|PTPRC_HUMAN » Receptor-type tyrosine-protein phosphatase C » Leukocyte common antigen;L-CA; T200;|
|Hydrophobic Thickness||31.6 ± 1.4 Å|
|Tilt Angle||0 ± 0°|
|Links||UniProtKB, Pfam, Interpro, iHOP, STRING, HGNC, HMDB|
|TM Segments||574-600 (571-605)|
Cell adhesion molecules (KEGG)
Developmental Biology (Reactome)
Immune System (Reactome)
Primary immunodeficiency (KEGG)
|PDB||1ygr (A/B=622-1231), 1ygu (A/B=622-1231)|
EPOR, Complex: EPOR:PTPRC
GHR, Complex: GHR:PTPRC
MET, Complex: PTPRC:MET
NTRK1, Complex: PTPRC:NTRK1
PGFRB, Complex: PTPRC:PGFRB
AA: 5-30, Protein tyrosine phosphatase N terminal
AA: 235-293, Leukocyte receptor CD45
|UniProt annotation for PTPRC_HUMAN » Receptor-type tyrosine-protein phosphatase C|
|FUNCTION: Protein tyrosine-protein phosphatase required for T-cell activation through the antigen receptor. Acts as a positive regulator of T-cell coactivation upon binding to DPP4. The first PTPase domain has enzymatic activity, while the second one seems to affect the substrate specificity of the first one. Upon T-cell activation, recruits and dephosphorylates SKAP1 and FYN. Dephosphorylates LYN, and thereby modulates LYN activity (By similarity). CATALYTIC ACTIVITY: Protein tyrosine phosphate + H(2)O = protein tyrosine + phosphate. SUBUNIT: Binds GANAB and PRKCSH (By similarity). Interacts with SKAP1. Interacts with DPP4; the interaction is enhanced in a interleukin-12-dependent manner in activated lymphocytes. Interacts with human cytomegalovirus protein UL11. DOMAIN: The first PTPase domain interacts with SKAP1. DISEASE: Severe combined immunodeficiency autosomal recessive T- cell-negative/B-cell-positive/NK-cell-positive (T(-)B(+)NK(+) SCID) OMIM: 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. mutations affecting the gene represented in this entry. DISEASE: Multiple sclerosis (MS) OMIM: 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. associated with variations affecting the gene represented in this entry.|
|UniProt features for PTPRC_HUMAN » Receptor-type tyrosine-protein phosphatase C|
SIGNAL 1 23 |
CHAIN 24 1304 Receptor-type tyrosine-protein phosphatase C.
DOMAIN 390 478 Fibronectin type-III 1.
DOMAIN 482 570 Fibronectin type-III 2.
DOMAIN 651 910 Tyrosine-protein phosphatase 1.
DOMAIN 942 1226 Tyrosine-protein phosphatase 2.
REGION 851 857 Substrate binding (By similarity).
ACT_SITE 851 851 Phosphocysteine intermediate.
ACT_SITE 1167 1167 Phosphocysteine intermediate (By similarity).
|Amino Acid Sequence for PTPRC_HUMAN » Receptor-type tyrosine-protein phosphatase C|
|MYLWLKLLAF GFAFLDTEVF VTGQSPTPSP TGLTTAKMPS VPLSSDPLPT HTTAFSPAST FERENDFSET TTSLSPDNTS TQVSPDSLDN ASAFNTTGVS SVQTPHLPTH ADSQTPSAGT DTQTFSGSAA NAKLNPTPGS NAISDVPGER STASTFPTDP VSPLTTTLSL AHHSSAALPA RTSNTTITAN TSDAYLNASE TTTLSPSGSA VISTTTIATT PSKPTCDEKY ANITVDYLYN KETKLFTAKL NVNENVECGN NTCTNNEVHN LTECKNASVS ISHNSCTAPD KTLILDVPPG VEKFQLHDCT QVEKADTTIC LKWKNIETFT CDTQNITYRF QCGNMIFDNK EIKLENLEPE HEYKCDSEIL YNNHKFTNAS KIIKTDFGSP GEPQIIFCRS EAAHQGVITW NPPQRSFHNF TLCYIKETEK DCLNLDKNLI KYDLQNLKPY TKYVLSLHAY IIAKVQRNGS AAMCHFTTKS APPSQVWNMT VSMTSDNSMH VKCRPPRDRN GPHERYHLEV EAGNTLVRNE SHKNCDFRVK DLQYSTDYTF KAYFHNGDYP GEPFILHHST SYNSKALIAF LAFLIIVTSI ALLVVLYKIY DLHKKRSCNL DEQQELVERD DEKQLMNVEP IHADILLETY KRKIADEGRL FLAEFQSIPR VFSKFPIKEA RKPFNQNKNR YVDILPYDYN RVELSEINGD AGSNYINASY IDGFKEPRKY IAAQGPRDET VDDFWRMIWE QKATVIVMVT RCEEGNRNKC AEYWPSMEEG TRAFGDVVVK INQHKRCPDY IIQKLNIVNK KEKATGREVT HIQFTSWPDH GVPEDPHLLL KLRRRVNAFS NFFSGPIVVH CSAGVGRTGT YIGIDAMLEG LEAENKVDVY GYVVKLRRQR CLMVQVEAQY ILIHQALVEY NQFGETEVNL SELHPYLHNM KKRDPPSEPS PLEAEFQRLP SYRSWRTQHI GNQEENKSKN RNSNVIPYDY NRVPLKHELE MSKESEHDSD ESSDDDSDSE EPSKYINASF IMSYWKPEVM IAAQGPLKET IGDFWQMIFQ RKVKVIVMLT ELKHGDQEIC AQYWGEGKQT YGDIEVDLKD TDKSSTYTLR VFELRHSKRK DSRTVYQYQY TNWSVEQLPA EPKELISMIQ VVKQKLPQKN SSEGNKHHKS TPLLIHCRDG SQQTGIFCAL LNLLESAETE EVVDIFQVVK ALRKARPGMV STFEQYQFLY DVIASTYPAQ NGQVKKNNHQ EDKIEFDNEV DKVKQDANCV NPLGAPEKLP EAKEQAEGSE PTSGTEGPEH SVNGPASPAL NQGS|