Text Size:AAA

CD127/IL-7RA Protein, Antibody, ELISA Kit, cDNA Clone

Human CD127/IL-7RA Protein

Description: Active
Expression host: Human Cells
  • Slide 1
  • Slide 1
10975-H03H-50
10975-H03H-100
50 µg / $178
100 µg / $298
Add to Cart
Description: Active
Expression host: Human Cells
  • Slide 1
10975-H08H-50
10975-H08H-100
50 µg / $178
100 µg / $298
Add to Cart

Mouse CD127/IL-7RA Protein

Expression host: Human Cells
  • Slide 1
50090-M08H-50
50090-M08H-100
50 µg / $178
100 µg / $298
Add to Cart

Rat CD127/IL-7RA Protein

Expression host: Human Cells
  • Slide 1
  • Slide 1
80083-R05H-20
80083-R05H-50
20 µg / $78
50 µg / $178
Add to Cart
Expression host: Human Cells
  • Slide 1
80083-R08H-50
80083-R08H-100
50 µg / $178
100 µg / $298
Add to Cart

Cynomolgus CD127/IL-7RA Protein

Expression host: Human Cells
  • Slide 1
  • Slide 1
90332-C08H-100
90332-C08H-50
100 µg / $298
50 µg / $178
Add to Cart

CD127/IL-7RA Related Areas

CD127/IL-7RA Related Pathways

CD127/IL-7RA Related Product

    CD127/IL-7RA Summary & Protein Information

    CD127/IL-7RA Related Information

    CD127/IL-7RA Background

    Gene Summary: The protein encoded by IL7R 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, Jul 2008]
    General information above from NCBI
    Subunit structure: The IL7 receptor is a heterodimer of IL7R and IL2RG. The TSLP receptor is a heterodimer of CRLF2 and IL7R.
    Domain: The WSXWS motif appears to be necessary for proper protein folding and thereby efficient intracellular transport and cell- surface receptor binding.
    The box 1 motif is required for JAK interaction and/or activation.
    Subcellular location: Isoform 1: Cell membrane; Single-pass type I membrane protein.
    Isoform 3: Cell membrane; Single-pass type I membrane protein.
    Isoform 4: Secreted.
    Post-translational: N-glycosylated IL-7Ralpha binds IL7 300-fold more tightly than the unglycosylated form.
    Involvement in disease: Severe combined immunodeficiency autosomal recessive T- cell-negative/B-cell-positive/NK-cell-positive (T(-)B(+)NK(+) SCID) [MIM:608971]: A form of severe combined immunodeficiency (SCID), a genetically and clinically heterogeneous group of rare congenital disorders characterized by impairment of both humoral and cell-mediated immunity, leukopenia, and low or absent antibody levels. Patients present in infancy recurrent, persistent infections by opportunistic organisms. The common characteristic of all types of SCID is absence of T-cell-mediated cellular immunity due to a defect in T-cell development. Note=The disease is caused by mutations affecting the gene represented in this entry.
    Multiple sclerosis 3 (MS3) [MIM:612595]: A multifactorial, inflammatory, demyelinating disease of the central nervous system. Sclerotic lesions are characterized by perivascular infiltration of monocytes and lymphocytes and appear as indurated areas in pathologic specimens (sclerosis in plaques). The pathological mechanism is regarded as an autoimmune attack of the myelin sheath, mediated by both cellular and humoral immunity. Clinical manifestations include visual loss, extra-ocular movement disorders, paresthesias, loss of sensation, weakness, dysarthria, spasticity, ataxia and bladder dysfunction. Genetic and environmental factors influence susceptibility to the disease. Note=Disease susceptibility is associated with variations affecting the gene represented in this entry. A polymorphism at position 244 strongly influences susceptibility to multiple sclerosis. Overtransmission of the major 'C' allele coding for Thr-244 is detected in offspring affected with multiple sclerosis. In vitro analysis of transcripts from minigenes containing either 'C' allele (Thr-244) or 'T' allele (Ile-244) shows that the 'C' allele results in an approximately two-fold increase in the skipping of exon 6, leading to increased production of a soluble form of IL7R. Thus, the multiple sclerosis associated 'C' risk allele of IL7R would probably decrease membrane-bound expression of IL7R. As this risk allele is common in the general population, some additional triggers are probably required for the development and progression of MS.
    Sequence similarity: Belongs to the type I cytokine receptor family. Type 4 subfamily.
    Contains 1 fibronectin type-III domain.
    General information above from UniProt

    Interleukin 7 Receptor alpha (IL-7RA), also known as CD127, is a 75 kDa hematopoietin receptor superfamily member that plays an important role in lymphocyte differentiation, proliferation, and survival. IL-7 receptor alpha (CD127) signaling is essential for T-cell development and regulation of naive and memory T-cell homeostasis. IL-7RA is critically required for the proper development and function of lymphoid cells. Therefore, the IL-7RA is critically required for the proper development and function of lymphoid cells. Studies from both pathogenic and controlled HIV infection indicate that the containment of immune activation and preservation of CD127 expression are critical to the stability of CD4(+) T cells in infection. A better understanding of the factors regulating CD127 expression in HIV disease, particularly on T(CM) cells, might unveil new approaches exploiting the IL-7/IL-7R receptor pathway to restore T cell homeostasis and promote immune reconstitution in HIV infection. Factors relevant to HIV infection that could potentially decrease CD127 expression on human CD8(+) T cells. CD127 down-regulation may be an important contributor to HIV-associated T-cell dysfunction. In addition to IL-7, IL-7RA also associates with TSLPR to form the functional receptor for thymic stromal lymphopoietin (TSLP) which indirectly regulates T cell development by modulating dendritic cell activation. Mutations in the human IL-7RA gene cause a type of severe combined immunodeficiency in which the major deficiencies are in T cell development, whereas B and NK cells are relatively normal in number. Variation in the IL7RA gene was recently found associated with multiple sclerosis (MS). The polymorphisms in the IL7RA gene is involved in MS pathogenesis and suggest that IL7RA variation may primarily affect chronic disease courses. Soluble CD127 (sCD127) appears to play an important role in the immunopathogenesis of several chronic infections, multiple sclerosis, and various cancers.

    CD127/IL-7RA Alternative Name

    CD127/IL-7RA Related Studies

  • Vranjkovic A, et al. (2007) IL-7 decreases IL-7 receptor alpha (CD127) expression and induces the shedding of CD127 by human CD8+ T cells. Int Immunol. 19(12): 1329-39.
  • Kiazyk SA, et al. (2008) Loss of CD127 expression links immune activation and CD4(+) T cell loss in HIV infection. Trends Microbiol. 16(12): 567-73.
  • Akkad DA, et al. (2009) Variation in the IL7RA and IL2RA genes in German multiple sclerosis patients. J Autoimmun. 32(2): 110-5.
  • Crawley AM, et al. (2010) Soluble IL-7R alpha (sCD127) inhibits IL-7 activity and is increased in HIV infection. J Immunol. 184(9): 4679-87.
  • Please note: All products are "FOR RESEARCH USE ONLY AND ARE NOT INTENDED FOR DIAGNOSTIC OR THERAPEUTIC USE"