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CaMKII Potentiates Store-Operated Ca2+ Entry Through Enhancing STIM1 Aggregation and Interaction with Orai1.
Cell Physiol Biochem 2018; 46(3):1042-1054CP

Abstract

BACKGROUND/AIMS

Upon Ca2+ store depletion, stromal interaction molecule 1 (STIM1) oligomerizes, redistributes near plasmalemma to interact with Ca2+ selective channel-forming subunit (Orai1) and initiates store-operated Ca2+ entry (SOCE). Ca2+/calmodulin-dependent protein kinase II (CaMKII) is a regulator of SOCE, but how CaMKII regulates SOCE remains obscure.

METHODS

Using Fura2, confocal microscopy, co-immunoprecipitation, specific blocker and overexpression/knockdown approaches, we evaluated STIM1 aggregation and its interaction with Orai1, and SOCE upon Ca2+ store depletion in thapsigargin (TG) treated HEK293 and HeLa cells.

RESULTS

Overexpression of CaMKIIδ enhanced TG-induced STIM1 co-localization and interaction with Orai1 as well as SOCE. In contrast, CaMKIIδ knockdown and a specific inhibitor of CaMKII suppressed them. In addition, overexpression or knockdown of CaMKIIδ in TG treated cells exhibited increased or reduced STIM1 clustering and plasmalemma redistribution, respectively.

CONCLUSION

CaMKII up-regulates SOCE by increasing STIM1 aggregation and interaction with Orai1. This study provides an additional insight into SOCE regulation and a potential mechanism for CaMKII involvement in some pathological situations through crosstalk with SOCE.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

29669320

Citation

Li, Shu, et al. "CaMKII Potentiates Store-Operated Ca2+ Entry Through Enhancing STIM1 Aggregation and Interaction With Orai1." Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology, vol. 46, no. 3, 2018, pp. 1042-1054.
Li S, Xue J, Sun Z, et al. CaMKII Potentiates Store-Operated Ca2+ Entry Through Enhancing STIM1 Aggregation and Interaction with Orai1. Cell Physiol Biochem. 2018;46(3):1042-1054.
Li, S., Xue, J., Sun, Z., Liu, T., Zhang, L., Wang, L., ... Luo, D. (2018). CaMKII Potentiates Store-Operated Ca2+ Entry Through Enhancing STIM1 Aggregation and Interaction with Orai1. Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology, 46(3), pp. 1042-1054. doi:10.1159/000488835.
Li S, et al. CaMKII Potentiates Store-Operated Ca2+ Entry Through Enhancing STIM1 Aggregation and Interaction With Orai1. Cell Physiol Biochem. 2018;46(3):1042-1054. PubMed PMID: 29669320.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - CaMKII Potentiates Store-Operated Ca2+ Entry Through Enhancing STIM1 Aggregation and Interaction with Orai1. AU - Li,Shu, AU - Xue,Jingyi, AU - Sun,Zhipeng, AU - Liu,Tiantian, AU - Zhang,Lane, AU - Wang,Limin, AU - You,Hongjie, AU - Fan,Zheng, AU - Zheng,Yuanyuan, AU - Luo,Dali, Y1 - 2018/04/13/ PY - 2017/07/24/received PY - 2018/02/27/accepted PY - 2018/4/19/pubmed PY - 2018/7/6/medline PY - 2018/4/19/entrez KW - CaMKII KW - Orai1 KW - STIM1 KW - Store-operated Ca2+ entry SP - 1042 EP - 1054 JF - Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology JO - Cell. Physiol. Biochem. VL - 46 IS - 3 N2 - BACKGROUND/AIMS: Upon Ca2+ store depletion, stromal interaction molecule 1 (STIM1) oligomerizes, redistributes near plasmalemma to interact with Ca2+ selective channel-forming subunit (Orai1) and initiates store-operated Ca2+ entry (SOCE). Ca2+/calmodulin-dependent protein kinase II (CaMKII) is a regulator of SOCE, but how CaMKII regulates SOCE remains obscure. METHODS: Using Fura2, confocal microscopy, co-immunoprecipitation, specific blocker and overexpression/knockdown approaches, we evaluated STIM1 aggregation and its interaction with Orai1, and SOCE upon Ca2+ store depletion in thapsigargin (TG) treated HEK293 and HeLa cells. RESULTS: Overexpression of CaMKIIδ enhanced TG-induced STIM1 co-localization and interaction with Orai1 as well as SOCE. In contrast, CaMKIIδ knockdown and a specific inhibitor of CaMKII suppressed them. In addition, overexpression or knockdown of CaMKIIδ in TG treated cells exhibited increased or reduced STIM1 clustering and plasmalemma redistribution, respectively. CONCLUSION: CaMKII up-regulates SOCE by increasing STIM1 aggregation and interaction with Orai1. This study provides an additional insight into SOCE regulation and a potential mechanism for CaMKII involvement in some pathological situations through crosstalk with SOCE. SN - 1421-9778 UR - https://www.unboundmedicine.com/medline/citation/29669320/CaMKII_Potentiates_Store_Operated_Ca2+_Entry_Through_Enhancing_STIM1_Aggregation_and_Interaction_with_Orai1_ L2 - https://www.karger.com?DOI=10.1159/000488835 DB - PRIME DP - Unbound Medicine ER -