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Validated All-in-One™ qPCR Primer for ICOS(NM_012092.2) Search again
Product ID:
HQP008554
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
AILIM, CD278, CVID1
Gene Description:
inducible T cell costimulator
Target Gene Accession:
NM_012092.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
The protein encoded by this gene belongs to the CD28 and CTLA-4 cell-surface receptor family. It forms homodimers and plays an important role in cell-cell signaling, immune responses, and regulation of cell proliferation. [provided by RefSeq].
Gene References into function
- its polymorphism may contributes to the pathogenesis of spondyloarthropathy
- Genetic polymorphism of the human ICOS gene.
- role of ligation in modulating TCR-induced transcriptional profiles
- ICOS reversely regulates IL-10 on re-activation of human effector T cells with mature dendritic cells. Interaction of ICOS with ICOS-L strongly promoted IL-10 secretion.
- ICOS provides co-stimulation to memory t-cells [review]
- Analysis of the upstream region of ICOS revealed an additional eight single nucleotide polymorphism
- local immune responses may be modulated by H4/ICOS expressed on T cells in the joints of patients with rheumatoid arthritis, and thus it may be involved in the pathogenetic mechanism of rheumatoid arthritis.
- ICOS is upregulated on human T cells after stimulation and can modulate both Th1 and Th2 cytokine production in the absence and presence of B7-1 (CD80) and B7-2 (CD86)costimulation.
- Targeting of specific chemokine and chemokine receptor pathways and/or ICOS may have clinical application in the prevention and treatment of chronic allograft nephropathy.
- AILIM has a role in regulating the signaling cascades for T-cell proliferation and IL-10 production
- ICOS does not belong to the group of genes that, if mutated, present clinically as the hyper-IgM syndrome.
- Highly expressed ICOS in activated CD4(+) lamina propria T cells of inflammatory bowel (IBD) contributes to dysregulated immune responses. Hyperexpression limited to inflammatory sites in IBD. Feasible therapeutic target for treatment of IBD.
- A subtype of regulatory T cells in human blood can be identified by expression of ICOS after activation; these ICOS-expressing cells block the capacity of reciprocal ICOS-negative cells to proliferate and to produce cytokines.
- ICOS expression on activated Th cells may provide a powerful means to amplify effector T cell responses in peripheral tissues, independently of the polarized state of the Th cells
- AILIM/ICOS-B7h interactions play an important role in the endothelium in controlling the entry of memory/effector T-cells into inflamed tissues in the periphery.
- The incidence of ICOS deficiency among patients with Common variable immunodeficiency is less than 5%
- invariant NKT cell activation is regulated by CD28 and IOCS independently
- A predominant effect of ICOS-mediated costimulation on T helper type 2 (Th2) cell differentiation in transgenic ICOS-deficient mice may be achieved by the enhancement of IL-4 receptor-mediated signaling.
- ICOS is an influential costimulatory pathway in atherosclerosis & may play a protective role. It localizes with T cells in human aortic plaque.
- This study could not confirm association with the CD28/CTLA4/ICOS gene region in multiple sclerosis.
- Two variants in the ICOS promoter region are significantly associated with allergic sensitization and production of type 2 T helper (Th2) cell cytokines
- ICOS is involved in abnormal T cell activation in systsemic lupus erythematosus (SLE) and blockade of the interaction between ICOS and its receptor may have therapeutic value in the treatment of this intractable disease.
- There are no major effects of the CD28/CTLA4/ICOS gene region on susceptibility to primary sclerosing cholangitis but minor contributions cannot be excluded.
- ICOS activation is associated with T helper type 1 (Th1) cell responses in human intracellular tuberculosis infection and may contribute to the amplification of those responses.
- This review summarizes the evidence that ICOS expression regulates T-cell-dependent B cell responses and proposes a model for the role of ICOS in diseases characterized by dysregulated humoral immunity.
- genetic variation in ICOS gene regulates the expression of both CTLA4 and ICOS and not only the splicing of sCTLA4 as suggested earlier.
- Both the PI3-kinase/Akt and Rho family cascades operate coordinately to induce the forward migration of activated T cells by AILIM/ICOS signaling.
- With multiethnic DNA panels that represent a wide spectrum of ethnic groups, we demonstrate long-range linkage disequilibrium among CD28, CTLA4, and ICOS costimulatory genes.
- ICOS may be relevant in inducing an acute immune response and may be critically involved in perpetuating inflammation in chronically immune-mediated disorders of the peripheral nervous system.
- These results define elevated populations of memory T-lymphocytes expressing B7 molecules in rheumatoid arthritis (RA) synovial fluid that either stimulate T cells through ICOS, or down-regulate RA synovial tissue T-lymphocytes through B7H1 and B7H2.
- The whole blood gene expression quantities of costimulatory molecules CD154 and ICOS reasonably robustly differentiated rejection patients from control patients.
- ICOS gene haplotypes correlate with IL10 secretion and multiple sclerosis.
- Of 9 CVID patients...No mutations of SAP, ICOS, TACI, BAFFR, and CD19 were identified
- definition of a newly discovered pathway that prevents autoimmunity by limiting the levels on T lymphocytes of aco-stimulatory receptor, the inducible T-cell co-stimulator(ICOS)
- Modulation of immune responses by ICOS-expressing naturally occurring T regulatory cells present in melanoma tissue depends upon costimulatory signals delivered to the CD4-positive CD25-negative responder cells and the cytokine milieu.
- p50alpha is likely a determining factor in ICOS-mediated PI3K activity in T cells
- Children with type 1 diabetes show decreased inducrion of ICOS in T cells.