STIM1 Knockout HEK293 Cell Line

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STIM1 Knockout HEK293 Cell Line
Cat.No.:

EDC09869

Species:

Human

Cell Name:

HEK293

Gene:

STIM1

Gene ID:

6786

Size:

1×10⁶cells

STIM1 Knockout Cell Line (HEK293) is an exclusive upgraded CRISPR/Cas9 system-mediated gene knockout cell, with the advantages of Optimized Strategy Design, Efficient Cell Transfection, High-Performance Cas9 Protein and Hassle-Free Cell Selection.
Cat.No. EDC09869
Product Name STIM1 Knockout Cell Line (HEK293)
Cell Line HEK293
Cellosaurus ID CVCL_0045
Cell Line Synonyms Hek293, HEK-293, HEK/293, (HEK)293, HEK 293, HEK,293, 293, 293 HEK, 293 Ad5, Graham 293, Graham-293, Human Embryonic Kidney 293
Gene STIM1
NCBI Gene ID
Gene Synonyms D11S4896E|GOK|IMD10|STRMK|TAM|TAM1
Summary
This gene encodes a type 1 transmembrane protein that mediates Ca2+ influx after depletion of intracellular Ca2+ stores by gating of store-operated Ca2+ influx channels (SOCs). It is one of several genes located in the imprinted gene domain of 11p15.5, an important tumor-suppressor gene region. Alterations in this region have been associated with the Beckwith-Wiedemann syndrome, Wilms tumor, rhabdomyosarcoma, adrenocrotical carcinoma, and lung, ovarian, and breast cancer. This gene may play a role in malignancies and disease that involve this region, as well as early hematopoiesis, by mediating attachment to stromal cells. Mutations in this gene are associated with fatal classic Kaposi sarcoma, immunodeficiency due to defects in store-operated calcium entry (SOCE) in fibroblasts, ectodermal dysplasia and tubular aggregate myopathy. This gene is oriented in a head-to-tail configuration with the ribonucleotide reductase 1 gene (RRM1), with the 3' end of this gene situated 1.6 kb from the 5' end of the RRM1 gene. Alternative splicing of this gene results in multiple transcript variants. [provided by RefSeq, May 2013]
Associated Diseases Non-tumor
Morphology Adherent
Passage Ratio 1/5，2days
Complete Culture Medium DMEM + 10% FBS
Freezing Medium 95% Complete culture medium+ 5% DMSO
QC Indels validated by Sanger sequencing; sterility confirmed via microbial testing.
* For research use only. Not intended for use in humans or animals, including clinical, therapeutic, or diagnostic purposes.
LociSTR Info (Sample Cell)
Sample Cell Line: HEK293		STR Info (Cell bank)
Cell Line: HEK293
Allele1Allele2Allele1Allele2
Amelogenin X X
CSF1P0 12 11 12
D2S1338 19 19
D3S1358 15 17 15 17
D5S818 8 8 9
D7S820 11 12 11 12
D8S1179 12 14 12 14
D13S317 12 14 12 14
D16S539 9 13 9 13
D18S51 17 18 17 18
D19S433 15 18 15 18
D21S11 28 30.2 28 30.2
FGA 23 23
Penta D 9 10 9 10
Penta E 7 15 7 15
TH01 7 9.3 7 9.3
TPOX 11 11
vWA 16 19 16 19
D6S1043 11 11
D12S391 19 21 11 15
D2S441 11 15 11 15
* STR authentication data of this cell line matches with that of cell lines sourced from ATCC, DSMZ, JCRB, and RIKEN databases.
Conclusion: The STR identification of this cell is correct.

