The two main components of store-operated calcium entry (SOCE) are the ion channel Orai1 and the multifunctional protein STIM1. Recently STIM1 has been recognized as a microtubule plus end tracking protein involved in remodeling of the endoplasmic reticulum. However, the relationship between ER remodeling and SOCE are poorly understood. In the present study we have found that activation of Orai1 channels by the expression of the SOAR (STIM1 Orai activating region) from STIM1 induces Orai1 puncta formation and SOCE but does not alter the role of STIM1 in ER remodeling. Furthermore, expression of the STIM1-EB1-D (the STIM1-EB1 association domain) from STIM1 significantly reduces SOCE and prevents the traveling of STIM1 in ER projections. However, ER projections driven by EB1 remained unaffected. These findings suggest that there may be several mechanisms responsible for ER remodeling but only one in which STIM1 participates. This type of ER remodeling mechanism where STIM1 plays an active role participates in the control of SOCE.