Characterization of the null murine sodium/myo-inositol cotransporter 1 (Smit1 or Slc5a3) phenotype: myo-inositol rescue is independent of expression of its cognate mitochondrial ribosomal protein subunit 6 (Mrps6) gene and of phosphatidylinositol levels in neonatal brain.

doi:10.1016/j.ymgme.2008.05.008

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Characterization of the null murine sodium/myo-inositol cotransporter 1 (Smit1 or Slc5a3) phenotype: myo-inositol rescue is independent of expression of its cognate mitochondrial ribosomal protein subunit 6 (Mrps6) gene and of phosphatidylinositol levels in neonatal brain.

Molecular genetics and metabolism - 1 Jan 2000

Buccafusca Roberto, Venditti Charles P, Kenyon Lawrence C, Johanson Roy A, Van Bockstaele Elisabeth, Ren Jun, Pagliardini Silvia, Minarcik Jeremy, Golden Jeffrey A, Coady Michael J, Greer John J, Berry Gerard T

Abstract excerpt

Ablation of the murine Slc5a3 gene results in severe myo-inositol (Ins) deficiency and congenital central apnea due to abnormal respiratory rhythmogenesis. The lethal knockout phenotype may be rescued by supplementing the maternal drinking water with 1% Ins. In order to test the hypothesis that Ins deficiency leads to inositide deficiencies, which are corrected by prenatal treatment, we measured the effects of...

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PMID: 18675571
DOI: 10.1016/j.ymgme.2008.05.008

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Characterization of the null murine sodium/myo-inositol cotransporter 1 (Smit1 or Slc5a3) phenotype: myo-inositol rescue is independent of expression of its cognate mitochondrial ribosomal protein subunit 6 (Mrps6) gene and of phosphatidylinositol levels in neonatal brain.PMID 18675571Read ↗

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