title: TGF-beta knockout and dominant-negative receptor transgenic mice.
abstract: Use of homologous recombination and transgenic technologies have provided mouse models to study the physiological roles of the three mammalian TGF-beta isoforms, and their regulation in the context of the intact animal. Mice harboring null mutations for TGF-beta isoforms demonstrate that each exerts discrete nonoverlapping functions during development. TGF-beta1 null mice reveal a crucial role for this cytokine in modulation of the immune system, with evidence for altered development, activation and function of various immune cell populations. New approaches to tissue- and cell-restricted disruption of TGF-beta signaling pathways in transgenic mice carrying dominant-negative mutant TGF-beta receptors will be discussed.
authors.affiliation: Laboratory of Chemoprevention, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-5055, USA. Letterij@pop.nci.nih.gov
authors.forename: J J
authors.initials: JJ
authors.lastname: Letterio
authors.forename: E P
authors.initials: EP
authors.lastname: Böttinger
mesh_terms: D000818:Animals; D015551:Autoimmunity; D006128:Growth; D007109:Immunity; D051379:Mice; D018345:Mice, Knockout; D008822:Mice, Transgenic; D018125:Receptors, Transforming Growth Factor beta / Q000235:genetics / Q000502:physiology*; D015398:Signal Transduction; D016212:Transforming Growth Factor beta / Q000235:genetics / Q000502:physiology*
chemical_list: D018125:Receptors, Transforming Growth Factor beta; D016212:Transforming Growth Factor beta