Yap and Taz promote osteogenesis and prevent chondrogenesis in neural crest cells in vitro and in vivo.

Neural crest cells (NCCs) are multipotent stem cells that can differentiate into multiple cell types, including the osteoblasts and chondrocytes, and constitute most of the craniofacial skeleton. Here, we show through in vitro and in vivo studies that the transcriptional regulators Yap and Taz have redundant functions as key determinants of the specification and differentiation of NCCs into osteoblasts or chondrocytes. Primary and cultured NCCs deficient in and switched from osteogenesis to chondrogenesis, and NCC-specific deficiency for and resulted in bone loss and ectopic cartilage in mice.

The subcellular redistribution of NLRC5 promotes angiogenesis via interacting with STAT3 in endothelial cells.

Angiogenesis is a critical step in repair of tissue injury. The pattern recognition receptors (PRRs) recognize pathogen and damage associated molecular patterns (DAMPs) during injury and achieve host defense directly. However, the role of NLR family CARD domain containing 5 (NLRC5), an important member of PPRs, beyond host defense in angiogenesis during tissue repair remains unknown.

Identification of NMU as a potential gene conferring alectinib resistance in non-small cell lung cancer based on bioinformatics analyses.

Non-small cell lung cancer (NSCLC) is the most common type of lung cancer, and adjuvant targeted therapy has shown great benefits for the NSCLC patients with specific genomic mutations. Alectinib, a selective anaplastic lymphoma kinase (ALK) inhibitor, has been clinically used for the NSCLC patients with ALK-rearrangement, however, irreversible therapeutic resistance for the patients receiving alectinib treatment frequently occurs. Here we show that neuromedin U (NMU) may confer the alectinib resistance in NSCLC via multiple mechanisms based on the integrative bioinformatics analyses.