The murine homolog of SALL4, a causative gene in Okihiro syndrome, is essential for embryonic stem cell proliferation, and cooperates with Sall1 in anorectal, heart, brain and kidney development.

@article{SakakiYumoto2006TheMH,
  title={The murine homolog of SALL4, a causative gene in Okihiro syndrome, is essential for embryonic stem cell proliferation, and cooperates with Sall1 in anorectal, heart, brain and kidney development.},
  author={Masayo Sakaki-Yumoto and Chiyoko Kobayashi and Akira Sato and Sayoko Fujimura and Yuko Mizuno Matsumoto and Minoru Takasato and Tatsuhiko Kodama and Hiroyuki Aburatani and Makoto Asashima and Nobuaki Yoshida and Ryuichi Nishinakamura},
  journal={Development},
  year={2006},
  volume={133 15},
  pages={
          3005-13
        }
}
Mutations in SALL4, the human homolog of the Drosophila homeotic gene spalt (sal), cause the autosomal dominant disorder known as Okihiro syndrome. In this study, we show that a targeted null mutation in the mouse Sall4 gene leads to lethality during peri-implantation. Growth of the inner cell mass from the knockout blastocysts was reduced, and Sall4-null embryonic stem (ES) cells proliferated poorly with no aberrant differentiation. Furthermore, we demonstrated that anorectal and heart… CONTINUE READING

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