anti-Stromal Interaction Molecule 2 (Stim2) Antibodies

Human Stromal Interaction Molecule 2 (Stim2) interaction partners

1. Cross-talk between N-terminal and C-terminal domains in stromal interaction molecule 2 (STIM2) determines enhanced STIM2 sensitivity.

2. STIM2 is constitutively localized within ER-PM junctions in ER-Ca(2+) store replete cells. STIM2 traps STIM1 and triggers remodeling of STIM1 C terminus, causing STIM1/Orai1 coupling and enhancement of Orai1 function in cells with relatively high ER-[Ca(2+)].

3. We identified the key structural determinants, especially the corresponding G residue in STIM1, which define the distinct activation dynamics of STIM2. The chimeric E470G mutation could switch STIM2 from a slow and weak Orai channel activator into a fast and potent one like STIM1 and vice versa.

4. Expression of full-length STIM1 with STIM2 in a 5:1 ratio causes suppression of sustained agonist-induced Ca(2+) oscillations and protects cells from Ca(2+) overload.

5. Stim2 deletion reduced SOCE by more than 90% in NIH 3T3 cells and abolishes STIM1 translocation to plasma membrane-associated ER membrane junctions.

6. With STIM2 being essential for life, but apparently not for development, newly available data demonstrate a complex and still intriguing behaviour that this review summarizes, updating current knowledge of STIM2 function [review]

7. The STIM2 protein play important roles in TGF-beta-induced EMT and these effects are related to both store-operated calcium entry and non-store-operated calcium entry.

8. What is less clear is how the spatial and temporal spread of intracellular Ca(2+) is shaped and regulated by differential expression of the individual SOCE genes and their splice variants, their heteromeric combinations and pre- and posttranslational modifications. This review focuses on principle mechanisms regulating expression, splicing, and targeting of Ca(2+) release-activated Ca(2+) (CRAC) channels.

9. While STIM1 is a full Orai1-agonist, leucine-replacement of this crucial residue in STIM2 endows it with partial agonist properties, which may be critical for limiting Orai1 activation stemming from its enhanced sensitivity to store-depletion

10. STIM2.1 cannot activate Orai1 due to splicing in residues within the channel-activating domain (CAD). STIM2.1 confers a calcium dependent dominant-negative function on both STIM1 and STIM2 (STIM2.2). Affinity of the STIM2.1 calmodulin binding site within the CAD domain is increased compared to STIM2.2.

11. STIM2 enhances receptor-stimulated Ca(2) signaling by promoting recruitment of STIM1 to the endoplasmic reticulum-plasma membrane junctions.

12. STIM2beta does not by itself strongly bind Orai1, it is recruited to Orai1 channels by forming heterodimers with other STIM isoforms.

13. Imin channels are regulated by STIM2, TRPC3-containing INS channels are induced by STIM1, and TRPC1-composed Imax channels are activated by both STIM1 and STIM2.

14. The higher amplitude of store-operated Ca2+ entry was associated to the over-expression for Stim2, Orai2-3, and TRPC1 while Stim2 levels remained constant and Stim1, Orai1, Orai3, TRPC1 and TRPC4 proteins were over-expressed in primary myelofibrosis.

15. the reciprocal shift in transient receptor potential channel 1 (TRPC1) and stromal interaction molecule 2 (STIM2) contributes to Ca2+ remodeling and cancer hallmarks in colorectal carcinoma cells

16. STIM2 is highly expressed and controls store-operated Ca(2+) entry in human melanoma. The invasive and migratory potential of melanoma cells was reduced upon silencing of STIM2.

17. Binding of the lysine rich domains of STIM1 and STIM2 to phosphatidylinositol 4,5 biphosphate rich liposomes depends on their oligomerization.

18. STIM2 is involved in spatial learning and plays an important role in ischemic-induced neuronal cell death during brain hypoxia. The absence of STIM2 reduces life expectancy in mice by sudden death.

19. STIM2 is involved in spatial learning and plays an important role in ischemic-induced neuronal cell death during brain hypoxia. The absence of STIM2 reduces life expectancy in mice by sudden death.

Mouse (Murine) Stromal Interaction Molecule 2 (Stim2) interaction partners

1. Results indicate that preformed clusters of STIM and ORAI1 enable local Ca(2+) entry events in unstimulated cells. Upon TCR activation, NAADP-evoked Ca(2+) release through RYR1, in coordination with Ca(2+) entry through ORAI1 and STIM, rapidly increases the number of Ca(2+) microdomains, thereby initiating spread of Ca(2+) signals deeper into the cytoplasm to promote full T cell activation.

2. data show that loss of SOCE in enamel cells has substantial detrimental effects on gene expression, cell function, and the mineralization of dental enamel

3. regulates both intracellular Ca2+ distribution and Ca2+ movement in skeletal myotubes

4. In contrast to wild-type controls or Stim2KO mice, isolated sweat glands from Stim1cKO mice showed no response to acetylcholine

5. Stim1 and Stim2 deficient B cells show an accelerated pace of affinity maturation but do not have dramatically impaired antibody production to T-independent antigen immunization

6. We found that STIM2 is required for the stable expression of both LTP and LTD at CA3-CA1 hippocampal synapses. Altered plasticity in Stim2 cKO mice is associated with subtle alterations in the shape and density of dendritic spines in CA1 neurons.

7. neutrophil cytokine production required STIM2, but not STIM1, at least in part as a result of redox regulation of cytokine gene expression

8. Expression of STIM2 protein rescued CaMKII activity and protected mushroom spines from Abeta42 oligomer toxicity in vitro and in vivo.

9. SOCE blockers or ablation of STIM1, STIM2, or Orai1 severely impaired nucleotide-induced migration and phagocytosis in microglia.

10. The data from this study indicate that upregulation of STIM2 and Orai2 is involved in the phenotypic transition of pulmonary arterial smooth muscle cells from a contractile state to a proliferative state.

11. STIM1, STIM2, and CRAC channel function play distinct but synergistic roles in CD4+ and CD8+ T cells during antiviral immunity

12. STIM2 deficiency significantly delays onset and attenuates the clinical course of experimental allergic encephalitis.

13. Using mice lacking STIM1 and its homologue STIM2, authors find that store-operated calcium entry in CD8(+) T cells is required to prevent the engraftment of melanoma and colon carcinoma cells and to control tumour growth.

14. STIM1 and STIM2-mediated store-operated Ca2+ influx, leading to efficient activation of NFAT (nuclear factor of activated T cells), is critical for the postselection maturation of agonist-selected T cells.

15. STIM1 and STIM2 protein deficiency in T lymphocytes underlies development of the exocrine gland autoimmune disease, Sjogren's syndrome.

16. show that endoplasmic reticulum calcium sensors STIM1- and STIM2-induced store-operated Ca(2+) influx is critical for B cell regulatory function

17. Absence of STIM2 in mouse embryonic fibroblasts results in a decreased store-operated calcium ion entry, although this inhibition is less pronounced than for STIM1.

18. both STIM1 and STIM2 are critical for T-cell function and autoimmunity in vivo.

19. Promote store-operated entry of calcium ions into T cells; required for the development and function of regulatory T cells.