Home / Products /Genome Editing /KO Cell Lines /GP1BB Knockout cell line (BEAS-2B)

GP1BB Knockout cell line (BEAS-2B)

Catalog Number: KOA31111

Price: Online Inquiry

Specifications Downloads Related products

Specifications

Product Information
Product Name GP1BB Knockout cell line (BEAS-2B)
specification 1*10^6
Storage and transportation Shipped on dry ice; Store in liquid nitrogen
Cell morphology Epithelial-like, adherent
Passage ratio 1:3~1:4
species Human
Gene GP1BB
Gene ID 2812
Build method Electroporation/Lentivirus
Mycoplasma testing negative
Cultivation system 90% DMEM+10% FBS
Parental Cell Line BEAS-2B
Quality Control Genotype: GP1BB Knockout cell line (BEAS-2B)>95% viability before freezing. All cells were tested and found to be free of bacterial, viruses,mycoplasma and other toxins.
Gene Information
Gene Official Full Name glycoprotein Ib platelet subunit betaprovided by HGNC
Also known as BS; CD42C; GPIBB; BDPLT1; GPIbbeta
Gene Description 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]
Expression Biased expression in brain (RPKM 9.9), skin (RPKM 3.4) and 10 other tissues See more

Downloads

Please note that all services are for research use only. Not intended for any clinical use.

Ask a Question

If your question is not addressed through these resources, you can fill out the online form below and we will answer your question as soon as possible.