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

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Gene Review: 

STT3A  -  STT3, subunit of the oligosaccharyltransfe...

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High impact information on STT3A

  • In contrast to embryonic cells, however, Chk1 is not required to delay mitosis when DNA synthesis is inhibited [1].
  • Furthermore, Chk1-dependent processes promote tumour cell survival after perturbations of DNA structure or metabolism [1].
  • Thus, Chk1 is dispensable for normal cell division in somatic DT40 cells but is essential for DNA damage-induced G(2)/M arrest and a subset of replication checkpoint responses [1].
  • These results suggest that Chk1 maintains the S-M checkpoint indirectly by preserving the viability of replication structures and that it is the continued presence of such structures, rather than the activation of Chk1 per se, which delays mitosis until DNA replication is complete [2].
 

Analytical, diagnostic and therapeutic context of STT3A

References

  1. Chk1-deficient tumour cells are viable but exhibit multiple checkpoint and survival defects. Zachos, G., Rainey, M.D., Gillespie, D.A. EMBO J. (2003) [Pubmed]
  2. Chk1-dependent S-M checkpoint delay in vertebrate cells is linked to maintenance of viable replication structures. Zachos, G., Rainey, M.D., Gillespie, D.A. Mol. Cell. Biol. (2005) [Pubmed]
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