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Protein Page:
ARSE (human)

Overview
ARSE May be essential for the correct composition of cartilage and bone matrix during development. Has no activity toward steroid sulfates. Defects in ARSE are the cause of chondrodysplasia punctata X-linked recessive type 1 (CDPX1). CDP is a clinically and genetically heterogeneous disorder characterized by punctiform calcification of the bones. CDPX1 is a congenital defect of bone and cartilage development characterized by aberrant bone mineralization, severe underdevelopment of nasal cartilage, and distal phalangeal hypoplasia. This disease can also be induced by inhibition with the drug warfarin. Belongs to the sulfatase family. Note: This description may include information from UniProtKB.
Protein type: Hydrolase; EC 3.1.6.-
Cellular Component: Golgi stack; endoplasmic reticulum lumen
Molecular Function: arylsulfatase activity; metal ion binding
Biological Process: cellular protein metabolic process; sphingolipid metabolic process; glycosphingolipid metabolic process; post-translational protein modification; skeletal development
Reference #:  P51690 (UniProtKB)
Alt. Names/Synonyms: ARSE; Arylsulfatase E; arylsulfatase E (chondrodysplasia punctata 1); ASE; CDPX; CDPX1; CDPXR; chondrodysplasia punctata 1; MGC163310
Gene Symbols: ARSE
Molecular weight: 65,669 Da
Basal Isoelectric point: 6.48  Predict pI for various phosphorylation states
Select Structure to View Below

ARSE

Protein Structure Not Found.


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Modification Sites and Domains  

Modification Sites in Parent Protein, Orthologs, and Isoforms  
 

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.


       human

 
0 1 S81-p VKLTQHIsAAsLCTP
0 1 S84-p TQHIsAAsLCTPSRA
0 1 Y98-p AAFLTGRyPVRSGMV
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