Although central nervous system (CNS) regeneration has been considered to be controlled by CNS microenvironment, CNS injury causes leading to leakage of circulating factors into CNS, which promotes CNS regeneration.

Overexpression of VPS9D1-AS1 is a lncRNA to activate TGF-β and IFN signaling pathways, regulates crosstalk between cancer cells and T lymphocytes in the tumor microenvironment.

Cryo-EM analysis of full-length human epidermal growth factor receptor provides a molecular explanation for how ligand-induced differential effect in the ligand-binding extracellular module tunes the transmembrane signaling mediated by epidermal growth factor receptor.

Parathyroid hormone attenuates osteoarthritis pain and joint degeneration by modification of subchondral bone remodeling and could be a potential disease-modifying therapy for osteoarthritis.

Differentiation of CD4 T cells into CD4 T follicular helper cells during viral infection in mice is promoted by tumor growth factor beta.

NODAL/Activin-induced SMAD2 binding directly drives remodeling of both open and closed chromatin and does not directly correlate with temporal patterns of gene expression upon prolonged signaling.

Neuronal activity modulates blood–brain barrier permeability, influencing synaptic plasticity and local network reorganization in the healthy brain.

Pathogen-specific CTLs are programmed to provide customized responses against infection, by inflammatory molecules that promote localization in peripheral and lymphoid tissues using alternative signaling mechanisms.

SMAD1/5 signaling is essential for the full transforming growth factor β (TGF-β)-induced transcriptional program and physiological responses and is induced via a novel receptor activation mechanism, involving two distinct type I receptors.