LAG3 antibody (N-term)
Purified Rabbit Polyclonal Antibody (Pab)
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Application ![]()
| WB, E |
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Primary Accession | P18627 |
Reactivity | Human, Mouse |
Host | Rabbit |
Clonality | polyclonal |
Isotype | Rabbit Ig |
Calculated MW | 57449 Da |
Gene ID | 3902 |
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Other Names | Lymphocyte activation gene 3 protein, LAG-3, CD223, Secreted lymphocyte activation gene 3 protein, sLAG-3, LAG3 (HGNC:6476), FDC |
Target/Specificity | This antibody is generated from a rabbit immunized with a KLH conjugated synthetic peptide between amino acids from human. |
Dilution | WB~~1:1000 E~~Use at an assay dependent concentration. |
Format | Purified polyclonal antibody supplied in PBS with 0.05% (V/V) Proclin 300. This antibody is purified through a protein A column, followed by peptide affinity purification. |
Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
Precautions | LAG3 antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | LAG3 (HGNC:6476) |
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Synonyms | FDC |
Function | Lymphocyte activation gene 3 protein: Inhibitory receptor on antigen activated T-cells (PubMed:20421648, PubMed:7805750, PubMed:8647185). Delivers inhibitory signals upon binding to ligands, such as FGL1 (By similarity). FGL1 constitutes a major ligand of LAG3 and is responsible for LAG3 T-cell inhibitory function (By similarity). Following TCR engagement, LAG3 associates with CD3-TCR in the immunological synapse and directly inhibits T-cell activation (By similarity). May inhibit antigen-specific T-cell activation in synergy with PDCD1/PD-1, possibly by acting as a coreceptor for PDCD1/PD-1 (By similarity). Negatively regulates the proliferation, activation, effector function and homeostasis of both CD8(+) and CD4(+) T-cells (PubMed:20421648, PubMed:7805750, PubMed:8647185). Also mediates immune tolerance: constitutively expressed on a subset of regulatory T-cells (Tregs) and contributes to their suppressive function (By similarity). Also acts as a negative regulator of plasmacytoid dendritic cell (pDCs) activation (By similarity). Binds MHC class II (MHC-II); the precise role of MHC-II-binding is however unclear (PubMed:8647185). |
Cellular Location | [Lymphocyte activation gene 3 protein]: Cell membrane; Single-pass type I membrane protein |
Tissue Location | Primarily expressed in activated T-cells and a subset of natural killer (NK) cells. |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
Lymphocyte activation gene 3 protein: Inhibitory receptor on antigen activated T-cells (PubMed:20421648, PubMed:7805750, PubMed:8647185). Delivers inhibitory signals upon binding to ligands, such as FGL1 (By similarity). FGL1 constitutes a major ligand of LAG3 and is responsible for LAG3 T-cell inhibitory function (By similarity). Following TCR engagement, LAG3 associates with CD3-TCR in the immunological synapse and directly inhibits T-cell activation (By similarity). May inhibit antigen-specific T-cell activation in synergy with PDCD1/PD-1, possibly by acting as a coreceptor for PDCD1/PD-1 (By similarity). Negatively regulates the proliferation, activation, effector function and homeostasis of both CD8(+) and CD4(+) T-cells (PubMed:20421648, PubMed:7805750, PubMed:8647185). Also mediates immune tolerance: constitutively expressed on a subset of regulatory T-cells (Tregs) and contributes to their suppressive function (By similarity). Also acts as a negative regulator of plasmacytoid dendritic cell (pDCs) activation (By similarity). Binds MHC class II (MHC-II); the precise role of MHC-II-binding is however unclear (PubMed:8647185).
REFERENCES
Triebel F.,et al.J. Exp. Med. 171:1393-1405(1990).
Triebel F.,et al.Submitted (SEP-2001) to the EMBL/GenBank/DDBJ databases.
Ota T.,et al.Nat. Genet. 36:40-45(2004).
Scherer S.E.,et al.Nature 440:346-351(2006).
Mural R.J.,et al.Submitted (SEP-2005) to the EMBL/GenBank/DDBJ databases.

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