Mouse Fasl activation kit by CRISPRa

SKU
GA201357
Fasl CRISPRa kit - CRISPR gene activation of mouse Fas ligand (TNF superfamily, member 6)
$1,657.00
2 Weeks*
Specifications
Product Data
Format 3 gRNAs (5ug each), 1 scramble ctrl (10ug) and 1 enhancer vector (10ug)
Target Symbol Fasl
Locus ID 14103
Components

GA201357G1, Fasl gRNA vector 1 in pCas-Guide-GFP-CRISPRa

GA201357G2, Fasl gRNA vector 2 in pCas-Guide-GFP-CRISPRa

GA201357G3, Fasl gRNA vector 3 in pCas-Guide-GFP-CRISPRa

1 CRISPRa-Enhancer vector, SKU GE100056

1 CRISPRa scramble vector, SKU GE100077

OTI Disclaimer These products are manufactured and supplied by OriGene under license from ERS. The kit is designed based on the best knowledge of CRISPRa SAM technology. The efficiency of the activation can be affected by many factors, including nucleosome occupancy status, chromatin structure and the gene expression level of the target, etc.
Shipping Ambient
Reference Data
RefSeq NM_001205243, NM_010177
UniProt ID P41047
Synonyms APT1LG1; CD95-L; CD95L; CD178; Fas-L; Faslg; gld; Tnfsf6; Tnlg1a
Summary Cytokine that binds to TNFRSF6/FAS, a receptor that transduces the apoptotic signal into cells (PubMed:7511063). Involved in cytotoxic T-cell-mediated apoptosis, natural killer cell-mediated apoptosis and in T-cell development (PubMed:19794494, PubMed:7532682). Initiates fratricidal/suicidal activation-induced cell death (AICD) in antigen-activated T-cells contributing to the termination of immune responses (PubMed:19794494). TNFRSF6/FAS-mediated apoptosis has also a role in the induction of peripheral tolerance (PubMed:10779162). Binds to TNFRSF6B/DcR3, a decoy receptor that blocks apoptosis (By similarity).[UniProtKB/Swiss-Prot Function]
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KN505762 Fasl - KN2.0, Mouse gene knockout kit via CRISPR, non-homology mediated. 1 kit
$1,657.00

Citations

*Delivery time may vary from web posted schedule. Occasional delays may occur due to unforeseen complexities in the preparation of your product. International customers may expect an additional 1-2 weeks in shipping.