Noggin was first discovered by its ability to induce secondary axis formation in Xenopus embryos. It is a secreted homodimeric glycoprotein that serves as a BMP (bone morphogenetic protein) antagonist. It has been found that noggin arrests the differentiation of stromal cells, preventing cellular maturation. In humans increased noggin activity results in skeletal dysplasia such as proximal symphalangism (SYM1) and multiple synostosis syndrome 1 (SYNS1). Noggin maintains prolonged growth of human embryonic stem cells in vitro and regulates the stem cell niche during neurogenesis.