IL7R alpha Active Protein | IL7RA active protein

Recombinant Human IL7R alpha Protein

Cat. Num. AAA9141734

• Gene Names: IL7R; ILRA; CD127; IL7RA; CDW127; IL-7R-alpha
• Purity: >95% by SDS-PAGE.
• Synonyms: IL7R alpha; Recombinant Human IL7R alpha Protein; CD127; CDW127; IL-7R; IL-7R-alpha; ILRA; IL7RA active protein

• Host: HEK293 Cells
• Purity/Purification: >95% by SDS-PAGE.
• Form/Format: Lyophilized from a 0.22 um filtered solution of PBS, pH 7.4.
• Sequence: ESGYAQNGDLEDAELDDYSFSCYSQLEVNGSQHSLTCAFEDPDVNITNLEFEICGALVEVKCLNFRKLQEIYFIETKKFLLIGKSNICVKVGEKSLTCKKIDLTTIVKPEAPFDLSVVYREGANDFVVTFNTSHLQKKYVKVLMHDVAYRQEKDENKWTHVNLSSTKLTLLQRKLQPAAMYEIKVRSIPDHYFKGFWSEWSPSYYFRTPEINNSSG
• Sequence Length: 459

• Species: Human
• Endotoxin: < 1.0 EU/ug of the protein by LAL method.
• Biological Activity: Measured by its binding ability in a functional ELISA. When Recombinant Human IL-7 R alpha /CD127 (0.25 ug/mL, 100 uL/well) is immobilized on a goat anti-human IgG Fc antibody coated plate, the concentration of recombinant human IL-7 that produces 50% of the optimal binding response is found to be approximately 30-150 ng/mL.
• Reconstitution: Reconstitute to a concentration of 0.1-0.5 mg/mL in sterile distilled water.
• Tag: Fc, 6xHis tag at the C-terminus
• Preparation and Storage: Store the lyophilized protein at -20 degree C to -80 degree C for long term.; After reconstitution, the protein solution is stable at -20 degree C for 3 months, at 2-8 degree C for up to 1 week.

SDS-Page

(Recombinant Human IL7R alpha Protein was determined by SDS-PAGE with Coomassie Blue, showing a band at 70-90 kDa.)

Related Product Information for IL7RA active protein

Description: Recombinant Human IL7R alpha Protein is produced by HEK293 expression system. The target protein is expressed with sequence (Glu21-Gly236) of human IL7R alpha (Accession #NP_002176.2) fused with an Fc, 6xHis tag at the C-terminus.

Background: This protein 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.

Product Categories/Family for IL7RA active protein

Cytokines & Cytokine Receptors

NCBI and Uniprot Product Information

• NCBI GI #: 28610151
• NCBI GeneID: 3575
• NCBI Accession #: NP_002176.2
• NCBI GenBank Nucleotide #: NP_002176.2
• UniProt Accession #: P16871
• NCBI Official Full Name: interleukin-7 receptor subunit alpha
• NCBI Official Synonym Full Names: interleukin 7 receptor
• NCBI Official Symbol: IL7R
• NCBI Official Synonym Symbols: ILRA; CD127; IL7RA; CDW127; IL-7R-alpha
• NCBI Protein Information: interleukin-7 receptor subunit alpha
• UniProt Protein Name: Interleukin-7 receptor subunit alpha
• UniProt Gene Name: IL7R
• UniProt Synonym Gene Names: IL-7 receptor subunit alpha; IL-7R subunit alpha; IL-7R-alpha; IL-7RA
• UniProt Entry Name: IL7RA_HUMAN

NCBI Description

The protein encoded by this gene is a receptor for interleukin 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 interleukins 2, 4, 7, 9, and 15. This protein has been shown to play a critical role in V(D)J recombination during lymphocyte development. Defects in this gene may be associated with severe combined immunodeficiency (SCID). Alternatively spliced transcript variants have been found. [provided by RefSeq, Dec 2015]

Uniprot Description

IL7R: Receptor for interleukin-7. Also acts as a receptor for thymic stromal lymphopoietin (TSLP). Defects in IL7R are a cause of severe combined immunodeficiency autosomal recessive T-cell-negative/B-cell- positive/NK-cell-positive (T(-)B(+)NK(+) SCID). 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. Genetic variations in IL7R are a cause of susceptibility to multiple sclerosis type 3 (MS3). 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 sheat, 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. 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. Belongs to the type I cytokine receptor family. Type 4 subfamily. 4 isoforms of the human protein are produced by alternative splicing.

Protein type: Receptor, cytokine; Membrane protein, integral

Chromosomal Location of Human Ortholog: 5p13

Cellular Component: plasma membrane; extracellular region; integral to membrane; external side of plasma membrane

Molecular Function: protein binding; interleukin-7 receptor activity; antigen binding

Biological Process: B cell proliferation; homeostasis of number of cells; cell morphogenesis; signal transduction; lymph node development; positive regulation of T cell differentiation in the thymus; cell surface receptor linked signal transduction; regulation of DNA recombination; negative regulation of T cell mediated cytotoxicity; immune response; immunoglobulin production; cell growth; regulation of cell size; T cell differentiation

Disease: Severe Combined Immunodeficiency, Autosomal Recessive, T Cell-negative, B Cell-positive, Nk Cell-positive