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Stim2 is a member of the stromal interaction molecule (STIM) family and likely arose, along with related family member STIM1, from a common ancestral gene. De plus, nous expédions Stim2 Protéines (8) et et beaucoup plus de produits pour cette protéine.
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Human Polyclonal Stim2 Primary Antibody pour IHC, ELISA - ABIN1003212
Luik, Lewis: New insights into the molecular mechanisms of store-operated Ca2+ signaling in T cells. dans Trends in molecular medicine 2007
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Human Polyclonal Stim2 Primary Antibody pour IHC, ELISA - ABIN1003213
Spassova, Soboloff, He, Xu, Dziadek, Gill: STIM1 has a plasma membrane role in the activation of store-operated Ca(2+) channels. dans Proceedings of the National Academy of Sciences of the United States of America 2006
Show all 4 Pubmed References
Stim2 deletion reduced SOCE by more than 90% in NIH 3T3 cells and abolishes STIM1 (Montrer STIM1 Anticorps) translocation to plasma membrane-associated ER membrane junctions.
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]
The STIM2 protein play important roles in TGF-beta (Montrer TGFB1 Anticorps)-induced EMT (Montrer ITK Anticorps) and these effects are related to both store-operated calcium entry and non-store-operated calcium entry.
What is less clear is how the spatial and temporal spread of intracellular Ca(2 (Montrer CA2 Anticorps)+) 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 (Montrer CA2 Anticorps)+) release-activated Ca(2 (Montrer CA2 Anticorps)+) (CRAC) channels.
While STIM1 (Montrer STIM1 Anticorps) is a full Orai1 (Montrer ORAI1 Anticorps)-agonist, leucine-replacement of this crucial residue in STIM2 endows it with partial agonist properties, which may be critical for limiting Orai1 (Montrer ORAI1 Anticorps) activation stemming from its enhanced sensitivity to store-depletion
STIM2.1 cannot activate Orai1 (Montrer ORAI1 Anticorps) due to splicing in residues within the channel-activating domain (CAD (Montrer CAD Anticorps)). STIM2.1 confers a calcium dependent dominant-negative function on both STIM1 (Montrer STIM1 Anticorps) and STIM2 (STIM2.2). Affinity of the STIM2.1 calmodulin binding site within the CAD (Montrer CAD Anticorps) domain is increased compared to STIM2.2.
STIM2 enhances receptor-stimulated Ca(2 (Montrer CA2 Anticorps)) signaling by promoting recruitment of STIM1 (Montrer STIM1 Anticorps) to the endoplasmic reticulum-plasma membrane junctions.
STIM2beta does not by itself strongly bind Orai1 (Montrer ORAI1 Anticorps), it is recruited to Orai1 (Montrer ORAI1 Anticorps) channels by forming heterodimers with other STIM isoforms.
Imin channels are regulated by STIM2, TRPC3 (Montrer TRPC3 Anticorps)-containing INS (Montrer INS Anticorps) channels are induced by STIM1 (Montrer STIM1 Anticorps), and TRPC1 (Montrer TRPC1 Anticorps)-composed Imax channels are activated by both STIM1 (Montrer STIM1 Anticorps) and STIM2.
The higher amplitude of store-operated Ca2 (Montrer CA2 Anticorps)+ entry was associated to the over-expression for Stim2, Orai2 (Montrer ORAI2 Anticorps)-3, and TRPC1 (Montrer TRPC1 Anticorps) while Stim2 levels remained constant and Stim1 (Montrer STIM1 Anticorps), Orai1 (Montrer ORAI1 Anticorps), Orai3 (Montrer ORAI3 Anticorps), TRPC1 (Montrer TRPC1 Anticorps) and TRPC4 (Montrer TRPC4 Anticorps) proteins were over-expressed in primary myelofibrosis.
Stim1 (Montrer STIM1 Anticorps) 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
We found that STIM2 is required for the stable expression of both LTP (Montrer SCP2 Anticorps) and LTD at CA3 (Montrer CA3 Anticorps)-CA1 (Montrer CA1 Anticorps) hippocampal synapses. Altered plasticity in Stim2 cKO mice is associated with subtle alterations in the shape and density of dendritic spines in CA1 (Montrer CA1 Anticorps) neurons.
neutrophil cytokine production required STIM2, but not STIM1 (Montrer STIM1 Anticorps), at least in part as a result of redox regulation of cytokine gene expression
Expression of STIM2 protein rescued CaMKII (Montrer CAMK2G Anticorps) activity and protected mushroom spines from Abeta42 oligomer toxicity in vitro and in vivo.
SOCE blockers or ablation of STIM1 (Montrer STIM1 Anticorps), STIM2, or Orai1 (Montrer TMEM132A Anticorps) severely impaired nucleotide-induced migration and phagocytosis in microglia.
The data from this study indicate that upregulation of STIM2 and Orai2 (Montrer ORAI2 Anticorps) is involved in the phenotypic transition of pulmonary arterial smooth muscle cells from a contractile state to a proliferative state.
STIM1 (Montrer STIM1 Anticorps), STIM2, and CRAC channel function play distinct but synergistic roles in CD4 (Montrer CD4 Anticorps)+ and CD8 (Montrer CD8A Anticorps)+ T cells during antiviral immunity
STIM2 deficiency significantly delays onset and attenuates the clinical course of experimental allergic encephalitis.
Using mice lacking STIM1 (Montrer STIM1 Anticorps) and its homologue STIM2, authors find that store-operated calcium entry in CD8 (Montrer CD8A Anticorps)(+) T cells is required to prevent the engraftment of melanoma and colon carcinoma cells and to control tumour growth.
STIM1 (Montrer STIM1 Anticorps) and STIM2-mediated store-operated Ca2 (Montrer CA2 Anticorps)+ influx, leading to efficient activation of NFAT (Montrer NFATC1 Anticorps) (nuclear factor of activated T cells), is critical for the postselection maturation of agonist-selected T cells.
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.
stromal interaction molecule 2