Anti-STIM1 Antibody (Rabbit Polyclonal antibody) General Information
Reacts with: Human
Recombinant Human STIM1 protein (Catalog#11434-H08H)
Produced in rabbits immunized with purified, recombinant Human STIM1 (rh STIM1; Catalog#11434-H08H; NP_003147.2; Met 1-Asp 213). Total IgG was purified by Protein A affinity chromatography
Polyclonal Rabbit IgG
0.2 μm filtered solution in PBS with 5% trehalose
This antibody is shipped as liquid solution at ambient temperature. Upon receipt, store it immediately at the temperature recommended below.
This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -80℃. Preservative-Free. Sodium azide is recommended to avoid contamination (final concentration 0.05%-0.1%). It is toxic to cells and should be disposed of properly. Avoid repeated freeze-thaw cycles.
Anti-STIM1 Antibody (Rabbit Polyclonal antibody) Validated Applications
**********Please Note: Optimal concentrations/dilutions should be determined by the end user.**********
Anti-STIM1 Antibody Alternative Names
Anti-D11S4896E Antibody;Anti-GOK Antibody;Anti-IMD10 Antibody;Anti-STRMK Antibody;Anti-TAM Antibody;Anti-TAM1 Antibody
STIM1 Background Information
Stromal interaction molecule 1, also known as STIM1 and GOK, is a cell membrane, a single-pass type I membrane protein and a endoplasmic reticulum membrane protein. STIM1 / GOK is ubiquitously expressed in various human primary cells and tumor cell lines. It contains one EF-hand domain and one SAM (sterile alpha motif) domain. STIM1 / GOK plays a role in mediating Ca2+ influx following depletion of intracellular Ca2+ stores. It acts as Ca2+ sensor in the endoplasmic reticulum via its EF-hand domain. Upon Ca2+ depletion, STIM1 / GOK translocates from the endoplasmic reticulum to the plasma membrane where it activates the Ca2+ release-activated Ca2+ (CRAC) channel subunit, TMEM142A / ORAI1. Transfection of STIM1 / GOK into cells derived from a rhabdoid tumor and from a rhabdomyosarcoma that do not express detectable levels of STIM1 can induce cell death, suggesting a possible role in the control of rhabdomyosarcomas and rhabdoid tumors. Defects in STIM1 are the cause of immune dysfunction with T-cell inactivation due to calcium entry defect type 2 (IDTICED2) which is an immune disorder characterized by recurrent infections, impaired T-cell activation and proliferative response, decreased T-cell production of cytokines, lymphadenopathy, and normal lymphocytes counts and serum immunoglobulin levels.
stromal interaction molecule 1
Sabbioni S. et al., 1997, Cancer Res. 57: 4493-7. Manji S.S. et al., 2000, Biochim. Biophys. Acta 1481: 147-55. Williams R.T. et al., 2002, Biochim. Biophys. Acta. 1596: 131-7. Spassova M.A. et al., 2006, Proc. Natl. Acad. Sci. USA. 103: 4040-5. Parvez S. et al., 2008, FASEB J. 22: 752-61.