Only the mutants that bound to YopJ, P15 and P16, were acetylated by YopJ (Figure 6B).
Nine rounds of FACS were used to isolate mutants that bound with high affinity to αvβ3 integrin (Table S2).
Those mutants that bound AZD9773 were analysed for their ability to induce cytotoxicity in L929 cells (Supplementary Table S1, available at http://www.bioscirep.org/bsr/033/bsr033e060add.htm) and their susceptibility to inhibition by AZD9773.
We will use ribosome display to select Cyt1Aa mutants that bind other Cry toxins as a way to develop tools for improving Bt Cry toxicity against specific insect targets.
More recent studies described 2 C3 mutants that bind CFB with higher affinity, resulting in a more stable C3 convertase complex.
Expression of activated Ras effector domain mutants that bind Raf, PI3K, or RalGEF are sufficient to induce the anchorage-independent growth of the human mammary epithelial cell line HME16C and are associated with up-regulation of EGFR ligands.
A breakthrough approach to identifying PARP-1 targets proteome-wide has been recently reported by Carter-O'Connell et al. using PARP-1 and PARP-2 mutants that bind a "clickable" NAD+ analog, followed by copper-catalyzed conjugation to an azidoalkyl reporter ("click" chemistry) and tandem mass spectrometry.
Noticeably, in both the MG-132 and concanamycin A experiments, co-expression of Oxr1-C with Fus and Tdp-43 mutants that bind poorly to Oxr1-C (Fus P517L, Tdp-43 and1G and Tdp-43 D169G; Fig. 2B) does not show a reduction in Fus or Tdp-43 cytoplasmic inclusions, suggesting that the binding of Oxr1 to Fus and Tdp-43 is necessary to influence inclusion formation.
Additionally, the ribbon organization of the Golgi is disturbed in KIF1C siRNA cells, a phenotype that can be suppressed by KIF1C expression, and not by the loop 6/10 mutant, but, significantly, can be rescued by a KIF1C mutant that binds Rab6 but not microtubules.
The circular dichroism spectra suggested that the structures of the single-mutant proteins that bound Cd or Zn were similar to that of the D11C/S28C double-mutant proteins.
Nonetheless, the RRM-deleted mutant (ΔRRM) that did not bind to U6 showed promotion in vitro pre-mRNA splicing, whereas the nuclear localization signal (NLS -deleted mutaNLS -deleted bound to U6 promutantthe pre-mRNA splicing both in vitro and in vivo.
