Inhibition of methionine aminopeptidase in C2C12 myoblasts disrupts cell integrity via increasing endoplasmic reticulum stress.

Proteasome-dependent protein degradation and the digestion of peptides by aminopeptidases are essential for myogenesis. Methionine aminopeptidases (MetAPs) are uniquely involved in, both, the proteasomal degradation of proteins and in the regulation of translation (via involvement in post-translational modification). Suppressing MetAP1 and MetAP2 expression inhibits the myogenic differentiation of C2C12 myoblasts.

The pericellular function of Fibulin-7 in the adhesion of oligodendrocyte lineage cells to neuronal axons during CNS myelination.

Myelin is an electrical insulator that enables saltatory nerve conduction and is essential for proper functioning of the central nervous system (CNS). It is formed by oligodendrocytes (OLs) in the CNS, and during OL development various molecules, including extracellular matrix (ECM) proteins, regulate OL differentiation and myelination; however, the role of ECM proteins in these processes is not well understood. Our present work is centered on the analyses of the expression and function of fibulin-7 (Fbln7), an ECM protein of the fibulin family, in OL differentiation.

Treatment outcomes and prognostic factors in patients with colorectal cancer and synchronous lung metastases in the conversion therapy era.

Purpose: The Japanese Grade Classification based on the status of pulmonary and mesenteric nodal metastases and the presence of extrapulmonary metastases had a prognostic value in patients with colorectal lung metastases previously. Because the survival of such patients has improved in the era of conversion therapy, this classification needs to be reaudited.

Methods: This study reviewed the treatment sequences of 126 colorectal cancer patients with synchronous lung metastases between 2010 and 2022 at our hospital.

Urodele amphibian newt bridges the missing link in evo-devo of the pancreas.

Background: The pancreas exhibits diverse structures and roles across vertebrates. The pancreas has evolved to include both endocrine and exocrine cells, a change that occurred during the transition from fish to amphibian. This event emphasizes the evolutionary significance of amphibians.

Q241R mutation of Braf causes neurological abnormalities in a mouse model of cardio-facio-cutaneous syndrome, independent of developmental malformations.

Constitutively active mutants of BRAF cause cardio-facio-cutaneous (CFC) syndrome, characterized by growth and developmental defects, cardiac malformations, facial features, cutaneous manifestations, and mental retardation. An animal model of human CFC syndrome, the systemic BrafQ241R/+ mutant mouse, has been reported to exhibit multiple CFC syndrome-like phenotypes. In this study, we analyzed the effects of Braf mutations on neural function, separately from their effects on developmental processes.