The availability of asparagine is important for cell growth and nascent peptide synthesis in certain sarcoma cells, and could be targeted therapeutically to inhibit tumor growth.

Osteoblasts utilize an elegant mechanism by which they obtain and subsequently synthesize the requisite amino acids to support osteoblast differentiation and bone formation.

Lineage resolved single-cell RNA-seq of mammary carcinoma models uncovers a metabolic vulnerability of taxane-resistant clones.

Mitochondrial electron transport chain dysfunction triggers the integrated stress response due to an asparagine deficiency downstream of impaired NADH oxidation in proliferating myoblasts, but not in differentiated myotubes.

Amphiphysin I is identified as a new substrate of AEP, and the resultant fragment induces synaptic dysfunction and promotes tau hyperphosphorylation via activating CDK5 kinase.

Multi-omic analyses reveal a connection between the integrated stress response and the regulation of redox and amino acid metabolism when the TCA cycle is impaired.

Precise hydrogen-bond stabilization of the neck linker docking onto the catalytic motor domain, is crucial for motor activity and intracellular functions of the bi-directional mitotic kinesin-5 Cin8.

Asp234 is deprotonated in the ground state and forms the proton transfer pathway that proceeds from the Schiff base toward Glu68 in the intermediate state of the anion channelrhodopsin GtACR1.

Kasugamycin potentiates rifampicin killing of Mycobacterium tuberculosis by targeting adaptive mistranslation.

Glutamine deprivation reprograms chondrocytes, attenuates inflammation, and such intervention may be protective against joint inflammation.