Neurofibromatosis type 1 gene (NF1) signaling is causally linked to the acquisition of a mesenchymal gene expression program in gliomas through the regulation of the AP-1 transcription factor FOSL1.

Newly prepared double gene-edited sheep provide excellent models for skeletal muscle growth and development, and muscle diseases such as muscle atrophy and sarcopenia.

A gene regulatory network model provides a simplified explanation of the molecular interactions that orchestrate muscle development in the sea urchin embryo.

Temporal changes in genome-wide enhancer transcription activity during a transdifferentiation event reveal additive and synergistic enhancer cooperation.

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.

The theory of Buffered Qualitative Stability uses the importance of biological robustness to explain many features of gene regulatory networks in a wide range of organisms, and has implications for diverse biological phenomena including the ability of bacteria and cancer cells to ‘loosen’ their robustness and hence evade treatment.

Cognate site identification uncovers the impact of combinatorial dimerization in specifying new DNA binding sites for human bZIP transcription factors and comprehensive specificity landscapes predict the impact of SNPs on bZIP binding at previously unannotated regulatory loci.

The transcription factor HAND2 evolved uterine expression during the origins of pregnancy and may be important for maternal-fetal immune signaling and parturition.

Single-cell chromatin accessibility analysis reveals the intricate regulatory landscape of mouse testicular development, uncovering novel cell subpopulations and transcription factors, and offering valuable insights into the molecular mechanisms driving germ cell and somatic cell maturation.

Genetic analyses reveal that the tropism towards specific Kras driver mutations during urethane carcinogenesis appears to arise from the selection of an oncogenic mutation in normal cells that imparts a narrow window of signaling conducive for tumorigenesis.