Murine Stim1 maps to distal Chromosome 7 and is not imprinted

Overall, Maree L.; Parker, Nigel; Scarcella, Deborah L.; Smith, Peter J.; Dziadek, Marie

doi:10.1007/s003359900839

Cited by 10 publications

(5 citation statements)

References 2 publications

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“…Despite some variations concerning STIM isoform abundance in certain tissues, similar expression pattern was observed in mouse (Table 1; Refs. [56, 70, 76, 79–80]). STIM1 is mainly expressed in murine skeletal muscle, cerebellum, spleen, thymus, lymph nodes and additionally in platelets, while is almost absent in brain and completely absent in kidney.…”

Section: Importance Of Orais and Stims In Tissuesmentioning

confidence: 99%

Orais and STIMs: physiological mechanisms and disease

Berna‐Erro

Woodard

Rosado

2012

J Cellular Molecular Medi

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The stromal interaction molecules STIM1 and STIM2 are Ca2+ sensors, mostly located in the endoplasmic reticulum, that detect changes in the intraluminal Ca2+ concentration and communicate this information to plasma membrane store-operated channels, including members of the Orai family, thus mediating store-operated Ca2+ entry (SOCE). Orai and STIM proteins are almost ubiquitously expressed in human cells, where SOCE has been reported to play a relevant functional role. The phenotype of patients bearing mutations in STIM and Orai proteins, together with models of STIM or Orai deficiency in mice, as well as other organisms such as Drosophila melanogaster, have provided compelling evidence on the relevant role of these proteins in cellular physiology and pathology. Orai1-deficient patients suffer from severe immunodeficiency, congenital myopathy, chronic pulmonary disease, anhydrotic ectodermal dysplasia and defective dental enamel calcification. STIM1-deficient patients showed similar abnormalities, as well as autoimmune disorders. This review summarizes the current evidence that identifies and explains diseases induced by disturbances in SOCE due to deficiencies or mutations in Orai and STIM proteins.

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Section: Importance Of Orais and Stims In Tissuesmentioning

confidence: 99%

Orais and STIMs: physiological mechanisms and disease

Berna‐Erro

Woodard

Rosado

2012

J Cellular Molecular Medi

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“…It has been described as a tumor suppressor acting in a recessive way (20). In a number of human tumor cell lines, STIM1 induces growth inhibition and cell degeneration (20–22). Further examination of STIM1 by Dziadek et al .…”

Section: Stim1mentioning

confidence: 99%

“…It has been described as a tumor suppressor acting in a recessive way (20). In a number of human tumor cell lines, STIM1 induces growth inhibition and cell degeneration (20)(21)(22). Further examination of STIM1 by Dziadek et al (23) using immunofluorescence and cell surface biotinylation revealed STIM1 expression in the plasma membrane.…”

Section: Stim1mentioning

confidence: 99%

Mechanistic view on domains mediating STIM1–Orai coupling

Fahrner

Muik

Derler

et al. 2009

Immunological Reviews

102

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Calcium (Ca2+) entry into non-excitable cells is mainly carried by store-operated channels, which serve essential functions ranging from regulation of transcription to cell growth. The best-characterized store-operated current, initially discovered in T lymphocytes and mast cells, is the Ca2+ release-activated Ca2+ (CRAC) current. The search for the molecular components of the CRAC channel has recently identified stromal interaction molecule 1 (STIM1) as the Ca2+ sensor in the endoplasmic reticulum (ER) and Orai1 as the CRAC channel pore. ER store depletion results in formation of STIM1 puncta that trigger Ca2+ influx via Orai1 channels. This review covers the role of domains within STIM1 and Orai and enlightens their function in the STIM1/Orai coupling process. Moreover, a molecular interpretation focuses on interactions between cytosolic portions of STIM1 and Orai together with a mechanistic view on the loss of function of the SCID (severe combined immunodeficiency)-linked Orai1 R91W mutant channel. The architecture of the selectivity filter of Orai channels is finally elucidated based on permeation properties of Orai pore mutants.

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“…Stim1 is an integral membrane N-glycosylated glycoprotein consisting of 746 amino acid residues [29,30] with 90% sequence identity in human and mouse proteins [31]. Using rhabdomyosarcoma cells in vitro and rhabdoid tumors in vivo, Stim1 was shown to inhibit the growth of tumor cells [32] and be expressed in many human primary and transformed cell lines [30].…”

Section: Introductionmentioning

confidence: 99%

Ganglioside GD1a regulation of caveolin-1 and Stim1 expression in mouse FBJ cells:Augmented expression of caveolin-1 and Stim1 in cells with increased GD1a content

et al. 2006

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GD1a was previously shown responsible for regulating cell motility, cellular adhesiveness to vitronectin, phosphorylation of c-Met and metastatic ability of mouse FBJ osteosarcoma cells. To determine the particular molecules regulated by GD1a, FBJ cells were assessed for tumor-related gene expression by semi-quantitative RT-PCR. Caveolin-1 and stromal interaction molecule 1 (Stim1) expression in FBJ-S1 cells, rich in GD1a, were found to be 6 and 4 times as much, respectively, than in FBJ-LL cells devoid of GD1a. Enhanced production of caveolin-1 in protein was confirmed by Western blotting. A low-metastatic FBJ-LL cell variant, having high GD1a expression through beta1-4GalNAcT-1 (GM2/GD2 synthase) cDNA transfection (Hyuga S, et al, Int J Cancer 83: 685-91, 1999), showed enhanced production of caveolin-1 and Stim1 in mRNA and protein, compared to mock-transfectant M5. Incubation of FBJ-M5 cells with exogenous GD1a augmented the expression of caveolin-1 in mRNA and protein and Stim1 in mRNA as well. Treatment of FBJ-S1 with fumonisin B1, an inhibitor of N-acylsphinganine synthesis, for 15 days caused the complete depletion of gangliosides and suppressed the expression of caveolin-1 and Stim1. St3gal5 siRNA transfected cells showed decreased expression of caveolin-1 and Stim1 mRNA, as well as St3gal5 mRNA. These findings clearly indicate ganglioside GD1a to be involved in the regulation of the transformation suppressor genes, caveolin-1 and Stim1. Moreover, treatment with GD1a of mouse melanoma B16 cells and human hepatoma HepG2 cells brought about elevated expression of caveolin-1 and Stim1.

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Murine Stim1 maps to distal Chromosome 7 and is not imprinted

Cited by 10 publications

References 2 publications

Orais and STIMs: physiological mechanisms and disease

Orais and STIMs: physiological mechanisms and disease

Mechanistic view on domains mediating STIM1–Orai coupling

Ganglioside GD1a regulation of caveolin-1 and Stim1 expression in mouse FBJ cells:Augmented expression of caveolin-1 and Stim1 in cells with increased GD1a content

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