A genetic discovery screen for epigenetic factors accelerating melanoma development in vivo identifies SATB2 as a driver of tumor invasion and resistance to FDA-approved BRAF-targeted inhibitor Vemurafenib.

Ts65dn mice exhibit structural, functional, molecular, and genetic alterations that are modulated but unrecovered by prenatal chronic GTE-EGCG, highlighting the importance of holistic studies to understand complex disorders and treatments.

Upon PDGFRα signaling in mouse embryonic palatal mesenchyme cells, Srsf3 exhibits differential transcript binding, resulting in retention of the receptor in early endosomes and increased downstream PI3K-mediated Akt signaling.

In addition to a neural crest cell specific role, AP-2α and AP-2ß cooperatively promote craniofacial development through regulating chromatin and gene expression dynamics in the facial surface ectoderm.

Inhibiting RNA N6-methyladenosine demethylase ALKBH5 promoted axonal regeneration of dorsal root ganglion neurons by regulating stability of Lpin2 mRNA and enhanced the survival and axonal regeneration of retinal ganglion cells.

Detailed molecular profiling investigations alongside antitumor testing and tolerability studies in animals suggest caution when considering the clinical development of inhibitors of CDK8 and CDK19, since a clear therapeutic window could not be demonstrated with two structurally distinct, potent and selective prototype drugs.

Normal hematopoietic stem and progenitor cells slow the regeneration of their niche after injury to minimize leakage from the niche vasculature.

The miR-106a-5p links STAT3 with TP73 to activate Pol III-dependent transcription and cancer cell proliferative activity.

Gene function can be revealed based on characteristic phenotypes using a Cell Painting microscopy assay.

Wound-specific notochord sheath cell subpopulations associate with notochord repair and adult vertebrae formation.