PhosSNP
PhosSNP catalogs and predicts phosphorylation-related single nucleotide polymorphisms (phosSNPs), identifying non-synonymous SNPs (nsSNPs) that influence protein phosphorylation status for functional analysis.
Key Features:
- Phosphorylation-Specific Analysis: Focuses on nsSNPs that affect protein phosphorylation, a post-translational modification that regulates protein activity, stability, and interactions.
- Kinase-Specific Prediction Tool (GPS 2.0): Uses the in-house kinase-specific phosphorylation site predictor GPS 2.0 to identify potential phosSNPs and assess impacts on kinase recognition.
- Detection Statistics: Reports that approximately 70% of nsSNPs are identified as potential phosSNPs and that about 74.6% of these may alter the types of kinases involved at adjacent phosphorylation sites.
- Database Integration (PhosSNP 1.0): Integrates identified phosSNPs into PhosSNP 1.0, with the database implementation using JAVA 1.5 (J2SE 5.0).
Scientific Applications:
- Personalized Medicine: Enables analysis of how nsSNP-driven phosphorylation changes can affect individual disease susceptibility and therapeutic response.
- Genomic Research: Supports genome-wide analyses of SNPs that influence protein function via phosphorylation alterations.
- Pathway Analysis: Identifies nsSNPs that may rewire biological pathways by changing phosphorylation characteristics and kinase interactions.
Methodology:
GPS 2.0 is applied to predict kinase-specific phosphorylation sites affected by nsSNPs for genome-wide identification of potential phosSNPs, and identified phosSNPs are integrated into the PhosSNP 1.0 database implemented in JAVA 1.5 (J2SE 5.0).
Topics
Details
- Tool Type:
- web application
- Operating Systems:
- Linux, Windows, Mac
- Programming Languages:
- Java
- Added:
- 3/30/2017
- Last Updated:
- 12/10/2018
Operations
Publications
Ren J, et al. PhosSNP for systematic analysis of genetic polymorphisms that influence protein phosphorylation. Mol Cell Proteomics. 2010; 9:623-34. doi: 10.1074/mcp.M900273-MCP200
PMID: 19995808