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Gene Review

IPW  -  imprinted in Prader-Willi syndrome (non...

Homo sapiens

Synonyms: NCRNA00002
 
 
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Disease relevance of IPW

 

High impact information on IPW

  • Methylation and expression studies indicate that the paternal SNRPN allele is unaffected by the translocation, while IPW and PAR1 are unexpressed [3].
  • An imprinted mouse transcript homologous to the human imprinted in Prader-Willi syndrome (IPW) gene [4].
  • Lack of expression of IPW may contribute to the PWS phenotype directly [1].
  • Both H19 and Insulin-like growth Factor 2 (IGF2), two additional imprinted genes, also showed biallelic expression in those same tumors that demonstrated IPW biallelic expression [2].
  • Biallelic expression of IPW was found in testicular germ cell tumor and bladder cancer cells, suggesting loss of imprinting in the latter case [2].
 

Biological context of IPW

  • Recent studies of mouse models carrying a cytogenetic deletion suggest that paternal deficiency of the SNRPN-IPW interval is critical for perinatal lethality of potential relevance to PWS [5].
  • The SNURF-SNRPN sense/UBE3A antisense transcription unit spans more than 460 kb and contains at least 148 exons, including the previously identified IPW exons [6].
  • A systematic search for other imprinted genes in the Prader-Willi syndrome region revealed a paternally expressed transcript (IPW, for imprinted in the Prader-Willi region) and a similarly imprinted mouse homologue (Ipw) in the conserved syntenic region on mouse chromosome 7 [7].
  • Differences in AW/IPW and left/right coronary artery autonomic receptors distribution and flow regulation and/or changes in cardiovascular homeostasis/coagulation, aggregation, viscosity, microcirculation, and so on connected with AMI expansion may be involved in these differences of AMI localization [8].
 

Anatomical context of IPW

  • Previous work has demonstrated IPW expression in the human fetus and adult, with monoallelic expression in adult lymphoblasts and fibroblasts, and in fetal tissues [2].
  • Exclusive paternal expression at both SNRPN and IPW was maintained in all T cell clones and correlated with maternal methylation of the intron 1 NotI site [9].
  • Clonal maintenance of imprinted expression of SNRPN and IPW in normal lymphocytes: correlation with allele-specific methylation of SNRPN intron 1 but not intron 7 [9].
 

Other interactions of IPW

  • Paternal specific expression of the known imprinted genes SNRPN (small nuclear ribonucleoprotein-associated polypeptide N gene) and IPW (imprinted gene in the Prader-Willi syndrome region) was maintained in the A9 hybrids [10].
 

Analytical, diagnostic and therapeutic context of IPW

  • To further examine the expression of IPW, a series of experiments were carried out using RT-PCR to measure IPW expression in placentae and various fetal and tumor tissues [2].

References

  1. Identification of a novel paternally expressed gene in the Prader-Willi syndrome region. Wevrick, R., Kerns, J.A., Francke, U. Hum. Mol. Genet. (1994) [Pubmed]
  2. Characterization of the imprinted IPW gene: allelic expression in normal and tumorigenic human tissues. Rachmilewitz, J., Elkin, M., Looijenga, L.H., Verkerk, A.J., Gonik, B., Lustig, O., Werner, D., de Groot, N., Hochberg, A. Oncogene (1996) [Pubmed]
  3. Exclusion of SNRPN as a major determinant of Prader-Willi syndrome by a translocation breakpoint. Schulze, A., Hansen, C., Skakkebaek, N.E., Brøndum-Nielsen, K., Ledbeter, D.H., Tommerup, N. Nat. Genet. (1996) [Pubmed]
  4. An imprinted mouse transcript homologous to the human imprinted in Prader-Willi syndrome (IPW) gene. Wevrick, R., Francke, U. Hum. Mol. Genet. (1997) [Pubmed]
  5. Large-scale evaluation of imprinting status in the Prader-Willi syndrome region: an imprinted direct repeat cluster resembling small nucleolar RNA genes. Meguro, M., Mitsuya, K., Nomura, N., Kohda, M., Kashiwagi, A., Nishigaki, R., Yoshioka, H., Nakao, M., Oishi, M., Oshimura, M. Hum. Mol. Genet. (2001) [Pubmed]
  6. The IC-SNURF-SNRPN transcript serves as a host for multiple small nucleolar RNA species and as an antisense RNA for UBE3A. Runte, M., Hüttenhofer, A., Gross, S., Kiefmann, M., Horsthemke, B., Buiting, K. Hum. Mol. Genet. (2001) [Pubmed]
  7. Imprinted genes in the Prader-Willi deletion. Francke, U. Novartis Found. Symp. (1998) [Pubmed]
  8. Is localization of acute myocardial infarction time related? Stoupel, E., Shimshoni, M., Agmon, J. Clinical cardiology. (1988) [Pubmed]
  9. Clonal maintenance of imprinted expression of SNRPN and IPW in normal lymphocytes: correlation with allele-specific methylation of SNRPN intron 1 but not intron 7. Balmer, D., LaSalle, J.M. Hum. Genet. (2001) [Pubmed]
  10. Evidence for uniparental, paternal expression of the human GABAA receptor subunit genes, using microcell-mediated chromosome transfer. Meguro, M., Mitsuya, K., Sui, H., Shigenami, K., Kugoh, H., Nakao, M., Oshimura, M. Hum. Mol. Genet. (1997) [Pubmed]
 
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