gopubmed logo
 
find other proteinsAll proteins
GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Stromal interaction molecule 2

STIM2
This gene is a member of the stromal interaction molecule (STIM) family and likely arose, along with related family member STIM1, from a common ancestral gene. The encoded protein functions to regulate calcium concentrations in the cytosol and endoplasmic reticulum, and is involved in the activation of plasma membrane Orai Ca(2+) entry channels. This gene initiates translation from a non-AUG (UUG) start site. A signal peptide is cleaved from the resulting protein. Multiple transcript variants result from alternative splicing. [provided by RefSeq, Dec 2009] (from NCBI)
Top mentioned proteins: Sim, Orai1, Orai2, CAN, HAD
Papers on STIM2
Enhanced Store-Operated Calcium Entry Leads to Striatal Synaptic Loss in a Huntington's Disease Mouse Model.
New
Bezprozvanny et al., Saint Petersburg, Russia. In J Neurosci, Feb 2016
The synaptic nSOC pathway is controlled by the ER resident protein STIM2.
ORAI Channel-Mediated Ca2+ Signals in Vascular and Airway Smooth Muscle.
Review
New
Trebak et al., United States. In Am J Physiol Cell Physiol, Jan 2016
UNASSIGNED: Orai proteins (Orai1-3) form a family of highly Ca(2+) selective plasma membrane channels that are regulated by stromal interacting molecules (STIM1 and STIM2); STIM proteins are Ca(2+) sensors located in the membrane of the endoplasmic reticulum (ER).
Junctate boosts phagocytosis by recruiting endoplasmic reticulum Ca2+ stores near phagosomes.
New
Nunes et al., Genève, Switzerland. In J Cell Sci, Dec 2015
Junctate expression in Stim1(-/-) and Stim1(-/-); Stim2(-/-) phagocytic fibroblasts increased phagocytosis and periphagosomal Ca(2+) elevations, yet with only a minimal impact on global SOCE.
Diseases caused by mutations in ORAI1 and STIM1.
Review
New
Feske et al., New York City, United States. In Ann N Y Acad Sci, Nov 2015
ORAI1 channels are activated by stromal interaction molecule (STIM) 1 and STIM2 located in the endoplasmic reticulum.
STIM and Orai proteins as novel targets for cancer therapy. A Review in the Theme: Cell and Molecular Processes in Cancer Metastasis.
Review
New
Motiani et al., New Delhi, India. In Am J Physiol Cell Physiol, Nov 2015
In this review, we will retrospect the data supporting a key role for STIM1, STIM2, Orai1, and Orai3 proteins in tumorigenesis and discuss the potential of targeting these proteins for cancer therapy.
Neuronal Store-Operated Calcium Entry and Mushroom Spine Loss in Amyloid Precursor Protein Knock-In Mouse Model of Alzheimer's Disease.
New
Bezprozvanny et al., Saint Petersburg, Russia. In J Neurosci, Oct 2015
We demonstrated previously that stromal interaction molecule 2 (STIM2)-regulated neuronal store-operated calcium entry (nSOC) in postsynaptic spines play a key role in stability of mushroom spines by maintaining activity of synaptic Ca(2+)/calmodulin kinase II (CaMKII).
Cooperative and alternate functions for STIM1 and STIM2 in macrophage activation and in the context of inflammation.
New
Gessner et al., Hannover, Germany. In Immun Inflamm Dis, Sep 2015
Here, we identify the closely related STIM2 as mediator of cell migration and cytokine production downstream of GPCR and TLR4 activation in macrophages and show that mice lacking STIM2 are partially resistant to inflammatory responses in peritonitis and LPS-induced inflammation.
Structural and functional mechanisms of CRAC channel regulation.
Review
New
Prakriya et al., Chicago, United States. In J Mol Biol, Feb 2015
Studies in the last two decades have revealed the cellular and molecular choreography of the CRAC channel activation process, and it is now established that opening of CRAC channels is governed through direct interactions between the pore-forming Orai proteins and the endoplasmic reticulum Ca(2+) sensors STIM1 and STIM2.
