Gulp1 regulates chondrocyte growth arrest and differentiation via the TGF-β/SMAD2/3 pathway.

Chondrocyte differentiation is crucial for cartilage formation. However, the complex processes and mechanisms coordinating chondrocyte proliferation and differentiation remain incompletely understood. Here, we report a novel function of the adaptor protein Gulp1 in chondrocyte differentiation.

Periostin is a novel histological biomarker for the diagnosis of chondroid tumor.

Background: The chondroid tumor is generally classified into three types, enchondroma, low-grade chondrosarcoma, and high-grade chondrosarcoma. A histological evaluation of a biopsy sample is the best predictor of the clinical course in most patients with carcinomas or sarcomas. Sometimes serological or molecular markers are used as prediction markers, but there has been no reliable marker for chondroid tumor diagnosis.

CFL2 is an essential mediator for myogenic differentiation in C2C12 myoblasts.

CFL2, a skeletal muscle-specific member of the actin depolymerizing factor/cofilin protein family, is known to be involved in the regulation of actin filament dynamics. Although the impact of CFL2 has been studied in human myopathy, its functional contribution to myogenic differentiation, in terms of its effects on cell proliferation, cell cycle, and myogenic factor modulation, remains largely unknown. Here, we report that CFL2 is required for the myogenic differentiation of C2C12 myoblasts by regulating proliferation and myogenic transcription factors expressions.

C1q and TNF related protein 1 regulates expression of inflammatory genes in vascular smooth muscle cells.

Background: C1q and TNF related protein 1 (C1QTNF1) is known to be associated with coronary artery diseases. However, the molecular function of C1QTNF1 on the vascular smooth muscles remains to be investigated.

Objective: This study was therefore undertaken to investigate the effect of C1QTNF1 on gene expression of human smooth muscle cells and to reveal potential molecular mechanisms mediated by C1QTNF1.