Human CD42c (GP1BB) activation kit by CRISPRa
CAT#: GA101879
GP1BB CRISPRa kit - CRISPR gene activation of human glycoprotein Ib platelet subunit beta
CNY 12,255.00
Specifications
Product Data | |
Format | 3 gRNAs (5ug each), 1 scramble ctrl (10ug) and 1 enhancer vector (10ug) |
Symbol | GP1BB |
Locus ID | 2812 |
Kit Components | GA101879G1, CD42c gRNA vector 1 in pCas-Guide-GFP-CRISPRa GA101879G2, CD42c gRNA vector 2 in pCas-Guide-GFP-CRISPRa GA101879G3, CD42c gRNA vector 3 in pCas-Guide-GFP-CRISPRa 1 CRISPRa-Enhancer vector, SKU GE100056 1 CRISPRa scramble vector, SKU GE100077 |
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. |
Reference Data | |
RefSeq | NM_000407 |
Synonyms | BDPLT1; BS; CD42C; GPIBB; GPIbbeta |
Summary | Platelet glycoprotein Ib (GPIb) is a heterodimeric transmembrane protein consisting of a disulfide-linked 140 kD alpha chain and 22 kD beta chain. It is part of the GPIb-V-IX system that constitutes the receptor for von Willebrand factor (VWF), and mediates platelet adhesion in the arterial circulation. GPIb alpha chain provides the VWF binding site, and GPIb beta contributes to surface expression of the receptor and participates in transmembrane signaling through phosphorylation of its intracellular domain. Mutations in the GPIb beta subunit have been associated with Bernard-Soulier syndrome, velocardiofacial syndrome and giant platelet disorder. The 206 amino acid precursor of GPIb beta is synthesized from a 1.0 kb mRNA expressed in plateletes and megakaryocytes. A 411 amino acid protein arising from a longer, unspliced transcript in endothelial cells has been described; however, the authenticity of this product has been questioned. Yet another less abundant GPIb beta mRNA species of 3.5 kb, expressed in nonhematopoietic tissues such as endothelium, brain and heart, was shown to result from inefficient usage of a non-consensus polyA signal in the neighboring upstream gene (SEPT5, septin 5). In the absence of polyadenylation from its own imperfect site, the SEPT5 gene produces read-through transcripts that use the consensus polyA signal of this gene. [provided by RefSeq, Dec 2010] |
Documents
Resources
基因表达相关资源 |
Other Versions
SKU | Description | Size | Price |
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KN416738 | GP1BB - KN2.0, Human gene knockout kit via CRISPR, non-homology mediated. |
CNY 8,680.00 |