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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
Gene Review

Hsdr1  -  hepatocyte specific developmental...

Mus musculus

Synonyms: Alf, albino-lethal factor, alf, hsdr-1
 
 
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Disease relevance of Hsdr1

 

High impact information on Hsdr1

  • This phenotype is thought to result from the loss of a positive transacting factor, denoted alf, in deletion homozygotes [2].
  • Surprisingly, a subset of these alf-responsive genes is negatively controlled by the tissue-specific extinguisher locus Tse-1 [2].
  • On the basis of this phenotype, it was proposed that these deletions remove a regulatory locus, alf or hsdr-1 [3].
  • Mice homozygous for albino deletions encompassing the locus alf/hsdr-1 die shortly after birth [4].
  • Mechanisms by which this metabolic defect might bring about alterations in gene expression characteristic of the alf/hsdr-1 deletion phenotype are discussed [4].
 

Biological context of Hsdr1

  • Here, we describe a detailed analysis of the region containing alf/hsdr-1 by means of chromosome jumping from flanking markers [5].
  • Using human radiation hybrid mapping and BAC contig construction, we have identified a conserved region of human chromosome 15 homologous to the mesd, nelg, and hsdr1 functional regions [6].
  • Genetic interaction between a maternal factor and the zygotic genome controls the intestine length in PRM/Alf mice [7].
 

Anatomical context of Hsdr1

 

Physical interactions of Hsdr1

  • Physical mapping of the albino-deletion complex in the mouse to localize alf/hsdr-1, a locus required for neonatal survival [9].
 

Other interactions of Hsdr1

 

Analytical, diagnostic and therapeutic context of Hsdr1

References

  1. Loss of fumarylacetoacetate hydrolase is responsible for the neonatal hepatic dysfunction phenotype of lethal albino mice. Grompe, M., al-Dhalimy, M., Finegold, M., Ou, C.N., Burlingame, T., Kennaway, N.G., Soriano, P. Genes Dev. (1993) [Pubmed]
  2. Two genetically defined trans-acting loci coordinately regulate overlapping sets of liver-specific genes. Ruppert, S., Boshart, M., Bosch, F.X., Schmid, W., Fournier, R.E., Schütz, G. Cell (1990) [Pubmed]
  3. Rescue of mice homozygous for lethal albino deletions: implications for an animal model for the human liver disease tyrosinemia type 1. Kelsey, G., Ruppert, S., Beermann, F., Grund, C., Tanguay, R.M., Schütz, G. Genes Dev. (1993) [Pubmed]
  4. Deficiency of an enzyme of tyrosine metabolism underlies altered gene expression in newborn liver of lethal albino mice. Ruppert, S., Kelsey, G., Schedl, A., Schmid, E., Thies, E., Schütz, G. Genes Dev. (1992) [Pubmed]
  5. Chromosome jumping from flanking markers defines the minimal region for alf/hsdr-1 within the albino-deletion complex. Schedl, A., Ruppert, S., Kelsey, G., Thies, E., Niswander, L., Magnuson, T., Klebig, M.L., Rinchik, E.M., Schütz, G. Genomics (1992) [Pubmed]
  6. Identification of mesoderm development (mesd) candidate genes by comparative mapping and genome sequence analysis. Wines, M.E., Lee, L., Katari, M.S., Zhang, L., DeRossi, C., Shi, Y., Perkins, S., Feldman, M., McCombie, W.R., Holdener, B.C. Genomics (2001) [Pubmed]
  7. Genetic interaction between a maternal factor and the zygotic genome controls the intestine length in PRM/Alf mice. Aubin-Houzelstein, G., Da Silva, N.R., Bellier, S., Salaün, P., Montagutelli, X., Panthier, J.J. Physiol. Genomics (2003) [Pubmed]
  8. Physical analysis of murine albino deletions that disrupt liver-specific gene regulation or mesoderm development. Klebig, M.L., Kwon, B.S., Rinchik, E.M. Mamm. Genome (1992) [Pubmed]
  9. Physical mapping of the albino-deletion complex in the mouse to localize alf/hsdr-1, a locus required for neonatal survival. Kelsey, G., Schedl, A., Ruppert, S., Niswander, L., Magnuson, T., Klebig, M.L., Rinchik, E.M., Schütz, G. Genomics (1992) [Pubmed]
  10. Transcriptional control in hepatocytes of normal and c14CoS albino deletion mice. Tönjes, R.R., Xanthopoulos, K.G., Darnell, J.E., Paul, D. EMBO J. (1992) [Pubmed]
 
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