Seven distinct cryo-electron microscopy structures delineate the elaborate mechanism for how E. coli Mfd, a transcription repair coupling factor, disassembles the RNA polymerase transcription elongation complex to initiate transcription-coupled repair.

Researchers are undertaking a systematic assessment of the reproducibility of biomedical science in Brazil.

Genetic interaction and biochemical analyses have unveiled the crucial involvement of CTPS in the regulation of adipocyte growth, lipid metabolism, and metabolic adaptation in Drosophila, achieved through activating the PI3K-Akt-SREBP pathway.

Network architecture and physiological features of the cell dictate asymmetric gene regulation between a negative autoregulatory TF gene and its target gene.

Modelling O-GlcNAc transferase intellectual disability reveals the roles of this post-translational modification in regulating normal axonal terminal morphology and maintaining appropriate sleep homeostasis, pharmacological and genetic rescues of O-GlcNAcylation highlight the complexities of addressing this disorder.

The structure of human PINK1 explains structural regulation and clarity on the impact of loss of function disease-associated mutations, which may stimulate future drug discovery efforts for both familial and idiopathic Parkinson's disease.

The capacity for new cerebellum-dependent learning is influenced by the recent history of neural activity in a mouse model of Fragile X syndrome, suggesting a role for metaplasticity.

Knocking out Folliculin (FLCN) in human renal epithelial cells activates STAT1/2-mediated gene expression, independent of interferon, uncovering a tissue-specific process potentially relevant in the cancer syndrome Birt-Hogg-Dubé (BHD).

Simultaneous stimulation and recording in awake-behaving pigeons showed that mid-infrared stimulation, as a promising neuromodulation approach, could facilitate or suppress neuronal firing activity depending on its ongoing sensory responsiveness levels, and cause reversible and gain modulation on sensorimotor behavior.

The use of a conformation-selective inhibitory nanobody provides critical information on MelB at a low-sugar affinity inward-facing Na⁺-bound state for establishing the mobile barrier and substrate-releasing mechanisms.