Download: Download high-res image (172KB) Download: Download full-size image Keiji Tanaka (photo courtesy of the Japanese Biochemical Society)

A study in Molecular Cell by Ramadhin et al.1 and two studies in Cell by van den Heuvel et al.2 and by Mevissen et al.3 show that STK19 is a key protein in transcription-coupled nucleotide excision repair (TC-NER) in mammalian cells by mediating the initial repair protein complex formation and subsequent TFIIH recruitment, thereby enabling the vital damage verification step.

In this issue of Molecular Cell, Sun et al. reveal that the long non-coding RNA (lncRNA) DNAJC3-AS1 plays a dual role in maintaining the rRNA processing function of fibrillarin (FBL) in cancer cells. It promotes FBL condensation while preventing abnormal aggregation, offering new therapeutic insights for cancer treatment by targeting lncRNAs involved in the regulation of FBL condensation.

Section snippets Main textFerroptosis, a cell death pathway triggered by iron-catalyzed peroxidation of phospholipids, has been implicated in both disease progression and cancer treatment.1 A major challenge in studying ferroptosis has been the difficulty in detecting ferroptotic cells under physiological conditions, owing to the lack of a specific marker for ferroptosis.1 This obstacle was recently

The regulatory mechanisms of silencers have remained poorly understood. In this issue, Hofbauer et al.1 conduct a genome-wide screen in Drosophila melanogaster and reveal three silencer types that appear to work alone—without the need for combinatorial action, traditional chromatin marks, or open chromatin regions.

In this issue of Molecular Cell, Ito et al.1 and Chen et al.2 identify peroxiredoxin 6 (PRDX6) as member of the selenoprotein (re)synthesis machinery, thereby linking PRDX6 to ferroptosis susceptibility of cancer cells.

In a recent study in Cell, Dopler et al.1 show that a subpopulation of P-stalk-containing ribosomes (PSRs) are generated following exposure to cytokines, and the data suggest that PSRs are central mediators of translational reprogramming during the cytokine- and immune-response.

Bacteria often defend against phage infection by deploying NADase effectors to degrade cellular NAD+, thereby halting both bacterial growth and phage replication. In a recent article in Nature, Osterman et al.1 identify phage-encoded counterdefense pathways that reconstitute NAD+ during infection, enabling phages to combat multiple unrelated antiphage systems.

In a recent paper at Nature, Li et al.1 reported that alanine-tRNA synthetases AARS1 and AARS2 are lactate sensors and mediate lactylation of cGAS, leading to its inactivation.

(Molecular Cell 84, 1–18.e1–e10; December 19, 2024)

In this issue, Devaiah et al.1 identify JNK-catalyzed phosphorylation to convert bromodomain-containing protein 4 (BRD4) from a chromatin regulator to a transcription activator.

In this issue of Molecular Cell, Chang et al.1 elaborate on the mechanisms by which CAT tail aggregation is mediated through threonine residues and how it contributes to the perturbation of proteostasis.

In this issue of Molecular Cell, Longo et al.1 reveal that AMPK, a regulatory kinase activated by metabolic stress, inhibits NIX/BNIP3-dependent mitophagy to preserve mitochondrial quantity and activates PINK1/Parkin-dependent mitophagy to ensure mitochondrial quality.

In a recent publication in Nature, Motone et al.1 report the development of a protein sequencing method using nanopores that enables the reading of long protein strands. This method allows for multi-pass re-reading and can detect single amino acid substitutions as well as post-translational modifications (PTMs).