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

GO curators for mouse genes have assigned the following annotations to the gene product of Tnfrsf1b. (This text reflects annotations as of Wednesday, January 23, 2013.)

---

Summary from NCBI RefSeq

[Summary is not available for the mouse gene. This summary is for the human ortholog.] The protein encoded by this gene is a member of the TNF-receptor superfamily. This protein and TNF-receptor 1 form a heterocomplex that mediates the recruitment of two anti-apoptotic proteins, c-IAP1 and c-IAP2, which possess E3 ubiquitin ligase activity. The function of IAPs in TNF-receptor signalling is unknown, however, c-IAP1 is thought to potentiate TNF-induced apoptosis by the ubiquitination and degradation of TNF-receptor-associated factor 2, which mediates anti-apoptotic signals. Knockout studies in mice also suggest a role of this protein in protecting neurons from apoptosis by stimulating antioxidative pathways. [provided by RefSeq, Jul 2008]

---

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

• Researchers have inferred from direct assay, that the gene product of Tnfrsf1b
  • is located in the following cellular components:
    • membrane ^[2]
    • membrane raft ^[6]
• The gene product of Tnfrsf1b has been shown to bind to the gene products of Krt18, Krt8. ^[2] Researchers have inferred, based on physical interactions, that the gene product of Tnfrsf1b
  • participates in the following biological processes:
    • tumor necrosis factor-mediated signaling pathway ^[4]
  • performs the following molecular functions:
    • tumor necrosis factor-activated receptor activity ^[4]
• Researchers have inferred, based on phenotypic analysis of mouse mutants, that the gene product of Tnfrsf1b
  • participates in the following biological processes:
    • cell death ^[3]
    • cell surface receptor signaling pathway ^[5]
    • inflammatory response ^[5]
    • negative regulation of inflammatory response ^[1]
    • RNA destabilization ^[1]

---

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 Tnfrsf1b:
  • participates in the following biological processes:
    • cellular response to lipopolysaccharide
    • immune response
    • positive regulation of membrane protein ectodomain proteolysis
  • performs the following molecular functions:
    • tumor necrosis factor-activated receptor activity
    • ubiquitin protein ligase binding
  • is located in the following cellular components:
    • axon
    • membrane
    • membrane raft
    • neuronal cell body
    • nucleus
    • perinuclear region of cytoplasm
    • varicosity

---

Summary text for additional MGI annotations

• Automated translation to GO terms of SwissProt keywords that describe Tnfrsf1b indicates that it:
  • is located in the following cellular components:
    • integral to membrane

---

References

1. Carballo E et al. (2001) Roles of tumor necrosis factor-alpha receptor subtypes in the pathogenesis of the tristetraprolin-deficiency syndrome. Blood, 98:2389-95. (PubMed:11588035)
2. Caulin C et al. (2000) Keratin-dependent, epithelial resistance to tumor necrosis factor-induced apoptosis. J Cell Biol, 149:17-22. (PubMed:10747083)
3. Erickson SL et al. (1994) Decreased sensitivity to tumour-necrosis factor but normal T-cell development in TNF receptor-2-deficient mice. Nature, 372:560-3. (PubMed:7990930)
4. Goodwin RG et al. (1991) Molecular cloning and expression of the type 1 and type 2 murine receptors for tumor necrosis factor. Mol Cell Biol, 11:3020-6. (PubMed:1645445)
5. Peschon JJ et al. (1998) TNF receptor-deficient mice reveal divergent roles for p55 and p75 in several models of inflammation. J Immunol, 160:943-52. (PubMed:9551933)
6. Tellier E et al. (2006) The shedding activity of ADAM17 is sequestered in lipid rafts. Exp Cell Res, 312:3969-80. (PubMed:17010968)

---

---

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

---