Chapter 2 69 formation of bone and cartilage. Bmps belong to the transforming growth factor beta (TGF-ß) superfamily. In recent years, Bmps are discovered to be key elements in the biological process of development and cellular functions. Fibroblast growth factor (Fgf): Fibroblast growth factor is a family of secreted proteins involved in a variety of biological activities including inhibition of cell proliferation, and regulation of cell survival and differentiation. Fgfs are heparin-binding proteins, which are required in the processes of angiogenesis, wound healing, and embryonic development. Ectodysplasin (Eda): Ectodysplasin (Eda) is a gene that encodes a type II membrane protein, Ectodysplasin-A. The Ectodysplasin-A protein, which belongs to the tumor necrosis factor family, acts as a homotrimer and is involved in cell-cell communication during the development of various skin appendages. Inactivating mutations in this gene are the cause of X-linked hypohidrotic ectodermal dysplasia, which results in the abnormal development of ectodermal structures before birth, including conical and missing teeth, lack of or malfunctioning sweat glands, and sparse hair. Several transcript variants encoding many different isoforms have been found for this gene. NF-ĸB: NF-ĸB is the abbreviation of nuclear factor kappa-light- chain-enhancer of activated B cells. NF-ĸB is a protein complex that controls gene transcription in cellular responses to stimuli such as stress, free radicals, ultraviolet irradiation, nutrition, and foreign antigens. While under normal conditions, NF-ĸB is located in the cytosol in complex with the inhibitory protein IĸBα without any activity. A variety of extracellular signals can activate the enzyme IĸB kinase (IKK). IKK, in turn, phosphorylates the IĸBα protein, which results in ubiquitination and dissociation of IκBα from NF-ĸβ. Subsequently NF-ĸB is activated and then translocated into the nucleus to initiate gene transcription. Noggin: Noggin is a protein that inhibits TGF-β signaling by binding to TGF-β family ligands and preventing them from binding to their corresponding receptors. Genetic experiments have