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Protein Page:
IL7R (mouse)
p Phosphorylation
ac Acetylation
me Methylation
m1 Mono-methylation
m2 Di-methylation
m3 Tri-methylation
ub Ubiquitination
sm Sumoylation
ne Neddylation
gl O-GlcNAc
ga O-GalNAc
pa Palmitoylation
ad Adenylylation
sn S-Nitrosylation
ca Caspase cleavage
sc Succinylation

Overview
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. Note: This description may include information from UniProtKB.
Protein type: Receptor, cytokine; Membrane protein, integral
Cellular Component: membrane; integral to membrane; external side of plasma membrane
Molecular Function: hematopoietin/interferon-class (D200-domain) cytokine receptor activity
Biological Process: B cell proliferation; positive regulation of T cell differentiation in the thymus; negative regulation of T cell mediated cytotoxicity; cell morphogenesis; homeostasis of number of cells; immunoglobulin production; cell growth; regulation of cell size; lymph node development; T cell differentiation
Reference #:  P16872 (UniProtKB)
Alt. Names/Synonyms: CD127; IL-7 receptor alpha chain; IL-7 receptor subunit alpha; IL-7R subunit alpha; IL-7R-alpha; IL-7RA; IL-7Ralpha; Il7r; IL7RA; interleukin 7 receptor; interleukin 7 receptor alpha chain; Interleukin-7 receptor subunit alpha; MGC107557
Gene Symbols: Il7r
Molecular weight: 51,605 Da
Basal Isoelectric point: 8.2  Predict pI for various phosphorylation states
Select Structure to View Below

IL7R

Protein Structure Not Found.


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Sites Implicated In
apoptosis, inhibited: Y449‑p
transcription, altered: Y449‑p
translation, altered: Y449‑p

Modification Sites and Domains Show Modification Legend
Click here to view phosphorylation modifications only

Modification Sites in Parent Protein, Orthologs, and Isoforms Show Modification Legend
 

Show Multiple Sequence Alignment


 SS 

SS: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.


 MS 

MS: The number of records in which this modification site was assigned using ONLY proteomic discovery-mode mass spectrometry.


       mouse

 
0 1 Y159 APHLKKKYLKKVKHD
0 1 Y169 KVKHDVAYRPARGES
0 1 T292 QLCKKPKTSLNVSFN
0 2 S297 PKTSLNVSFNPESFL
0 1 T337 AQPEELETQGHRAAV
0 4 S346-p GHRAAVHsANRSPET
0 1 S356-p RSPETSVsPPETVRR
0 1 S365 PETVRRESPLRCLAR
0 2 S375-p RCLARNLsTCNAPPL
4 0 Y449-p VLNQEEAyVTMSSFY
  human

 
Y159-p TSHLQKKyVKVLMHD
Y169-p VLMHDVAyRQEKDEN
K292-ub HLCKKPRkNLNVsFN
S297-p PRkNLNVsFNPESFL
K337-ub QQLEESEkQRLGGDV
S346-p RLGGDVQsPNCPSED
I356 CPSEDVVITPESFGR
S365-p PESFGRDsSLTCLAG
S375-p TCLAGNVsACDAPIL
Y449-p GSNQEEAyVTMSSFY
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