Human CD95 (FAS) activation kit by CRISPRa

CAT#: GA100252

FAS CRISPRa kit - CRISPR gene activation of human Fas cell surface death receptor

Product Images

Specifications

Product Data

• Format: 3gRNAs, 1 scramble ctrl and 1 enhancer vector
• Symbol: FAS
• Locus ID: 355
• Kit Components:

  GA100252G1, CD95 gRNA vector 1 in pCas-Guide-GFP-CRISPRa

  GA100252G2, CD95 gRNA vector 2 in pCas-Guide-GFP-CRISPRa

  GA100252G3, CD95 gRNA vector 3 in pCas-Guide-GFP-CRISPRa

  1 CRISPRa-Enhancer vector, SKU GE100056

  1 CRISPRa scramble vector, SKU GE100077

• Disclaimer: The kit is designed based on the best knowledge of CRISPa 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.

Reference Data

• RefSeq: NM_000043, NM_001320619, NM_152871, NM_152872, NM_152873, NM_152874, NM_152875, NM_152876, NM_152877, NR_028033, NR_028034, NR_028035, NR_028036, NR_135313, NR_135314, NR_135315
• Synonyms: ALPS1A; APO-1; APT1; CD95; FAS1; FASTM; TNFRSF6
• Summary: 'The protein encoded by this gene is a member of the TNF-receptor superfamily. This receptor contains a death domain. It has been shown to play a central role in the physiological regulation of programmed cell death, and has been implicated in the pathogenesis of various malignancies and diseases of the immune system. The interaction of this receptor with its ligand allows the formation of a death-inducing signaling complex that includes Fas-associated death domain protein (FADD), caspase 8, and caspase 10. The autoproteolytic processing of the caspases in the complex triggers a downstream caspase cascade, and leads to apoptosis. This receptor has been also shown to activate NF-kappaB, MAPK3/ERK1, and MAPK8/JNK, and is found to be involved in transducing the proliferating signals in normal diploid fibroblast and T cells. Several alternatively spliced transcript variants have been described, some of which are candidates for nonsense-mediated mRNA decay (NMD). The isoforms lacking the transmembrane domain may negatively regulate the apoptosis mediated by the full length isoform. [provided by RefSeq, Mar 2011]'