Go Annotations as Summary Text (Tabular View) (GO Graph)

GO curators for mouse genes have assigned the following annotations to the gene product of Tgfb2. (This text reflects annotations as of Wednesday, January 23, 2013.)

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Summary from NCBI RefSeq

[Summary is not available for the mouse gene. This summary is for the human ortholog.] This gene encodes a member of the transforming growth factor beta (TGFB) family of cytokines, which are multifunctional peptides that regulate proliferation, differentiation, adhesion, migration, and other functions in many cell types by transducing their signal through combinations of transmembrane type I and type II receptors (TGFBR1 and TGFBR2) and their downstream effectors, the SMAD proteins. Disruption of the TGFB/SMAD pathway has been implicated in a variety of human cancers. The encoded protein is secreted and has suppressive effects of interleukin-2 dependent T-cell growth. Translocation t(1;7)(q41;p21) between this gene and HDAC9 is associated with Peters' anomaly, a congenital defect of the anterior chamber of the eye. The knockout mice lacking this gene show perinatal mortality and a wide range of developmental, including cardiac, defects. Alternatively spliced transcript variants encoding different isoforms have been identified. [provided by RefSeq, Sep 2010]

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Summary text based on GO annotations supported by experimental evidence in mouse

• Researchers have inferred from direct assay, that the gene product of Tgfb2
  • participates in the following biological processes:
    • activation-induced cell death of T cells ^[16]
    • induction of apoptosis ^[16]
    • neuron fate commitment ^[11]
    • pathway-restricted SMAD protein phosphorylation ^[14]
    • positive regulation of gene expression ^[2]
    • somatic stem cell division ^[8]
  • is located in the following cellular components:
    • axon ^[1]
    • extracellular space ^[4]
    • neuronal cell body ^[1]
• The gene product of Tgfb2 has been shown to bind to the gene products of D0H4S114, Htra3. ^{[12, 15]}
• Researchers have inferred, based on phenotypic analysis of mouse mutants, that the gene product of Tgfb2
  • participates in the following biological processes:
    • axon guidance ^[10]
    • blood vessel development ^[10]
    • blood vessel remodeling ^[9]
    • dopamine biosynthetic process ^[1]
    • extracellular matrix organization ^{[10, 13]}
    • hair follicle development ^{[5, 7]}
    • hair follicle morphogenesis ^[5]
    • heart development ^[10]
    • hemopoiesis ^[8]
    • neuron development ^[1]
    • positive regulation of cell cycle ^[8]
    • regulation of apoptotic process ^[9]
    • skeletal system development ^[3]
• Researchers have inferred, based on genetic interactions, that the gene product of Tgfb2
  • participates in the following biological processes:
    • cartilage condensation based on interactions with Fgf4, Fgf6 ^[6]

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Summary text based on GO annotations supported by experimental evidence in other organisms

• From comparative sequence analysis (see table for details), MGI curators have determined that the gene product of Tgfb2:
  • participates in the following biological processes:
    • activation of protein kinase activity
    • cardiac epithelial to mesenchymal transition
    • cardiac muscle cell proliferation
    • cardioblast differentiation
    • catagen
    • cell cycle arrest
    • cell death
    • cell migration
    • cell morphogenesis
    • cell-cell junction organization
    • collagen fibril organization
    • embryonic neurocranium morphogenesis
    • epithelial to mesenchymal transition
    • eye development
    • glial cell migration
    • hair follicle development
    • heart development
    • heart morphogenesis
    • negative regulation of alkaline phosphatase activity
    • negative regulation of apoptotic process
    • negative regulation of cell growth
    • negative regulation of cell proliferation
    • negative regulation of epithelial cell proliferation
    • negative regulation of immune response
    • negative regulation of macrophage cytokine production
    • negative regulation of release of sequestered calcium ion into cytosol
    • pathway-restricted SMAD protein phosphorylation
    • positive regulation of apoptotic process
    • positive regulation of cardioblast differentiation
    • positive regulation of catagen
    • positive regulation of cell adhesion mediated by integrin
    • positive regulation of cell growth
    • positive regulation of cell migration
    • positive regulation of cell proliferation
    • positive regulation of epithelial cell migration
    • positive regulation of epithelial to mesenchymal transition
    • positive regulation of heart contraction
    • positive regulation of integrin biosynthetic process
    • positive regulation of neuron apoptotic process
    • positive regulation of phosphatidylinositol 3-kinase cascade
    • positive regulation of protein secretion
    • positive regulation of stress-activated MAPK cascade
    • protein phosphorylation
    • regulation of transforming growth factor beta2 production
    • response to estrogen stimulus
    • response to hypoxia
    • response to progesterone stimulus
    • signal transduction by phosphorylation
    • SMAD protein import into nucleus
    • transforming growth factor beta receptor signaling pathway
    • wound healing
  • performs the following molecular functions:
    • beta-amyloid binding
    • protein heterodimerization activity
    • protein homodimerization activity
    • protein N-terminus binding
    • receptor binding
    • receptor signaling protein serine/threonine kinase activity
    • transforming growth factor beta receptor binding
    • type II transforming growth factor beta receptor binding
  • is located in the following cellular components:
    • basement membrane
    • cell surface
    • cytoplasm
    • extracellular matrix
    • extracellular region
    • extracellular space
    • secretory granule
    • trans-Golgi network

