Differential hepatocyte toxicity of recombinant Apo2L/TRAIL versions
By D. Lawrence, Z. Shahrokh, S. Marsters, Kirsten A. Achilles, Danny Shih, B. Mounho, Kenneth J. Hillan, K. Totpal, L. Deforge, P. Schow and 13 more. Nature Medicine, 2001
757 citations recorded by the source corpus.
Subfields: Hepatology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/c3e1ec076d1af38b4d95701c7c7e561b04bb6a2a
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In Molecular Biology
Citations in the corpus
- Apo2L/TRAIL and its death and decoy receptors (2003, background): “It is not fully understood why normal cells and certain tumour cells are resistant to Apo2L/TRAIL.”
- Extrinsic versus intrinsic apoptosis pathways in anticancer chemotherapy (2006, background): “…may be related to the TRAIL preparations used in these studies, since TRAIL preparations, which are antibody-crosslinked or not optimized for Zn content, have been reported to form multimeric aggregates thereby overpassing the threshold of sensitivity of normal cells (Lawrence et al., 2001).”
- Death-receptor O-glycosylation controls tumor-cell sensitivity to the proapoptotic ligand Apo2L/TRAIL (2007, methodology): “0 4 12 37 111 333 1000 C el l V ia bi lit y (% ) siControl siCASP8 siGALNT3 (1) siGALNT3 (2) siGALNT3 (3)”
- Apo2L/TRAIL: apoptosis signaling, biology, and potential for cancer therapy. (2003, methodology): “[26] Lawrence D, Shahrokh Z, Marsters S, Achilles K, Shih D, Mounho B, et al.”