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To address these potential mechanisms, we generated an N-terminal FLAG epitope-tagged derivative of c-Myb, expressed from a lentiviral vector, which we used to transduce the Jurkat T-cells so that it was stably expressed.
To separately evaluate these mechanisms, we generated D/− mice carrying a single copy of the mutant allele but lacking wild-type Nav1.6.
In order to further clarify the functions of gankyrin and better understand its molecular mechanisms, we generated a gankyrin null cell line from the human colon cancer cell line, HCT116, by gene targeting.
To address the question whether Bcl11b regulates neuronal differentiation cell autonomously or through indirect mechanisms, we generated a mosaic deletion of Bcl11b by ex utero electroporation of Cre recombinase into Bcl11bflox/flox brains at E15.5 followed by organotypic slice culture up to 14 DIV.
To determine which DPR is toxic in vivo and identify the mechanisms, we generated DNA constructs containing 80 copies of GGXGCX, GGXCGX, or CCXCGX (with X being randomly any one of the four nucleotides) that can be transcribed under the control of UAS elements and translated into (GA 80, (GR 80, or (PR 80, respectively.
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To investigate the functional consequence of Rnd3 downregulation and the associated molecular mechanism, we generated Rnd3+/− haploinsufficient mice to mimic the downregulation of Rnd3 observed in the failing human heart.
To investigate this dimerization mechanism, we generated a substrate-binding-deficient variant of Hsp70 E.coli (V438F), which also includes the phosphomimic T504E and was shown to be unable to bind substrates in DnaK and Hsp70 (Mayer et al., 2000, Rohrer et al., 2014).
Based on known data about the behavior of the sound transmission mechanism, we generate a model that reproduces the real mechanics of the middle ear by the finite elements method in the most exact manner possible.
To explore these mechanisms further, we generated catalogs of somatic mutation from 21 breast cancers and applied mathematical methods to extract mutational signatures of the underlying processes.
To investigate this compensatory mechanism further, we generated a series of double mutants for lys-7 and the three candidate genes (abl-1, fat-5 and rga-6) identified by resistance analysis, and tested their susceptibility to infection with C. neoformans and S. Typhimurium.
To further elucidate the physiological role of PINK1 in mammalian tissue and to gain insight in the disease mechanisms of PARK6, we generated a PINK1 deficient mouse and assessed degrees of mitochondrial dysfunction at old age and the consequences for growth, motor performance, neuronal activity and aggregation/degeneration.
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