Similar observations about the subcellular localization of Yap1 were made with mouse MIN6 β-cells (Fig. 2D-F′), indicating that it might be a general response for Yap1 to be activated after palmitate-induced apoptosis in mammalian β-cell lines.
Interestingly, we also have initial observations that the subcellular distribution of Gαs changes upon odorant exposure, with Gαs showing a marked redistribution from the dendrites of the sensory neurons to the base of the sensilla upon odorant exposure, providing further indication of an involvement of the protein in the signaling cascade (Figure S6).
Our observations regarding the subcellular responses of somata vs. dendrites to excitotoxic insults suggest a disconnection between the severity of ATP depletion and the degree of mitochondrial depolarisation.
However, we had not yet published our detailed observations on the subcellular localization of ESCRT-III and report them here.
The reconstitution of IFP fluorescence, representing the formation of a stabilized PDK1-IFPC::IFPN-AKT1 complex, allowed direct observation of the subcellular localization of the complex.
Observation of the subcellular localization of NHERF1 protein in tumor and contiguous non-involved tissues from the same patient revealed that cytoplasmic NHERF1 expression progressively increased in tumors cells from normal to invasive and metastatic tissues.
After evaluating possible effects of incomplete or incorrect annotations, we conclude that our observation of the subcellular relocalization after gene duplication on the genomic scale was robust to misannotations.
Our observation that the subcellular localization of Par3 and aPKC is altered in polarized numb-shRNA cells before HGF treatment strongly suggests that Numb also has an important function in regulating the stability of TJs.
For observation of the subcellular localization of PIN GFP after BFA, MG132, auxin, or wortmannin treatment, seedlings were incubated in half-strength liquid MS medium for the indicated time periods.
To confirm these observations we analyzed the subcellular distribution of STAT5A-eYFP and STAT5AR618Q-eYFP, which harbors an inactivating mutation in the SH2 domain, in the presence of vSrc-dsRed in HeLa T-REx FRT cells.
