The SMADIP1 gene (also known as SIP1) is a member of the delta-EF1 (TCF8)/Zfh1 family of 2-handed zinc finger/homeodomain proteins. SMADIP1 interacts with receptor-mediated, activated full-length SMADs.[1]
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Wakamatsu N; Yamada Y; Yamada K et al. (2001). "Mutations in SIP1, encoding Smad interacting protein-1, cause a form of Hirschsprung disease". Nat. Genet.27 (4): 369–70. doi:10.1038/86860. PMID11279515.Cite uses deprecated parameter |author-separator= (help)
Comijn J; Berx G; Vermassen P et al. (2001). "The two-handed E box binding zinc finger protein SIP1 downregulates E-cadherin and induces invasion". Mol. Cell7 (6): 1267–78. doi:10.1016/S1097-2765(01)00260-X. PMID11430829.Cite uses deprecated parameter |author-separator= (help)
Cacheux V; Dastot-Le Moal F; Kääriäinen H et al. (2001). "Loss-of-function mutations in SIP1 Smad interacting protein 1 result in a syndromic Hirschsprung disease". Hum. Mol. Genet.10 (14): 1503–10. doi:10.1093/hmg/10.14.1503. PMID11448942.Cite uses deprecated parameter |author-separator= (help)
Tylzanowski P, Verschueren K, Huylebroeck D, Luyten FP (2001). "Smad-interacting protein 1 is a repressor of liver/bone/kidney alkaline phosphatase transcription in bone morphogenetic protein-induced osteogenic differentiation of C2C12 cells". J. Biol. Chem.276 (43): 40001–7. doi:10.1074/jbc.M104112200. PMID11477103.
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Espinosa-Parrilla Y; Amiel J; Augé J et al. (2003). "Expression of the SMADIP1 gene during early human development". Mech. Dev.114 (1–2): 187–91. doi:10.1016/S0925-4773(02)00062-X. PMID12175509.Cite uses deprecated parameter |author-separator= (help)
Yoneda M; Fujita T; Yamada Y et al. (2002). "Late infantile Hirschsprung disease-mental retardation syndrome with a 3-bp deletion in ZFHX1B". Neurology59 (10): 1637–40. doi:10.1212/01.wnl.0000034842.78350.4e. PMID12451214.Cite uses deprecated parameter |author-separator= (help)