Identification of a Primary Target of Thalidomide Teratogenicity
By Takumi Ito, H. Ando, Takayuki Suzuki, T. Ogura, K. Hotta, Yoshimasa Imamura, Y. Yamaguchi, H. Handa. Science, 2010
1,868 citations recorded by the source corpus.
Subfields: Hematology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/23455446b96033d52607b743dde2c3e2a25b6685
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In Hematology
In Molecular Biology
- Steven A. Carr
- Yang Xie
- Benjamin L. Ebert
- Andrei N. Lupas
- N. Vargesson
- M. Coles
- Marcus D. Hartmann
- Johannes Söding
Citations in the corpus
- Lenalidomide induces ubiquitination and degradation of CK1α in del(5q) MDS (2015, background): “b, Immunoblot of CK1α protein levels in the bone marrow (1,2) and peripheral blood (3,4) mononuclear cells of AML patients treated with lenalidomide as part of a clinical trial.”
- Thalidomide‐induced teratogenesis: History and mechanisms (2015, background): “Several studies have demonstrated that Fgf8 signaling is reduced or lost in developing chicken and rabbit limbs, and zebrafish fins following thalidomide exposure (Hansen et al., 2002; Ito et al., 2010; Knobloch et al., 2011).”
- Anticancer sulfonamides target splicing by inducing RBM39 degradation via recruitment to DCAF15 (2017, background): “In another example of how chemical structure can influence neosubstrate preference, CC-885 was identified in a screen of IMiD derivatives as catalyzing the recruitment of GSPT1, a translation termination factor essential for myeloid leukemia cell proliferation, to CUL4-CRBN (44).”