Browse our latest Biochemistry and Chemical Biology articles

An image-based multiplex autophagosome RNAi screen targeting all Rab GTPases as well as their GAPs and GEFs identifies the Rab GEF SMCR8 as multifaceted autophagy modulator, which regulates kinase activity and gene expression of ULK1.

The small subunit ribosomal protein uS7/Rps5 interacts with translation initiation factor eIF2α to stabilize first the open, and then the closed conformation of the pre-initiation complex to promote accurate start codon selection in vivo.

Accessible cholesterol levels in human red blood cells were found to be stable within individuals but vary >10-fold among individuals and this variability may contribute to differences in cholesterol trafficking among tissues.

The kinase Mps1, long known to be the 'boss' in mitotic checkpoint signaling, phosphorylates multiple proteins in the checkpoint signaling cascade.

First two transmembrane segments of Tim17 are involved in interaction with the channel and the second two with the motor of the presequence translocase suggesting how proteins are handed over during their translocation into mitochondria.

Differential eIF4E binding to transcription initiation nucleotides and alternative promoter usage of eIF1A, PABP and other genes are involved in the response of the translation machinery to energy stress.

The N-terminal domain of the chromatin remodeler ISWI contains previously uncharacterized conserved motifs that maintain structure, prevent ATP hydrolysis unless nucleosomes are bound, and confer H4-tail sensitivity without directly competing with the H4 tail.

A method for determining how many ions are required to drive transport in an electrogenic secondary active transporter will help understand the mechanisms of bacterial transporters whose structures have been solved.

Transport-based high-throughput identification of cargo proteins specific to all 12 human importin-β family nuclear import receptors revealed biological processes that the cargo cohorts of each receptor are involved in.

Prostate cancer resistance to androgen receptor antagonist therapy occurs by way of tumors impeding local glucocorticoid metabolism and inactivation and thereby permitting sustained glucocorticoids to stimulate up-regulated glucocorticoid receptor.