FAQ

The choice depends on whether you are studying STIM1's role in store-operated calcium entry (SOCE) or its emerging functions in arachidonate-regulated calcium channels and calcium-mediated cancer biology. The Knockout line is the standard tool for asking whether STIM1 is required for SOCE — STIM1 senses ER calcium depletion and activates Orai1 channels at ER-plasma membrane junctions. Overexpression is useful for studying constitutively-active STIM1 mutations (e.g., R304W from Stormorken syndrome) or for testing SOCE enhancement. For SOCE research, the EDITGENE STIM1 Knockout in HEK293 is the gold-standard platform — HEK293 has long been the standard heterologous system for SOCE reconstitution and biophysical characterization. STIM2 paralog compensation should be assessed in parallel. Rescue with wild-type, gain-of-function, or activation-deficient STIM1 enables comprehensive structure-function dissection of this pathway.
Primary applications: • SOCE measurement: calcium imaging (Fura-2, Fluo-4, GCaMP) with thapsigargin or cyclopiazonic acid-induced store depletion to quantify store-operated calcium entry capacity. • STIM1-Orai1 interaction: imaging of ER-PM junction puncta formation following calcium store depletion using fluorescently-tagged STIM1 rescue constructs. • Disease mutation modeling: rescue with Stormorken syndrome (R304W) or York platelet syndrome variants for genotype-function studies. • SOCE inhibitor specificity: genetic control for testing SOCE-targeting compounds (BTP2, GSK-7975A) for on-target activity. EDITGENE recommends this model for researchers investigating store-operated calcium entry, calcium-dependent signaling, and STIM1-related disease mechanisms.
Yes. STIM1 rescue experiments are extensively established in SOCE research: • Construct design: use a codon-modified STIM1 sequence with a small C-terminal tag (FLAG, HA, YFP for imaging). STIM1 is a type II ER membrane protein — N-terminal signal sequence and EF-hand calcium-sensing domain must be preserved. • Activation-deficient rescue: the D76A mutation in the EF-hand abolishes ER calcium sensing — STIM1 with this mutation is constitutively active. • Disease mutation rescue: Stormorken syndrome variants (R304W, gain-of-function) and York platelet syndrome variants enable disease modeling in a controlled background. • Functional readout: rescue should restore thapsigargin-induced SOCE measured by calcium imaging, and Orai1-STIM1 puncta formation at ER-PM junctions. HEK293 is the gold-standard heterologous expression system for SOCE reconstitution, with extensive established protocols for STIM1 rescue and live-cell calcium imaging.
* Research Use Disclaimer: Content is generated from publicly available research data, bioinformatic resources, and computational analyses for research reference only.

Related Publications

IF=2.4
Cerebellum (London, England)
Responding to burst stimulation of parallel fibers (PFs), cerebellar Purkinje neurons (PNs) generate a convolved synaptic response displaying a fast excitatory postsynaptic current (EPSC) followed by a slow EPSC (EPSC). The latter is companied with a rise of intracellular Ca and critical for motor coordination. The genesis of EPSC in PNs results from activation of metabotropic type 1 glutamate receptor (mGluR1), oligomerization of stromal interaction molecule 1 (STIM1) on the membrane of endoplasmic reticulum (ER) and opening of transient receptor potential canonical 3 (TRPC3) channels on the plasma membrane. Neuronal nitric oxide synthase (nNOS) is abundantly expressed in PFs and granule neurons (GNs), catalyzing the production of nitric oxide (NO) hence regulating PF-PN synaptic function. We recently found that nNOS/NO regulates the morphological development of PNs through mGluR1-regulated Ca-dependent mechanism. This study investigated the role of nNOS/NO in regulating EPSC. Electrophysiological analyses showed that EPSC in cerebellar slices of nNOS knockout (nNOS) mice was significantly larger than that in wildtype (WT) mice. Activation of mGluR1 in cultured PNs from nNOS mice evoked larger TRPC3-channel mediated currents and intracellular Ca rise than that in PNs from WT mice. In addition, nNOS inhibitor and NO-donor increased and decreased, respectively, the TRPC3-current and Ca rise in PNs. Moreover, the NO-donor effectively decreased TRPC3 currents in HEK293 cells expressing WT STIM1, but not cells expressing a STIM1 with cysteine mutants. These novel findings indicate that nNOS/NO inhibits TRPC3-containig channel mediated cation influx during EPSC, at least in part, by S-nitrosylation of STIM1.
This KO model may be useful for: - Investigating S-nitrosylation regulation of STIM1 and its effect on TRPC3 channel activity - Studying mGluR1-dependent slow EPSC generation and intracellular calcium dynamics in cerebellar Purkinje neurons - Modeling the role of nNOS/NO signaling in motor coordination and synaptic transmission at parallel fiber-Purkinje neuron synapses - Examining the functional interaction between STIM1 and TRPC3-containing channels in response to burst stimulation - Evaluating the effects of nitric oxide donors or nNOS inhibitors on STIM1-mediated cation influx in heterologous expression systems

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