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TGF beta 3
From Wikipedia, the free encyclopedia
| Transforming growth factor beta-3 | |
|---|---|
| Other names: | TGF-beta-3 |
| Genetic data | |
| Locus: | Chr. 14 q24 |
| Gene code: | HUGO code:TGFB3 |
| Protein Structure/Function | |
| Structure: | Molecular structure |
| Protein type: | TGF beta family |
| Functions: | cell differentiation, embryogenesis |
| Other | |
| Taxa expressing: | Homo sapiens; homologs: many metazoan phyla |
| Cell types: | many |
| Subcellular localization: | extracellular |
| Covalent modifications: | glycosylation |
| Medical/Biotechnological data | |
| Diseases: | Arrhythmogenic Right Ventricular Dysplasia 1 |
| Database Links | |
| Entrez: | 7043 |
| OMIM: | 190230 |
| RefSeq: | NM_003239 |
| UniProt: | P10600 |
Transforming growth factor-beta 3 (TGF-β3) is a type of protein, known as a cytokine, which is involved in cell differentiation, embryogenesis and development. It belongs to a large family of cytokines called the Transforming growth factor beta superfamily, which includes the TGF-β family, Bone morphogenetic proteins (BMPs), growth and differentiation factors (GDFs), inhibins and activins.[1]
TGF-β3 is believed to regulate molecules involved in cellular adhesion and extracellular matrix (ECM) formation during the process of palate development. Without TGF-β3, mammals develop a deformity known as a cleft palate.[2][3] This is caused by failure of epithelial cells in both sides of the developing palate to fuse. TGF-β3 also plays an essential role in controlling the development of lungs in mammals, by also regulating cell adhesion and ECM formation in this tissue,[4] and controls wound healing by regulating the movements of epidermal and dermal cells in injured skin.[5]
- ^ Herpin A, Lelong C, Favrel P (2004). "Transforming growth factor-beta-related proteins: an ancestral and widespread superfamily of cytokines in metazoans". Dev Comp Immunol 28 (5): 461-85. PMID 15062644.
- ^ Taya Y, O'Kane S, Ferguson M (1999). "Pathogenesis of cleft palate in TGF-beta3 knockout mice". Development 126 (17): 3869-79. PMID 10433915.
- ^ Dudas M, Nagy A, Laping N, Moustakas A, Kaartinen V (2004). "Tgf-beta3-induced palatal fusion is mediated by Alk-5/Smad pathway". Dev Biol 266 (1): 96-108. PMID 14729481.
- ^ Kaartinen V, Voncken J, Shuler C, Warburton D, Bu D, Heisterkamp N, Groffen J (1995). "Abnormal lung development and cleft palate in mice lacking TGF-beta 3 indicates defects of epithelial-mesenchymal interaction". Nat Genet 11 (4): 415-21. PMID 7493022.
- ^ Bandyopadhyay B, Fan J, Guan S, Li Y, Chen M, Woodley DT, Li W (2006). "A "traffic control" role for TGFbeta3: orchestrating dermal and epidermal cell motility during wound healing". J Cell Biol. 172 (7): 1093-105. PMID 16549496.
TGF beta superfamily of ligands:
Activin A and B - Anti-müllerian hormone - Bone morphogenetic proteins (BMP2, BMP3, BMP4, BMP5, BMP6, BMP7, BMP8a, BMP8b, BMP10 , BMP15) - Growth differentiation factors (GDF1, GDF2, GDF3, GDF5, GDF6, GDF7, GDF9, GDF10, GDF11, GDF15) - Inhibin A and B - Myostatin - Nodal - TGF beta family (TGF-β1, TGF-β2, TGF-β3)
Type II receptors:ACVR2A - ACVR2B - AMHR2 - BMPR2 - TGFBR2 - TGFBR3
Type I receptors: ACVR1A - ACVR1B - ACVR1C - ACVRL1 - BMPR1A - BMPR1B - TGFBR1
Signal transducers/SMAD: R-SMAD (SMAD1, SMAD2, SMAD3, SMAD5, SMAD9) - I-SMAD (SMAD6, SMAD7) - SMAD4
Ligand Inhibitors: Cerberus - Chordin - DAN - Decorin - Follistatin - Gremlin - Lefty - LTBP1 - Noggin - THBS1
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