Additional file 2 of STIM1 at the plasma membrane as a new target in progressive chronic lymphocytic leukemia

Table S1. B cell receptors (BCR) and co-receptors analysis in B-CLL cells (n = 30) according to the capacity of the cells to possess an elevated constitutive Ca2+ entry (CE+) and their capacity to mobilize Ca2+ in response to BCR engagement (IgM+). The phosphorylated phospholipase Cγ2 (pPLCγ2), an immediate downstream BCR effector, was added to the list. Figure S2. Representative kinetic plots of anti-IgM Ca2+ response (A), and thapsigargin (TG) Ca2+ response (B) in representative healthy donor (HD) control B cells (n = 8), CE- B-CLL (n = 13) and CE+ B-CLL (n = 16) samples. Cox regression model of progression free survival (PFS) was used to dichotomize CLL patients in IgM- and IgM+ (dash line). From the TG Ca2+ response analysis, the basal Ca2+ level was evaluated before normalization (1), the TG capacity to release Ca2+ from the endoplasmic reticulum (ER), and the TG capacity to release SOCE following extracellular medium supplementation with 1.8 mM Ca2+. P values are indicated when significant. Figure S3. Basal calcium (Ca2+) entry is related to constitutive calcium entry (CE) but not to store operated Ca2+ entry (SOCE), while the anti-IgM Ca2+ response correlated to thapsigargin (TG) capacity to induce endoplasmic reticulum (ER) Ca2+ release and SOCE. Figure S4. The pool of STIM1 in plasma membrane (STIM1PM) is correlated with basal Ca2+ levels but independent from anti-IgM Ca2+ response and thapsigargin (TG) capacity to release Ca2+ from the endoplasmic reticulum (ER) and to induce SOCE. Correlations between STIM1PM levels with basal Ca2+ (A), anti-IgM Ca2+ response (B), TG capacity to induce ER Ca2+ release (C), and TG SOCE (D). Values were obtained from 18 CLL, see material and methods for details. P and r2 values are indicated when significant. (DOCX 531 kb)