Close to the Tyr, mutation of C206 caused loss of flavin from the complex, and within the same region of the protein, but at increased distance from the flavin are A211 (non-conserved) and E214 (intermediate behavior).
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Previous studies have shown that disruption of TZ complexes causes loss of Y-links and/or changes in microxtubule-membrane linkage [ 20, 23]; as such, the correlation between absence of both TZ complex proteins and ciliary Y-links in the non-seed land plants is consistent with the theory that the TZ complex proteins are involved in the formation of Y-links [ 21, 22].
SGF29 deletion causes loss of H3K9ac and loss of SAGA complex at target sites 49.
Given that several of these proteins contain transmembrane domains, and that disruption of TZ complex proteins often causes loss of ciliary Y-links [ 20, 23, 24], the model also suggests that TZ complex proteins may make up the Y-links connecting the axonemal doublets to the membrane [ 21, 22].
During wing disc development, the mutant clone cells, containing a deficiency that eliminates all the members of this complex, did not cause loss of wing margin; however, the differentiation of sensory structures and the pattern of veins was affected (de Celis et al., 1996b).
Knockdown of PHB1 causes loss of PHB1 membrane localization and disruption of the PHB1/C-Raf complex, which further attenuate Tan IIA-induced apoptosis of activated HSCs [ 9].
A high rate of complex internalization may result in high intracellular concentrations of DM1, and deceleration of the endocytosis rate might cause loss of sensitivity to T-DM1.
Our studies implicate a more complex, lineage-dependent mechanism in which TCDD stimulates growth of rHpSCs and, in parallel, causes loss of viability of rHBs.
Although different more complex recalibration functions may provide better recalibration on training data, they are inadvisable because they can cause loss of generalization.
