Description: SH2 domain protein 2A RefSeq Summary (NM_003975): This gene encodes an adaptor protein thought to function in T-cell signal transduction. A related protein in mouse is responsible for the activation of lymphocyte-specific protein-tyrosine kinase and functions in downstream signaling. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Mar 2010]. Transcript (Including UTRs) Position: hg18 chr1:155,042,659-155,053,226 Size: 10,568 Total Exon Count: 9 Strand: - Coding Region Position: hg18 chr1:155,043,594-155,053,124 Size: 9,531 Coding Exon Count: 8
multiple sclerosis Dai KZ 2001, The T cell regulator gene SH2D2A contributes to the genetic susceptibility of multiple sclerosis, Genes and immunity. 2001 Aug;2(5):263-8.
[PubMed 11528519]
Since the SH2D2A protein modulates T cell activation, this may be a mechanism for how short SH2D2A alleles confer susceptibility to develop MS.
rheumatoid arthritis Smerdel, A. et al. 2004, Genetic association between juvenile rheumatoid arthritis and polymorphism in the SH2D2A gene., Genes and immunity. 2004 Jun;5(4):310-2.
[PubMed 15129233]
Our data indicate that the 'short' alleles of the SH2D2A promoter could contribute to the genetic susceptibility to JRA.
The RNAfold program from the Vienna RNA Package is used to perform the secondary structure predictions and folding calculations. The estimated folding energy is in kcal/mol. The more negative the energy, the more secondary structure the RNA is likely to have.
ModBase Predicted Comparative 3D Structure on Q9NP31-3
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Orthologous Genes in Other Species
Orthologies between human, mouse, and rat are computed by taking the best BLASTP hit, and filtering out non-syntenic hits. For more distant species reciprocal-best BLASTP hits are used. Note that the absence of an ortholog in the table below may reflect incomplete annotations in the other species rather than a true absence of the orthologous gene.