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Invitrogen
CD127 Polyclonal Antibody, PE
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Please note: We are reviewing Western blot images included in the antibody testing data in our catalog, including those provided by third parties. Unless expressly labeled or annotated as “raw-unedited”, Western blot images included in the antibody testing data in our catalog may have been edited, optimized or otherwise adjusted for presentation.
Product Details
PA5-46900
Product Specifications
Species Reactivity
Rat
Host/Isotype
Sheep
/ IgG
Class
Polyclonal
Type
Antibody
Immunogen
Mouse myeloma cell line NS0-derived recombinant rat IL-7 R alpha/CD127 Glu21-Asp239
Conjugate
PE
PE
PE
Excitation/Emission Max
565/576 nm
View spectra
Form
Liquid
Purification
Antigen affinity chromatography
Storage buffer
Buffered saline solution with ≤ 0.5% BSA
Contains
0.09% sodium azide
Storage conditions
4°C, store in dark, DO NOT FREEZE!
Shipping conditions
Ambient (domestic); Wet ice (international)
RRID
Product Specific Information
In direct ELISAs, approximately 60% cross-reactivity with recombinant mouse IL-7 R alpha and less than 10% cross-reactivity with recombinant human IL-7 R alpha is observed.
Target Information
CD127, also known as the Interleukin-7 receptor alpha chain (IL-7Ralpha), is a type I glycoprotein with a molecular weight of 75-80 kDa. It forms a multi-functional receptor complex with CD132, the common gamma chain, to create the IL-7 receptor (IL-7R), which is crucial for lymphopoiesis. The active IL-7 receptor is an alpha/gamma chain heterodimer, where the gamma chain also associates with the interleukin-2 receptor and primarily activates signal transduction, while the alpha chain determines specific signaling events through its association with cytoplasmic signaling molecules. CD127 is expressed by immature B cells through the early pre-B stage, thymocytes during various stages of development, and most mature T cells, with transient down-regulation upon activation. It promotes the proliferation of precursor B cells, thymocytes, T cell progenitors, and mature CD4+ and CD8+ T cells. Binding of IL-7 to CD127 results in signal transduction through several tyrosine kinase pathways, including the Jak/STAT pathway, and is indispensable for lymphocyte development and the control of homeostatic proliferation of T cells in the periphery. Additionally, IL-7R signaling is involved in the regulation of T cell receptor (TCR) locus rearrangement in gamma delta T cells. Interestingly, CD127 expression is down-regulated on CD4+CD25+ regulatory T cells (T regs). While CD4 and CD25 co-expression is commonly used to identify T regs, this method may include cells without suppressive activity. CD4+CD25+ cells that have down-regulated CD127 expression are significantly enriched for the regulatory T cell population, as defined by the expression of the T reg-specific transcription factor Foxp3 and their suppressive activity in vitro. Diseases associated with CD127 dysfunction include severe combined immunodeficiency and T cell negative/B cell negative/NK positive severe combined immunodeficiency.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
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Bioinformatics
Protein Aliases: IL 7 receptor; IL 7R a; IL 7R subunit alpha; IL 7R α; IL 7Ra; IL 7Rα; IL-7R; IL7 receptor; IL7 receptor subunit alpha; IL7R a; IL7R alpha; IL7R subunit alpha; IL7R α; IL7Rα; Interleukin7 receptor subunit alpha; MGC107557; sCD127; soluble IL 7 receptor; soluble IL 7R
Entrez Gene ID: (Rat) 294797
cell morphogenesis
negative regulation of T cell mediated cytotoxicity
biological_process
positive regulation of cell proliferation
regulation of cell size
positive regulation of gene expression
cellular homeostasis
hemopoiesis
T cell differentiation
positive regulation of T cell differentiation in thymus
interleukin-7-mediated signaling pathway
B cell proliferation
positive regulation of JAK-STAT cascade
lymph node development
homeostasis of number of cells
defense response to Gram-positive bacterium
negative regulation of T cell apoptotic process
positive regulation of STAT cascade
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