This paper reviews the basic biology and biochemistry of the TGF-P iso
forms including their unique serine-threonine receptors and signaling
intermediates. Dysregulation of TGF-beta expression and/or recepotr/si
gnaling function have been implicated in a wide variety of pathologies
. We will discuss mechanisms underlying some of these disease processe
s as gained from study of transgenic mice in which expression of TGF-b
eta 1 has either been lost by targeted deletion of its gene, is overex
pressed in a tissue-specific manner, or blocked by its latency associa
ted peptide.