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

GO curators for mouse genes have assigned the following annotations to the gene product of Sh3bp2. (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 has an N-terminal pleckstrin homology (PH) domain, an SH3-binding proline-rich region, and a C-terminal SH2 domain. The protein binds to the SH3 domains of several proteins including the ABL1 and SYK protein tyrosine kinases , and functions as a cytoplasmic adaptor protein to positively regulate transcriptional activity in T, natural killer (NK), and basophilic cells. Mutations in this gene result in cherubism. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Mar 2009]

---

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

• Researchers have inferred, based on physical interactions, that the gene product of Sh3bp2
  • performs the following molecular functions:
    • SH3 domain binding ^[3]

---

Summary text based on GO annotations supported by structural data

• Sh3bp2 encodes a protein or proteins that contain the following InterPro domains: Pleckstrin homology domain, Pleckstrin homology-like domain, SH2 domain, indicating that the gene product:
  • performs the following molecular functions:
    • phospholipid binding

---

References

1. Guettler S et al. (2011) Structural basis and sequence rules for substrate recognition by Tankyrase explain the basis for cherubism disease. Cell, 147:1340-54. (PubMed:22153077)
2. Levaot N et al. (2011) Loss of Tankyrase-Mediated Destruction of 3BP2 Is the Underlying Pathogenic Mechanism of Cherubism. Cell, 147:1324-39. (PubMed:22153076)
3. Ren R et al. (1993) Identification of a ten-amino acid proline-rich SH3 binding site. Science, 259:1157-61. (PubMed:8438166)

---

---

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

---