Anti-PDCD1 (clone PD1-17) Recombinant Antibody Coupled Liposome (VS-1024-FY255)
CAT#: VS-1024-FY255
Anti-PD-1 antibody conjugated liposomes hold significant potential in the treatment of Adrenocortical carcinoma by enhancing the immune response against tumor cells. By targeting the PD-1 immune checkpoint pathway, these liposomes could improve T-cell activation and promote antitumor immunity, potentially leading to better patient outcomes. Additionally, the liposomal delivery system can enhance the bioavailability and stability of the conjugated antibodies, ensuring sustained therapeutic effects at the tumor site. Overall, this innovative approach may pave the way for more effective immunotherapies in combating Adrenocortical carcinoma and other malignancies.



Specifications
- Potential Clinical Applications
- Adrenocortical carcinoma
Product Composition
- Clone
- PD1-17
- Antibody Type
- IgG
- Antibody Host
- Mouse
- Antibody Reactivity
- Human
- Antibody Description
- This is a recombinant mouse monoclonal antibody that was engineered to specifically bind to Programmed Cell Death Protein 1 (PD-1), an important checkpoint inhibitor in the immune system. The antibody's high affinity and specificity towards PD-1 make it a powerful tool in immunological research and therapeutic development, particularly in the context of cancer treatment. By blocking PD-1 interactions, this antibody can potentially restore immune responses against tumors, thus playing a pivotal role in cancer immunotherapy.
Product Property
- Storage
- See in the COA
- Storage Shelf Time
- See in the COA
Target Information
- Target
- PDCD1
- Introduction
- This gene encodes a cell surface membrane protein of the immunoglobulin superfamily. This protein is expressed in pro-B-cells and is thought to play a role in their differentiation. In mice, expression of this gene is induced in the thymus when anti-CD3 antibodies are injected and large numbers of thymocytes undergo apoptosis. Mice deficient for this gene bred on a BALB/c background developed dilated cardiomyopathy and died from congestive heart failure. These studies suggest that this gene product may also be important in T cell function and contribute to the prevention of autoimmune diseases.
- Alternative Names
- Programmed Cell Death 1; Systemic Lupus Erythematosus Susceptibility 2; Protein PD-1; HPD-1; PD1; Programmed Cell Death 1 Protein; Programmed Cell Death Protein 1
- Full Name
- Programmed Cell Death 1
- Gene ID
- 5133
- UniProt ID
- Q15116
- Cellular Localization
- Cell membrane; Membrane
- Post Translation Modifications
- Ubiquitinated at Lys-233 by the SCF(FBXO38) complex, leading to its proteasomal degradation (PubMed:30487606).
Ubiquitinated via 'Lys-48'-linked polyubiquitin chains (PubMed:30487606).
Tyrosine phosphorylated at Tyr-223 (within ITIM motif) and Tyr-248 (ITSM motif) upon ligand binding. Phosphorylation at Tyr-248 promotes 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.
N-glycosylation at Asn-58 contains at least two N-acetylglucosamine units and one fucose (PubMed:28165004).
- Protein Refseq
- NP_005009.2
- Function
- 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).
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).
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Datasheet
MSDS
COA
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