A Heteromorphic Protein-tyrosine Phosphatase, PTPϕ, Is Regulated by CSF-1 in Macrophages ()

A novel protein-tyrosine phosphatase, PTPϕ, was cloned from a murine macrophage cDNA library. As a result of alternative splicing, macrophage PTPϕ mRNAs are predicted to encode two membrane-spanning molecules and a cytosolic enzyme with identical catalytic domains. The membrane-spanning forms differ...

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Bibliographic Details
Published inThe Journal of biological chemistry Vol. 270; no. 45; pp. 27339 - 27347
Main Authors Pixley, Fiona J., Lee, Pierre S.W., Dominguez, Melissa G., Einstein, Douglas B., Stanley, E. Richard
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 10.11.1995
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Summary:A novel protein-tyrosine phosphatase, PTPϕ, was cloned from a murine macrophage cDNA library. As a result of alternative splicing, macrophage PTPϕ mRNAs are predicted to encode two membrane-spanning molecules and a cytosolic enzyme with identical catalytic domains. The membrane-spanning forms differ in the juxtamembrane region, while a start codon downstream of this region is utilized in the translation of the putative cytosolic form. Expression of PTPϕ mRNA is low and restricted to macrophage cell lines, macrophage-rich tissues, and brain, kidney, and heart. The mRNA in macrophages and heart is ∼2.8 kilobases (kb). However, a ∼5.5-kb transcript in brain and kidney indicates a fourth isoform encoding a large extracellular domain. The ∼5.5-kb PTPϕ brain mRNA encodes the mouse homolog of GLEPP1, a recently reported glomerular epithelial protein. The level of expression of the mRNA encoding the cytosolic form was very low, and only the membrane-spanning proteins (43 and 47 kDa) could be detected in macrophages. Following addition of colony stimulating factor-1 to quiescent BAC1.2F5 macrophages, PTPϕ mRNA and protein were down-regulated. The restricted expression of the shorter isoforms of PTPϕ and their regulation by colony stimulating factor-1 in macrophages suggest that PTPϕ may play a role in mononuclear phagocyte survival, proliferation, and/or differentiation.
Bibliography:ObjectType-Article-2
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ISSN:0021-9258
1083-351X
DOI:10.1074/jbc.270.45.27339