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Gene Review

Blm  -  Bloom syndrome, RecQ helicase-like

Mus musculus

Synonyms: Bloom syndrome protein homolog, RecQ helicase homolog, mBLM
 
 
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Disease relevance of Blm

  • The proportional dwarfism seen in the human is consistent with the small size and developmental delay (12-24 hr) seen during mid-gestation in murine Blm-/- embryos [1].
  • Blm-deficient mice, like Bloom syndrome patients, have increased frequencies of mitotic recombination owing to a mutation in the RecQ protein-like-3 helicase gene [2].
 

High impact information on Blm

 

Biological context of Blm

 

Anatomical context of Blm

  • Embryonic stem cells deficient for Brca2 or Blm exhibit divergent genotoxic profiles that support opposing activities during homologous recombination [8].
  • The mBLM mRNA level in the testis began to increase 12-14 days after birth, corresponding to the appearance of cells in the pachytene phase [9].
 

Associations of Blm with chemical compounds

  • However, the same approach was hampered in mouse tissues owing to leaky expression of the Blm gene, which is the major obstacle in the tetracycline regulatory system [5].
  • A cassette containing both sc rtTS and tTA was introduced into the Blm allele in ES cells and reduction of basal activity was observed upon doxycycline treatment [5].
  • By contrast, Blm-impaired cells are hypersensitive to ICRF-193, mildly resistant to camptothecin and mitomycin C and more strongly resistant to hydroxyurea [8].
  • Indeed, a combination of N-ethyl-N-nitrosourea mutagenesis and transient loss of Blm expression enabled us to generate an ES cell library with genome-wide bi-allelic mutations [10].
 

Other interactions of Blm

References

  1. Stage-specific apoptosis, developmental delay, and embryonic lethality in mice homozygous for a targeted disruption in the murine Bloom's syndrome gene. Chester, N., Kuo, F., Kozak, C., O'Hara, C.D., Leder, P. Genes Dev. (1998) [Pubmed]
  2. Tumor suppressor gene identification using retroviral insertional mutagenesis in Blm-deficient mice. Suzuki, T., Minehata, K., Akagi, K., Jenkins, N.A., Copeland, N.G. EMBO J. (2006) [Pubmed]
  3. Mutation of the murine Bloom's syndrome gene produces global genome destabilization. Chester, N., Babbe, H., Pinkas, J., Manning, C., Leder, P. Mol. Cell. Biol. (2006) [Pubmed]
  4. Recql5 and Blm RecQ DNA helicases have nonredundant roles in suppressing crossovers. Hu, Y., Lu, X., Barnes, E., Yan, M., Lou, H., Luo, G. Mol. Cell. Biol. (2005) [Pubmed]
  5. Bloom's syndrome gene-deficient phenotype in mouse primary cells induced by a modified tetracycline-controlled trans-silencer. Hayakawa, T., Yusa, K., Kouno, M., Takeda, J., Horie, K. Gene (2006) [Pubmed]
  6. Induction of renal tumorigenesis with elevated levels of somatic loss of heterozygosity in Tsc1+/- mice on a Blm-deficient background. Wilson, C., Idziaszczyk, S., Colley, J., Humphreys, V., Guy, C., Maynard, J., Sampson, J.R., Cheadle, J.P. Cancer Res. (2005) [Pubmed]
  7. Analysis of the role of RecQ helicases in RNAi in mammals. Stein, P., Svoboda, P., Stumpo, D.J., Blackshear, P.J., Lombard, D.B., Johnson, B., Schultz, R.M. Biochem. Biophys. Res. Commun. (2002) [Pubmed]
  8. Embryonic stem cells deficient for Brca2 or Blm exhibit divergent genotoxic profiles that support opposing activities during homologous recombination. Marple, T., Kim, T.M., Hasty, P. Mutat. Res. (2006) [Pubmed]
  9. cDNA cloning of mouse BLM gene, the homologue to human Bloom's syndrome gene, which is highly expressed in the testis at the mRNA level. Seki, T., Wang, W.S., Okumura, N., Seki, M., Katada, T., Enomoto, T. Biochim. Biophys. Acta (1998) [Pubmed]
  10. Genome-wide phenotype analysis in ES cells by regulated disruption of Bloom's syndrome gene. Yusa, K., Horie, K., Kondoh, G., Kouno, M., Maeda, Y., Kinoshita, T., Takeda, J. Nature (2004) [Pubmed]
  11. Mismatch repair genes identified using genetic screens in Blm-deficient embryonic stem cells. Guo, G., Wang, W., Bradley, A. Nature (2004) [Pubmed]
 
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