Lamp2 Mouse Gene Knockout Kit (CRISPR)

Specifications

Product Data
Format	2 gRNA vectors, 1 RFP-BSD donor, 1 scramble control
Donor DNA	RFP-BSD
Symbol	Lamp2
Locus ID	16784
Kit Components	KN309118G1, Lamp2 gRNA vector 1 in pCas-Guide CRISPR vector KN309118G2, Lamp2 gRNA vector 2 in pCas-Guide CRISPR vector KN309118RB-D, donor DNA containing left and right homologous arms and RFP-BSD functional cassette. GE100003, scramble sequence in pCas-Guide vector
Disclaimer	These products are manufactured and supplied by OriGene under license from ERS. The kit is designed based on the best knowledge of CRISPR technology. The system has been functionally validated for knocking-in the cassette downstream the native promoter. The efficiency of the knock-out varies due to the nature of the biology and the complexity of the experimental process.
Reference Data
RefSeq	NM_001017959, NM_001290485, NM_010685, NR_152733
Synonyms	CD107b; Lamp-2; Lamp-2a; Lamp-2b; Lamp-2c; Lamp II; LGP-B; Mac3
Summary	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 (PubMed:10972293). Functions by binding target proteins, such as GAPDH and MLLT11, and targeting them for lysosomal degradation (By similarity). Required for the fusion of autophagosomes with lysosomes during autophagy (PubMed:27628032). 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 (PubMed:27628032). Required for normal degradation of the contents of autophagosomes (PubMed:10972293, PubMed:12221139). Plays a role in lysosomal protein degradation in response to starvation (PubMed:27628032). 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 (By similarity).[UniProtKB/Swiss-Prot Function]

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