|
ORF cDNA clones
|
CRISPR / TALEN
|
Lentivirus
|
AAV
|
TALE-TF
|
ORF knockin clones
|
|
Antibody
|
Proteins
|
miRNA target clones
|
qPCR primers
|
shRNA clones
|
miRNA products
|
Promoter clones
|
Validated All-in-One™ qPCR Primer for IL7R(NM_002185.4) Search again
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:
Summary
The protein encoded by this gene is a receptor for interleukine 7 (IL7). The function of this receptor requires the interleukin 2 receptor, gamma chain (IL2RG), which is a common gamma chain shared by the receptors of various cytokines, including interleukine 2, 4, 7, 9, and 15. This protein has been shown to play a critical role in the V(D)J recombination during lymphocyte development. This protein is also found to control the accessibility of the TCR gamma locus by STAT5 and histone acetylation. Knockout studies in mice suggested that blocking apoptosis is an essential function of this protein during differentiation and activation of T lymphocytes. The functional defects in this protein may be associated with the pathogenesis of the severe combined immunodeficiency (SCID). [provided by RefSeq].
Gene References into function
- IL-7 may function to regulate the milieu of the microenvironment by modulating IL-6 secretion by the IL-7R-expressing stromal elements
- IL-2 signaling can diminish IL-7Ralpha expression via a phosphatidylinositol 3-kinase/Akt-dependent mechanism.
- IL-7R has a role in some human solid malignancies [review]
- Interaction between IL-7 and its receptor has the major role in modulating T-ALL survival within the microenvironment generated by the T-ALL/TEC interaction.
- Expansion of CD8 positive, CD127 negative effector-like T cells is identified as a novel feature of HIV-associated immune perturbation.
- Maturation of memory CD4 and CD8 T cells is associated with a CD127high phenotype and the expression of CD127 serves as a predictor of the functional quality of antiviral T cells.
- Virus-specific IL-7Ralpha+ cells proliferated vigorously in response to IL-7, IL-15, or peptide, whereas IL-7Ralpha- cells required both peptide and helper-cell activation or IL-2 or IL-15 for optimal expansion
- Altogether, we show that gamma(c) is the target of an ubiquitination mechanism and its expression level can be regulated through the activities of a couple of ubiquitin-ligase/ubiquitin-hydrolase enzymes, namely c-Cbl/DUB-2.
- The T cell proliferation gene IL7R (CD127) was also underexpressed in PPMS, but was up-regulated in SPMS compared to the controls.
- Aging affects IL-7Ralpha expression by T cells, leading to impaired signaling and survival responses to IL-7.
- HIV infection produces the Tat protein, which in turn may up-regulate IL-7R in a paracrine manner, which ultimately promotes early events in HIV replication.
- Transcription of the IL-7R alpha subunit is suppressed in both naive and memory T cells following IL-7 stimulation.
- Cell surface expression of CD127 therefore allows accurate estimation of regulatory T cell numbers and isolation of pure populations for in vitro studies and should contribute to our understanding of regulatory abnormalities in immunopathic diseases.
- CD127 can be used to quantitate regulatory T (Treg) cell subsets in individuals with type 1 diabetes supporting the use of CD127 as a biomarker for human Treg cells.
- CD127 expression on T cells remains low in HIV-infected patients despite antiretroviral therapy
- IL-7 receptor and Notch1 pathways cooperate to synchronize cell proliferation and suppression of non-T lineage choices in primitive intrathymic progenitors.
- CD127 uniquely enables the purification of FOXP3+ Treg cells and, potentially, also "adaptive" regulatory T-cell subsets from the CD4+CD25- T-cell population.
- A large fraction of peripheral HCV-specific CD8+ T cells were CD127+ and KLRG1-. Intrahepatic virus-specific CD8+ T cells displayed significantly reduced levels of CD127 expression but similar levels of KLRG1 expression compared to the peripheral blood.
- CD4+ regulatory T-cells exhibiting suppressive activity in vitro display distinctly lower surface expression of CD127, irrespective of their level of CD25 expression.
- results confirm that signal transduction via the IL-15R, and hence NK ontogeny, is preferentially retained relative to the IL-7R as gammac expression becomes limiting.
- These findings suggest that DNA methylation is involved in regulating IL-7Ralpha expression in T cells via affecting IL-7Ralpha gene promoter activity.
- gene encoding the IL-7Ralpha chain is polymorphic, and investigation of inhalation allergic patients compared with controls showed significant association with two alleles at position +1237 and +2087
- A subset of naive CD8-positive cells characterized by low interleukin-7 receptor alpha message and protein expression may encompass cells that have recently received homeostatic signals.
- CD4(+)CD25(+)CD45RO(+)IL-7Ralpha(high) cell population contained allospecific CD4 T cells and secreted effector cytokines.
- Increased constitutive interleukin-7 receptor alpha expression has minimal effects on the numbers or function of effector and memory CD8 T cells formed.
- Alleles of IL2RA and IL7RA and those in the HLA locus are identified as heritable risk factors for multiple sclerosis.
- Results provide compelling evidence that polymorphisms in IL7R, which encodes the interleukin 7 receptor alpha chain (IL7Ralpha), indeed contribute to the non-HLA genetic risk in multiple sclerosis.
- Results show allelic association of a polymorphism in interleukin 7 receptor alpha chain (IL7R) as a significant risk factor for multiple sclerosis in four independent family-based or case-control data sets.
- Immunolocalization of IL-7, IL-7Ralpha, SDF-1alpha, and CXCR4 resulted in a diffuse but specific labeling. RT-PCR analysis confirmed the expression of the above-mentioned transcripts.
- Stimulation of the IL-7 pathway begins with IL-7 binding to unglycosylated and glycosylated forms of its alpha-receptor, IL-7 receptor alpha.
- Haplotypes of the IL7R gene are correlated with altered expression in whole blood cells in multiple sclerosis.
- IL-7 reduced CD127-surface expression and shedding by CD8+ T cells; results support a role for IL-7 in the down-regulation of CD127 expression and impairment of CTL function observed in HIV infection
- We report that loss of CD127 defines terminally differentiated B cell-helping effector T cells in human tonsils.
- The association between rs6897932 and multiple sclerosis in the Olmsted County collection appeared to be much stronger than anticipated on the basis of recent studies
- Expression of transgenic IL-7 receptor alpha by itself does not support increased survival of effector antigen-specific CD4 or CD8 T cells into the memory phase following infection with Listeria monocytogenes.
- IL2RA and IL7RA genes confer susceptibility for multiple sclerosis in two independent European populations.
- IL-7- and TCR/CD28-mediated signaling data show that differentially regulate IL-7Ralpha expression on human T cells with a transient and chronic effect, respectively.
- during HIV infection, specific changes in the fraction of CD4(+) T cells expressing CD25 and/or CD127 are associated with disease progression
- Independent replication of the association between the CAPSL and IL7R locus and type 1 diabetes, especially for early-onset type 1 diabetes patients.
- Association studies between IL7RA rs6897932 and multiple sclerosis.
- Down-regulation of CD127 was mainly associated with T cell activation and reverted only partially after suppression of detectable plasma HIV RNA with HAART
- CD8+ T-cell CD127 expression is significantly higher in children with better HIV disease control, and may have a role as an immunologic indicator of disease status.
- The SCID mutations of IL-7Ralpha locate outside the binding interface with IL-7, suggesting that the expressed mutations cause protein folding defects in IL-7Ralpha
