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Mcl-1 deficiency results in peri-implantation embryonic lethality.

Genes & development | Jan 1, 2000

http://www.ncbi.nlm.nih.gov/pubmed/10640272

We disrupted the Mcl-1 locus in murine ES cells to determine the developmental roles of this Bcl-2 family member. Deletion of Mcl-1 resulted in peri-implantation embryonic lethality. Mcl-1(-/-) embryos do not implant in utero, but could be recovered at E3.5-4.0. Null blastocysts failed to hatch or attach in vitro, indicating a trophectoderm defect, although the inner cell mass could grow in culture. Of note, Mcl-1(-/-) blastocysts showed no evidence of increased apoptosis, but exhibited a delay in maturation beyond the precompaction stage. This model indicates that Mcl-1 is essential for preimplantation development and implantation, and suggests that it has a function beyond regulating apoptosis.

Pubmed ID: 10640272 RIS Download

Mesh terms: Animals | Apoptosis | Crosses, Genetic | Embryo Implantation | Female | Fetal Death | Humans | In Situ Hybridization | In Situ Nick-End Labeling | Myeloid Cell Leukemia Sequence 1 Protein | Neoplasm Proteins | Polymerase Chain Reaction | Proto-Oncogene Proteins c-bcl-2

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Associated grants

  • Agency: NCI NIH HHS, Id: CA49712-10

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