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This product is an unconjugated anti-human LAMP2 monoclonal antibody gernerated from the mouse. This antibody can be used for applications: ELISA, Western Blotting, Immunohistochemistry.
Please feel free to contact us for a quote and further discussion with our scientists. Datasheets
specifications |
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Antibody Isotype | IgA |
Clone | NGA03-TT |
Applications | ELISA; WB; IHC |
Target | LAMP-2 |
Host | Mouse |
Clonality | Monoclonal |
Antibody Type | Primary antibody |
Species Reactivity | Human |
Immunogen | Lysosomal-associated membrane protein 2 |
Format | Liquid |
Buffer | PBS with 50% glycerol, pH7.3 |
Storage | Store at -20°C. Avoid repeated freeze-thaw cycles. |
Target Information |
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Target Name | LAMP-2 |
Alternative Names | Lysosomal Associated Membrane Protein 2; Lysosome-Associated Membrane Glycoprotein 2; CD107 Antigen-Like Family Member B; CD107b; LGP-96; Lysosomal-Associated Membrane Protein 2; CD107b Antigen; LGP110; LAMPB; LAMP2; DND |
Related Disease | Danon Disease; Hypertrophic Cardiomyopathy |
Gene ID | 3920 |
UniProt ID | P13473 |
Target Overview | Plays an important role in chaperone-mediated autophagy, a process that mediates lysosomal degradation of proteins in response to various stresses and as part of the normal turnover of proteins with a long biological half-live. Functions by binding target proteins, such as GAPDH and MLLT11, and targeting them for lysosomal degradation. Plays a role in lysosomal protein degradation in response to starvation. Required for the fusion of autophagosomes with lysosomes during autophagy. Cells that lack LAMP2 express normal levels of VAMP8, but fail to accumulate STX17 on autophagosomes, which is the most likely explanation for the lack of fusion between autophagosomes and lysosomes. Required for normal degradation of the contents of autophagosomes. Required for efficient MHCII-mediated presentation of exogenous antigens via its function in lysosomal protein degradation; antigenic peptides generated by proteases in the endosomal/lysosomal compartment are captured by nascent MHCII subunits. Is not required for efficient MHCII-mediated presentation of endogenous antigens. |
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