PD-1
Human Recombinant PDCD1 - Fc Tagged
Reference ID:KB-3666
Western Blot
ELISA
FACS
Protein:Protein
Flow Cytometry
Gene of Interest
Gene Synonyms:PDCD1;PD1
Protein Names:Programmed cell death protein 1 (Protein PD-1) (hPD-1) (CD antigen CD279)
Accession Data
Organism:Homo sapiens (Human)
Mass (kDa):316.47
Length (aa):288
Sequence:MQIPQAPWPVVWAVLQLGWRPGWFLDSPDRPWNPPTFSPALLVVTEGDNATFTCSFSNTSESFVLNWYRMSPSNQTDKLAAFPEDRSQPGQDCRFRVTQLPNGRDFHMSVVRARRNDSGTYLCGAISLAPKAQIKESLRAELRVTERRAEVPTAHPSPSPRPAGQFQTLVVGVVGGLLGSLVLLVWVLAVICSRAARGTIGARRTGQPLKEDPSAVPVFSVDYGELDFQWREKTPEPPVPCVPEQTEYATIVFPSGMGTSSPARRGSADGPRSAQPLRPEDGHCSWPL
Proteomics (Proteome ID):UP000005640
Proteomics (Chromosome): Chromosome 2
Activity Regulation: Inhibited by pembrolizumab (also named MK-3475 or lambrolizumab), a monoclonal antibody that prevents the interaction with CD274/PDCD1L1 (PubMed:27734966, PubMed:27325296). Inhibited by nivolumab (also named ONO-4538, BMS-936558 or Opdivo), a monoclonal antibody that prevents the interaction with CD274/PDCD1L1 (PubMed:28165004). The interaction with nivolumab is not dependent on glycosylation and depends on a loop at the N-terminus (N-terminal loop, corresponding to residues 25-34) (PubMed:28165004). Targeting the interaction between PDCD1 and CD274/PDCD1L1 with pembrolizumab and nivolumab antibodies has demonstrated great promise as a strategy for controlling and eradicating cancer (PubMed:22658127, PubMed:25034862, PubMed:25399552). Pembrolizumab and nivolumab are used for treatment of patients with advanced melanoma (PubMed:25034862, PubMed:25399552). These antibodies are also effective against other cancers, such as non-small cell lung cancer, renal cell carcinoma, bladder cancer and Hodgkin's lymphoma (PubMed:25034862). {ECO:0000269|PubMed:22658127, ECO:0000269|PubMed:25034862, ECO:0000269|PubMed:25399552, ECO:0000269|PubMed:27325296, ECO:0000269|PubMed:27734966, ECO:0000269|PubMed:28165004}.
Function [CC]:Inhibitory receptor on antigen activated T-cells that plays a critical role in induction and maintenance of immune tolerance to self (PubMed:21276005). Delivers inhibitory signals upon binding to ligands CD274/PDCD1L1 and CD273/PDCD1LG2 (PubMed:21276005). Following T-cell receptor (TCR) engagement, PDCD1 associates with CD3-TCR in the immunological synapse and directly inhibits T-cell activation (By similarity). Suppresses T-cell activation through the recruitment of PTPN11/SHP-2: following ligand-binding, PDCD1 is phosphorylated within the ITSM motif, leading to the recruitment of the protein tyrosine phosphatase PTPN11/SHP-2 that mediates dephosphorylation of key TCR proximal signaling molecules, such as ZAP70, PRKCQ/PKCtheta and CD247/CD3zeta (By similarity). {ECO:0000250|UniProtKB:Q02242, ECO:0000269|PubMed:21276005}.; The PDCD1-mediated inhibitory pathway is exploited by tumors to attenuate anti-tumor immunity and escape destruction by the immune system, thereby facilitating tumor survival (PubMed:28951311). The interaction with CD274/PDCD1L1 inhibits cytotoxic T lymphocytes (CTLs) effector function (PubMed:28951311). The blockage of the PDCD1-mediated pathway results in the reversal of the exhausted T-cell phenotype and the normalization of the anti-tumor response, providing a rationale for cancer immunotherapy (PubMed:22658127, PubMed:25034862, PubMed:25399552). {ECO:0000269|PubMed:22658127, ECO:0000269|PubMed:25034862, ECO:0000269|PubMed:25399552, ECO:0000303|PubMed:28951311}.
Developmental Stage:Induced at programmed cell death. {ECO:0000269|PubMed:7851902}.
Disease:Systemic lupus erythematosus 2 (SLEB2) [MIM:605218]: A chronic, relapsing, inflammatory, and often febrile multisystemic disorder of connective tissue, characterized principally by involvement of the skin, joints, kidneys and serosal membranes. It is of unknown etiology, but is thought to represent a failure of the regulatory mechanisms of the autoimmune system. The disease is marked by a wide range of system dysfunctions, an elevated erythrocyte sedimentation rate, and the formation of LE cells in the blood or bone marrow. {ECO:0000269|PubMed:12402038}. Note=Disease susceptibility is associated with variations affecting the gene represented in this entry.
Mutagenesis:MUTAGEN 49 49 N->A: Decreased N-glycosylation without affecting binding to binding to nivolumab drug. {ECO:0000269|PubMed:28165004}.; MUTAGEN 58 58 N->A: Decreased N-glycosylation without affecting binding to binding to nivolumab drug. {ECO:0000269|PubMed:28165004}.; MUTAGEN 74 74 N->A: Decreased N-glycosylation without affecting binding to binding to nivolumab drug. {ECO:0000269|PubMed:28165004}.; MUTAGEN 116 116 N->A: Decreased N-glycosylation without affecting binding to binding to nivolumab drug. {ECO:0000269|PubMed:28165004}.; MUTAGEN 210 210 K->R: Does not affect ubiquitination by the SCF(FBXO38) complex. {ECO:0000269|PubMed:30487606}.; MUTAGEN 233 233 K->R: Abolishes ubiquitination by the SCF(FBXO38) complex. {ECO:0000269|PubMed:30487606}.
Reagent Data
Name:PD-1
Class:Fluorecent Labeled
Subcategory:Protein
Region:Leu 25 - Gln 167
Molecular Weight:42.6
Source:HEK293
Species:Human
Tag:Fc
Conjugation:FITC
Format:Lyophilized
Purification System:Chromatography
Formulation:Sterile-filtered colorless solution
Formulation Concentration:1 mg/ml
Buffer Volume:Standard
Buffer Solution:PBS
pH:7.4-7.5
Toxicity
Endotoxin Level:< 1%
Aggregate Tested By:SDS-PAGE
Endotoxin Screened:< 0.1 ng/ug
Purity:> 98%
Determined: SDS-PAGE
Stain:Blue
Chromotography:Anion-exchange
Validated: RP-HPLC
Sample Handling
Storage:-20°C
Stability:This bioreagent is stable at 4°C (short-term) and -70°C(long-term). After reconstitution, sample may be stored at 4°C for 2-7 days and below -18°C for future use.
Preparation:Reconstitute in sterile distilled H2O to no less than 100 ug/ml; dilute reconstituted stock further in other aqueous solutions if needed. Please review COA for lot-specific instructions. Final measurements should be determined by the end-user for optimal performance.