In vitro binding assays with recombinant tTG and immobilized membrane lipids (Fig. S5A) or phosphoinositides (Fig. S5B) showed its interaction with PA, phosphatidylserine (PS), PI(4 P, PI(3 P, phosphatidylinositol (5 -phosphate [PI(5 -phosphate)P2, PI(4,5)P2, phosphatidyl-inositol (3,4)-diphosphate [PI 5 P]PI 3,5 P2non-PI 4,5 P2pid membrane compounds cardiolipin and sulfatide.
STRING database analysis shows its interaction with GTP cyclohydrolase I and 6-pyruvoyl tetrahydropterin synthase.
STRING database analysis shows its interaction with other P. falciparum phosphatases.
STRING database analysis shows its interaction with GAP50 acid phosphatase on the basis of binding evidences.
It is modeled to show its potential interaction with Asp95 in Rap.
Following the cellular uptake of a fluorescent analog of farnesol, we showed its close interaction with tobacco plastids and modification of plastid homeostasis.
Peptides 400 417, 435 452 and 547 564 from the HCV E2 protein did not give rise to any significant differences in the DEPE SAXD reflections, showing that its interaction with the membrane did not have any significant changes in the membrane structure of DEPE (Figures 4A, 4B and 4C).
As observed in Figure 5, peptides pertaining to sequences750 767, 771 788, and 785 802 did not give rise to any significant differences in the DEPE SAXD reflections, showing that its interaction with the membrane did not have any significant changes in the membrane structure of DEPE (Figures 5A, 5B and 5C).
Peptides 197 214 and 260 277 from E1 did not give rise to any significant differences in DEPE SAXD reflections, showing that its interaction with the membrane did not induce any significant changes in the membrane structure of DEPE (Figures 3A and 3B).
