Human CD40 activation kit by CRISPRa

CAT#: GA100680

CD40 CRISPRa kit - CRISPR gene activation of human CD40 molecule

Product Images

Specifications

Product Data

• Format: 3gRNAs, 1 scramble ctrl and 1 enhancer vector
• Symbol: CD40
• Locus ID: 958
• Kit Components:

  GA100680G1, CD40 gRNA vector 1 in pCas-Guide-GFP-CRISPRa

  GA100680G2, CD40 gRNA vector 2 in pCas-Guide-GFP-CRISPRa

  GA100680G3, CD40 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_001250, NM_001302753, NM_001322421, NM_001322422, NM_152854, NR_126502, NR_136327, NM_001362758, NM_001302753.2
• Synonyms: Bp50; CDW40; p50; TNFRSF5
• Summary: 'This gene is a member of the TNF-receptor superfamily. The encoded protein is a receptor on antigen-presenting cells of the immune system and is essential for mediating a broad variety of immune and inflammatory responses including T cell-dependent immunoglobulin class switching, memory B cell development, and germinal center formation. AT-hook transcription factor AKNA is reported to coordinately regulate the expression of this receptor and its ligand, which may be important for homotypic cell interactions. Adaptor protein TNFR2 interacts with this receptor and serves as a mediator of the signal transduction. The interaction of this receptor and its ligand is found to be necessary for amyloid-beta-induced microglial activation, and thus is thought to be an early event in Alzheimer disease pathogenesis. Mutations affecting this gene are the cause of autosomal recessive hyper-IgM immunodeficiency type 3 (HIGM3). Multiple alternatively spliced transcript variants of this gene encoding distinct isoforms have been reported. [provided by RefSeq, Nov 2014]'