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Ptpro  -  protein tyrosine phosphatase, receptor...

Rattus norvegicus

Synonyms: GLEPP1, RPTP-BK
 
 
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Disease relevance of Ptpro

 

High impact information on Ptpro

  • These data support the conclusion that the GLEPP1 (Ptpro) receptor plays a role in regulating the glomerular pressure/filtration rate relationship through an effect on podocyte structure and function [3].
  • Reduced filtration surface area in association with these structural changes was confirmed by finding reduced glomerular nephrin content and reduced glomerular filtration rate in Ptpro(-/-) mice [3].
  • After removal of one or more kidneys, Ptpro(-/-) mice had higher blood pressure than did their wild-type littermates [3].
  • Heterozygote mating produced the expected genotypic ratio of 1:2:1, indicating that the Ptpro(-/-) genotype does not lead to embryonic or neonatal lethality [3].
  • Bisulfite genomic sequencing of the CpG island encompassing exon 1 of the PTPRO gene revealed dense methylation in the PNNs and tumors, whereas it was methylation free in the livers of animals on normal diet [2].
 

Chemical compound and disease context of Ptpro

 

Biological context of Ptpro

 

Anatomical context of Ptpro

 

Associations of Ptpro with chemical compounds

  • METHODS: The number of podocytes per glomerular section and the podocyte density in glomeruli from rats and mice with streptozotocin (STZ)-diabetes mellitus was determined at several time points based on detection of the glomerular podocyte specific antigens, WT-1 and GLEPP1 [5].
 

Other interactions of Ptpro

  • RPTP-BK has seven fibronectin type III-like repeats in the extracellular region and a unique catalytic phosphatase domain in the cytoplasmic region [4].
  • RESULTS: Cells obtained in the urine from PHN rats were positive for synaptopodin, nephrin, podocin, WT-1, and GLEPP1 (podocyte-specific antigens) [6].
 

Analytical, diagnostic and therapeutic context of Ptpro

  • To better understand the utility of GLEPP1 as a marker of glomerular injury, the amount and distribution of GLEPP1 protein and mRNA were examined by immunohistochemistry, Western blot and RNase protection assay in a model of podocyte injury in the rat [1].
  • Scanning and transmission electron microscopy showed that Ptpro(-/-) mice had an amoeboid rather than the typical octopoid structure seen in the wild-type mouse podocyte and that there were blunting and widening of the minor (foot) processes in association with altered distribution of the podocyte intermediate cytoskeletal protein vimentin [3].

References

  1. GLEPP1 receptor tyrosine phosphatase (Ptpro) in rat PAN nephrosis. A marker of acute podocyte injury. Kim, Y.H., Goyal, M., Wharram, B., Wiggins, J., Kershaw, D., Wiggins, R. Nephron (2002) [Pubmed]
  2. Suppression of the protein tyrosine phosphatase receptor type O gene (PTPRO) by methylation in hepatocellular carcinomas. Motiwala, T., Ghoshal, K., Das, A., Majumder, S., Weichenhan, D., Wu, Y.Z., Holman, K., James, S.J., Jacob, S.T., Plass, C. Oncogene (2003) [Pubmed]
  3. Altered podocyte structure in GLEPP1 (Ptpro)-deficient mice associated with hypertension and low glomerular filtration rate. Wharram, B.L., Goyal, M., Gillespie, P.J., Wiggins, J.E., Kershaw, D.B., Holzman, L.B., Dysko, R.C., Saunders, T.L., Samuelson, L.C., Wiggins, R.C. J. Clin. Invest. (2000) [Pubmed]
  4. Identification of a receptor-type protein tyrosine phosphatase expressed in postmitotic maturing neurons: its structure and expression in the central nervous system. Tagawa, M., Shirasawa, T., Yahagi, Y., Tomoda, T., Kuroyanagi, H., Fujimura, S., Sakiyama, S., Maruyama, N. Biochem. J. (1997) [Pubmed]
  5. Reduction in podocyte density as a pathologic feature in early diabetic nephropathy in rodents: prevention by lipoic acid treatment. Siu, B., Saha, J., Smoyer, W.E., Sullivan, K.A., Brosius, F.C. BMC nephrology [electronic resource]. (2006) [Pubmed]
  6. Podocytes that detach in experimental membranous nephropathy are viable. Petermann, A.T., Krofft, R., Blonski, M., Hiromura, K., Vaughn, M., Pichler, R., Griffin, S., Wada, T., Pippin, J., Durvasula, R., Shankland, S.J. Kidney Int. (2003) [Pubmed]
 
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