Our hosting provider will be undergoing maintenance on Tuesday, August 30 between 8am and 5pm PDT. SciCrunch services may be offline during the maintenance.

Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

The murine SNF5/INI1 chromatin remodeling factor is essential for embryonic development and tumor suppression.

The assembly of eukaryotic DNA into nucleosomes and derived higher order structures constitutes a barrier for transcription, replication and repair. A number of chromatin remodeling complexes, as well as histone acetylation, were shown to facilitate gene activation. To investigate the function of two closely related mammalian SWI/SNF complexes in vivo, we inactivated the murine SNF5/INI1 gene, a common subunit of these two complexes. Mice lacking SNF5 protein stop developing at the peri-implantation stage, showing that the SWI/SNF complex is essential for early development and viability of early embryonic cells. Furthermore, heterozygous mice develop nervous system and soft tissue sarcomas. In these tumors the wild-type allele was lost, providing further evidence that SNF5 functions as a tumor suppressor gene in certain cell types.

Pubmed ID: 11263494

Authors

  • Klochendler-Yeivin A
  • Fiette L
  • Barra J
  • Muchardt C
  • Babinet C
  • Yaniv M

Journal

EMBO reports

Publication Data

December 23, 2000

Associated Grants

None

Mesh Terms

  • Alleles
  • Animals
  • Apoptosis
  • Blastocyst
  • Blotting, Southern
  • Cell Death
  • Chromosomal Proteins, Non-Histone
  • Crosses, Genetic
  • DNA-Binding Proteins
  • Embryo, Mammalian
  • Exons
  • Female
  • Gene Expression Regulation
  • Gene Expression Regulation, Developmental
  • Genetic Predisposition to Disease
  • Genotype
  • Heterozygote
  • Immunohistochemistry
  • In Situ Nick-End Labeling
  • Lac Operon
  • Loss of Heterozygosity
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Models, Genetic
  • Mutagenesis
  • Neoplasms
  • Polymerase Chain Reaction
  • Stem Cells
  • Time Factors
  • Transcription Factors
  • Transcription, Genetic
  • Transcriptional Activation
  • Vimentin
  • beta-Galactosidase