological and genetic analyses reveal a biophysical mechanism in parvalbumin interneurons, uncoupled from changes in gene expression, resulting in reduced cortical inhibition in early-stage Alzheimer's disease.