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Summary text based on GO annotations supported by structural data

• Tgfb2 encodes a protein or proteins that contain the following InterPro domains: Transforming growth factor beta, conserved site, Transforming growth factor, beta 2, Transforming growth factor-beta, Transforming growth factor-beta, C-terminal, Transforming growth factor-beta, N-terminal, Transforming growth factor-beta-related, indicating that the gene product:
  • participates in the following biological processes:
    • cell growth
    • growth

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Summary text for additional MGI annotations

• Automated translation to GO terms of SwissProt keywords that describe Tgfb2 indicates that it:
  • participates in the following biological processes:
    • positive regulation of cell division

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References

1. Andrews ZB et al. (2006) Transforming growth factor beta2 haploinsufficient mice develop age-related nigrostriatal dopamine deficits. Neurobiol Dis, 21:568-75. (PubMed:16257223)
2. Anthwal N et al. (2008) The role of transforming growth factor-beta signalling in the patterning of the proximal processes of the murine dentary. Dev Dyn, 237:1604-13. (PubMed:18498113)
3. Baffi MO et al. (2004) Conditional deletion of the TGF-beta type II receptor in Col2a expressing cells results in defects in the axial skeleton without alterations in chondrocyte differentiation or embryonic development of long bones. Dev Biol, 276:124-42. (PubMed:15531369)
4. Cheng HL et al. (1993) TGF-beta 2 gene and protein expression in maternal and fetal tissues at various stages of murine development. J Reprod Immunol, 25:133-48. (PubMed:8164195)
5. Foitzik K et al. (1999) The TGF-beta2 isoform is both a required and sufficient inducer of murine hair follicle morphogenesis. Dev Biol, 212:278-89. (PubMed:10433821)
6. Grass S et al. (1996) Alterations in somite patterning of Myf-5-deficient mice: a possible role for FGF-4 and FGF-6. Development, 122:141-50. (PubMed:8565825)
7. Jamora C et al. (2005) A signaling pathway involving TGF-beta2 and snail in hair follicle morphogenesis. PLoS Biol, 3:e11. (PubMed:15630473)
8. Langer JC et al. (2004) Quantitative Trait Analysis Reveals Transforming Growth Factor-{beta}2 as a Positive Regulator of Early Hematopoietic Progenitor and Stem Cell Function. J Exp Med, 199:5-14. (PubMed:14707111)
9. Molin DG et al. (2002) Altered apoptosis pattern during pharyngeal arch artery remodelling is associated with aortic arch malformations in Tgfbeta2 knock-out mice. Cardiovasc Res, 56:312-22. (PubMed:12393102)
10. Molin DG et al. (2004) Transforming growth factor beta-SMAD2 signaling regulates aortic arch innervation and development. Circ Res, 95:1109-17. (PubMed:15528466)
11. Okano J et al. (2005) Transforming growth factor beta2 promotes the formation of the mouse cochleovestibular ganglion in organ culture. Int J Dev Biol, 49:23-31. (PubMed:15744664)
12. Paliwal S et al. (2004) P311 binds to the latency associated protein and downregulates the expression of TGF-beta1 and TGF-beta2. Biochem Biophys Res Commun, 315:1104-9. (PubMed:14985127)
13. Saika S et al. (2001) TGFbeta2 in corneal morphogenesis during mouse embryonic development. Dev Biol, 240:419-32. (PubMed:11784073)
14. Stenvers KL et al. (2003) Heart and liver defects and reduced transforming growth factor beta2 sensitivity in transforming growth factor beta type III receptor-deficient embryos. Mol Cell Biol, 23:4371-85. (PubMed:12773577)
15. Tocharus J et al. (2004) Developmentally regulated expression of mouse HtrA3 and its role as an inhibitor of TGF-beta signaling. Dev Growth Differ, 46:257-74. (PubMed:15206957)
16. Weller M et al. (1994) Transforming growth factor-beta 2 induces apoptosis of murine T cell clones without down-regulating bcl-2 mRNA expression. Eur J Immunol, 24:1293-300. (PubMed:8206089)

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Gene Ontology Evidence Code Abbreviations:

EXP Inferred from experiment

IC Inferred by curator

IDA Inferred from direct assay

IEA Inferred from electronic annotation

IGI Inferred from genetic interaction

IMP Inferred from mutant phenotype

IPI Inferred from physical interaction

ISS Inferred from sequence or structural similarity

ISO Inferred from sequence orthology

ISA Inferred from sequence alignment

ISM Inferred from sequence model

NAS Non-traceable author statement

ND No biological data available

RCA Reviewed computational analysis

TAS Traceable author statement

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