GP1BB purified MaxPab mouse polyclonal antibody (B01P)
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Specification
Product Description
Mouse polyclonal antibody raised against a full-length human GP1BB protein.
Immunogen
GP1BB (AAI60146.1, 1 a.a. ~ 206 a.a) full-length human protein.
Sequence
MGSGPRGALSLLLLLLAPPSRPAAGCPAPCSCAGTLVDCGRRGLTWASLPTAFPVDTTELVLTGNNLTALPPGLLDALPALRTAHLGANPWRCDCRLVPLRAWLAGRPERAPYRDLRCVAPPALRGRLLPYLAEDELRAACAPGPLCWGALAAQLALLGLGLLHALLLVLLLCRLRRLRARARARAAARLSLTDPLVAERAGTDES
Host
Mouse
Reactivity
Human
Interspecies Antigen Sequence
Mouse (90); Rat (84)
Quality Control Testing
Antibody reactive against mammalian transfected lysate.
Storage Buffer
In 1x PBS, pH 7.4
Storage Instruction
Store at -20°C or lower. Aliquot to avoid repeated freezing and thawing.
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Applications
Western Blot (Transfected lysate)
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Gene Info — GP1BB
Entrez GeneID
2812GeneBank Accession#
BC160146.1Protein Accession#
AAI60146.1Gene Name
GP1BB
Gene Alias
CD42c
Gene Description
glycoprotein Ib (platelet), beta polypeptide
Gene Ontology
HyperlinkGene 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 within a separate gene (septin 5) located upstream of this gene. In the absence of polyadenylation from its own imperfect site, the septin 5 gene uses the consensus polyA signal of this gene. [provided by RefSeq
Other Designations
glycoprotein Ib, beta polypeptide|nuclear localization signal deleted in velocardiofacial syndrome
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