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Our design considered up to three tandemly arranged BP100 units and peptide accumulation in the endoplasmic reticulum (ER), analyzing five BP100 derivatives.
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ER analyzed the data and drafted the manuscript.
CK and ER analyzed the data, drafted the manuscript and revised the manuscript.
Using a cell line that contains a visible prolactin enhancer/promoter array (PRL-HeLa) regulated by ER, we analyzed ER response to E2 and EGF by quantifying image-based results.
To test whether other ER family members compensate for the mutation in ER, we analyzed the expression of ER, ERECTA LIKE 1 and ERECTA LIKE 2 (ERL1 and ERL2).
We tested this by crossing the Ac (No-0) parent to wild type La-er, and analyzing marker segregation in F2 lines that were either selected or not selected on NAM.
The numerical aberrations were classified into DP, PP, and ER, and the frequencies of PP + ER were analyzed.
Er/APv showed selectivity towards platelets and αIIbβ3 integrin transfected cells and reacted with the same region as unlabeled Er, as analyzed in competition assays.
Figure 5A shows an IPA network of these various ER components (analyzed separately from other differentially expressed genes).
To further assess the NPA insensitivity of putative auxin carriers at the ER, we analyzed PILS putative auxin carrier activity in our system.
Although our data already argue against svt2 being a result of an artifact of the experiment or a contamination with L er, we analyzed subsequent svt2 generations and discovered additional characteristics that are unique to svt2.
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