Loss-of-function screening identified transglutaminase 2 (TGM2) as a putative tumor suppressor in the TP53 pathway and revealed that TGM2-mediated autophagy and CDKN1A-mediated cell cycle arrest are two critical barriers that prevent oncogenic transformation.
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.
A combined approach of unbiased proteomics, biochemistry, genetics, and transgenic animal models reveals that GPR56/ADGRG1 regulates myelin formation and repair by interacting with its microglial-derived ligand transglutaminase 2.
The structure-based design established a new approach to control pathway-selective activation of opioid receptors, resulting in new dual MOR/KOR G-protein biased agonist analgesics with attenuated liabilities.
The activation and membrane localization of the broadly-tuned noxious chemosensory cation channel TRPA1 are regulated by direct interactions with cholesterol via CRAC motifs in transmembane segments 2 and 4.
Electrophysiological and molecular modeling studies identify a sulfur-aromatic interaction between the hydrophobic channel gate and a nearby methionine residue, termed the "gate latch", which is essential for Orai1 pore opening.