Description: Homo sapiens protein tyrosine phosphatase, receptor type, S (PTPRS), transcript variant 4, mRNA. RefSeq Summary (NM_130855): The protein encoded by this gene is a member of the protein tyrosine phosphatase (PTP) family. PTPs are known to be signaling molecules that regulate a variety of cellular processes including cell growth, differentiation, mitotic cycle, and oncogenic transformation. This PTP contains an extracellular region, a single transmembrane segment and two tandem intracytoplasmic catalytic domains, and thus represents a receptor-type PTP. The extracellular region of this protein is composed of multiple Ig-like and fibronectin type III-like domains. Studies of the similar gene in mice suggested that this PTP may be involved in cell-cell interaction, primary axonogenesis, and axon guidance during embryogenesis. This PTP has been also implicated in the molecular control of adult nerve repair. Four alternatively spliced transcript variants, which encode distinct proteins, have been reported. [provided by RefSeq, Jul 2008]. Transcript (Including UTRs) Position: hg19 chr19:5,205,519-5,340,814 Size: 135,296 Total Exon Count: 30 Strand: - Coding Region Position: hg19 chr19:5,206,785-5,286,151 Size: 79,367 Coding Exon Count: 29
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.
SCOP Domains: 48726 - Immunoglobulin 49265 - Fibronectin type III 52799 - (Phosphotyrosine protein) phosphatases II
ModBase Predicted Comparative 3D Structure on Q13332-7
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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.