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TRACC (Transcriptional Readout Activated by Cell-cell Contacts) is an engineered molecular tool that detects and records cell-cell contacts in mammalian systems.

Timing of neural precursor cells division controls the order of development of sensory neurons, which in turn determines their axon terminal pattern and ultimately fly behaviour.

Quantitative proteomics reveals the diversity and heterogeneity of nuclear proteomes in mammalian organs and identifies the molecular features of ageing.

Ribosomal protein mutations, mutations that affect ribosomal RNA synthesis, or function of the mature ribosome, trigger a transcriptional response mediated by Xrp1 expression which reduces cellular translation via eIF2-alpha phosphorylation and renders cells liable to competition with wild-type neighbors.

Irradiation of normal human fibroblasts and mice in conditions mimicking standard external X-ray radiotherapy protocols highlights that noncancerous cells surrounding the planning target volume accumulate DNA single-strand breaks but almost no double-strand breaks, putting them in a pre-cancerous senescent state.

Cell encapsulation-based transcriptional profiling using myogenic progenitors reveals that long-range factors in the aged systemic environment induce a wide range of signaling pathways in a niche-independent manner.

Tom70 connects the mitochondrial import to the nuclear transcriptional activity of mitochondrial proteins and controls mitochondrial biogenesis defects during aging.

A biochemical approach shows that SOX4 guaranteed the PGR protein stability through repressing the ubiquitin E3 ligase HERC4, to make the stroma cell conducive for response to progesterone and decidualization.

Membrane potential adjustment required for growth plate chondrocytic signal conversion from cGMP to Ca²⁺ influx toward long bone outgrowth.

Axon degeneration due to loss of mitochondria is suppressed by CaMKII activity and MAP kinase signaling.