When wild type αSNAP was added to the assay, exocytosis was completely recovered, suggesting that the primary defect in these cells is a deficient amount of functional αSNAP and not an abnormal maturation of sperm in SP mice (Fig. 7).
Mutant mice deficient for functional Smad3 show abnormally increased numbers of type X collagen-expressing chondrocytes in articular cartilage.
Post-mitotic nuclei deficient for functional cohesin exhibit global architectural changes associated with loss of cohesin/CTCF contacts and relaxation of topological domains.
In addition, ectopic expression of Serrate was shown to partially rescue the severe neuronal hyperplasia observed in Delta-deficient embryos [17], reinforcing the notion of functional redundancy between different ligands.
It has been demonstrated in CRB1-deficient (Crb1−/−) mice that the absence of functional CRB1 leads to a loss of interaction between Müller glial cells and photoreceptor cells which causes retinal disorganization followed relatively late by retinal degeneration accompanied by Müller cell gliosis [19], [20].
The ability of IL-6-deficient DCs to promote the generation of functional CD8+ Tm cells indicates that other soluble factors (IL-12 and IL-23) produced by DCs are sufficient to induce the generation of CD8+ Tm cells.
Our results demonstrate that in p53-deficient human gastric cancer cells, restoration of functional miR-34 inhibits cell growth and induces chemosensitization and apoptosis, indicating that miR-34 may restore p53 function.
Our results demonstrate that in p53-deficient human gastric cancer cells, restoration of functional microRNA miR-34 inhibits cell growth, induces apoptosis, and leads to chemosensitization, indicating that miR-34 may restore, at least in part, the p53 tumor-suppressing function.
To refine UGT73C6 function in the context of functional redundancy it was therefore aimed to generate plants deficient in the expression of both UGT73C6 and UGT73C5.
