We are proud to mention publications in which DAPCEL, Inc. technology was successfully utilized:
Skabkin, M.A., Skabkina, O.V., Dhote, V., Komar, A.A., Hellen, C.U., Pestova, T.V. (2010) Activities of Ligatin and MCT-1/DENR in eukaryotic translation initiation and ribosomal recycling. Genes Dev. 24, 1787-1801.
This is a first manuscript in which DAPCEL, Inc gene redesign technology was utilized. In this paper a gene of the human DHX29 (1369 amino acid long DExH-box protein) was reverse engineered by selection of rare synonymous codons to ensure correct co-translational folding of DHX29 in a heterologous host (E. coli). The protein was expressed in its active, soluble form and purified to homogeneity. Activity of the recombinant protein was found to be identical to that of the protein purified previously from mammalian cells (Pisareva, V.P., Pisarev, A.V., Komar, A.A., Hellen, C.U., Pestova, T.V. (2008) Translation initiation on mammalian mRNAs with structured 5'UTRs requires DExH-box protein DHX29. Cell 135, 1237-1250).
DAPCEL, Inc optimized genes have been successfully used in the following additional papers:
Dhote, V., Sweeney, T.R., Kim, N., Hellen, C.U., Pestova, T.V. (2012) Roles of individual domains in the function of DHX29, an essential factor required for translation of structured mammalian mRNAs. Proc Natl Acad Sci U S A 109, E3150-E3159.
Garcia, H., Miecznikowski, J.C., Safina, A., Commane, M., Ruusulehto, A., Kilpinen, S., Leach, R.W., Attwood, K., Li, Y., Degan, S., Omilian, A.R., Guryanova, O., Papantonopoulou, O., Wang, J., Buck, M., Liu, S., Morrison, C., Gurova, K.V. (2013) Facilitates chromatin transcription complex is an "accelerator" of tumor transformation and potential marker and target of aggressive cancers. Cell Rep. 4, 159-173.
Publications utilizing DAPCEL, Inc. products
We are proud to mention several recent publications in which DAPCEL, Inc. products (and in particular our highest specific activity Oncostatin M) were successfully utilized:
Bryson, B.L., Junk, D.J., Cipriano, R., Jackson, M.W. (2017) STAT3-mediated SMAD3 activation underlies Oncostatin M-induced Senescence. Cell Cycle. 16, 319-334.
Junk, D.J., Bryson, B.L., Smigiel, J.M., Parameswaran, N., Bartel, C.A., Jackson, M.W. (2017) Oncostatin M promotes cancer cell plasticity through cooperative STAT3-SMAD3 signaling. Oncogene. Mar 13. doi: 10.1038/onc.2017.33. [Epub ahead of print].
Smigiel, J.M., Parameswaran, N., Jackson, M.W. (2017) Potent EMT and CSC Phenotypes Are Induced By Oncostatin-M in Pancreatic Cancer. Mol Cancer Res. 15, 478-488.