Stim and Orai proteins in neuronal Ca(2+) signaling and excitability.
Review
D'Angelo et al., Pavia, Italy. In Front Cell Neurosci, 2014
Their paralogs, Stim2, Orai2 and Orai3, support SOCE in heterologous expression systems, but their physiological role is still obscure.
Dental enamel cells express functional SOCE channels.
Lacruz et al., New York City, United States. In Sci Rep, 2014
Investigating primary murine enamel cells, we found that key components of CRAC channels (ORAI1, ORAI2, ORAI3, STIM1, STIM2) were expressed and most abundant during the maturation stage of enamel development.
Agonist-selected T cell development requires strong T cell receptor signaling and store-operated calcium entry.
Impact
Takayanagi et al., Tokyo, Japan. In Immunity, 2013
Here we have used mice lacking the endoplasmic reticulum Ca2+ sensors stromal interaction molecule 1 (STIM1) and STIM2 to show that STIM-induced store-operated Ca2+ entry is not essential for thymic development of conventional TCRαβ+ T cells but is specifically required for the development of agonist-selected T cells (regulatory T cells, invariant natural killer T cells, and TCRαβ+ CD8αα+ intestinal intraepithelial lymphocytes).
Stromal interaction molecule 2 (STIM2) is frequently overexpressed in colorectal tumors and confers a tumor cell growth suppressor phenotype.
GeneRIF
Villanueva et al., Barcelona, Spain. In Mol Carcinog, 2012
Stromal interaction molecule 2 is frequently overexpressed in colorectal tumors and confers a tumor cell growth suppressor phenotype.
STIM proteins: dynamic calcium signal transducers.
Impact
GeneRIF
Gill et al., Philadelphia, United States. In Nat Rev Mol Cell Biol, 2012
Studies indicate that in vertebrates, stromal interaction molecule proteins STIM1 and STIM2 are expressed ubiquitously
Polyamines regulate intestinal epithelial restitution through TRPC1-mediated Ca²+ signaling by differentially modulating STIM1 and STIM2.
GeneRIF
Wang et al., Baltimore, United States. In Am J Physiol Cell Physiol, 2012
It was shown that polyamines regulate intestinal epithelial restitution through TRPC1-mediated Ca2+ signaling by altering the ratio of STIM1 to STIM2. Overexpression of ornithine decarboxylase resulted in increased STIM1 but decreased STIM2 expression.
Store-operated calcium entry modulates neuronal network activity in a model of chronic epilepsy.
GeneRIF
Methner et al., Bonn, Germany. In Exp Neurol, 2011
Stim1 and Stim2 were increased in brains of chronic epileptic rodents and strongly expressed in hippocampal specimens from medial temporal lobe epilepsy patients.
The calcium sensors STIM1 and STIM2 control B cell regulatory function through interleukin-10 production.
Impact
GeneRIF
Baba et al., Suita, Japan. In Immunity, 2011
show that endoplasmic reticulum calcium sensors STIM1- and STIM2-induced store-operated Ca(2+) influx is critical for B cell regulatory function
Store-independent activation of Orai1 by SPCA2 in mammary tumors.
Impact
Rao et al., Baltimore, United States. In Cell, 2010
Unexpectedly, SPCA2-Orai1 signaling was independent of ER Ca(2+) stores or STIM1 and STIM2 sensors and uncoupled from Ca(2+)-ATPase activity of SPCA2.
Molecular basis of calcium signaling in lymphocytes: STIM and ORAI.
Review
Impact
Rao et al., Boston, United States. In Annu Rev Immunol, 2009
STIM1 and STIM2 sense the depletion of ER Ca(2+) stores, whereas ORAI1 is a pore subunit of the CRAC channel.
Dual functions for the endoplasmic reticulum calcium sensors STIM1 and STIM2 in T cell activation and tolerance.
Impact
GeneRIF
Rao et al., Boston, United States. In Nat Immunol, 2008
Promote store-operated entry of calcium ions into T cells; required for the development and function of regulatory T cells.
share on facebooktweetadd +1mail to friends