ephb2

Expression system: HEK293 Cells
Length: 19-482, Full Length of Mature Protein
Activity: Not Tested

EphB2, a receptor tyrosine kinase for ephrin ligands, is overexpressed in various cancers and plays an important role in tumor progression. EPHB2 promotes endothelial-mesenchymal transition (EMT) and elicits associated pathologic characteristics of glioblastoma multiforme (GBM) such as invasion and migration. EPHB2 is epigenetically overexpressed in hypoxia, a condition highly prevalent in malignancy. Furthermore, HIF-2α is required for EPHB2 stabilization by hypoxia.

EphB2 Protein, Human, Recombinant (aa 570-987, His & GST) is expressed in Baculovirus insect cells with His and GST tag. The predicted molecular weight is 75.2 kDa and the accession number is P29323-3.

EphB2 Protein, Mouse, Recombinant (hFc) is expressed in HEK293 mammalian cells with hFc tag. The predicted molecular weight is 84.6 kDa and the accession number is P54763-3.

EphB2 Protein, Human, Recombinant (His & hFc) is expressed in HEK293 mammalian cells with His and hFc tag. The predicted molecular weight is 86 kDa and the accession number is P29323-2.

EphB2 Protein, Human, Recombinant (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 59.7 kDa and the accession number is P29323-2.

EphB2 Protein, Mouse, Recombinant (His) is expressed in HEK293 mammalian cells with His tag. The predicted molecular weight is 59.3 kDa and the accession number is P54763-3.

B-cell linker protein, also known as B-cell adapter containing a SH2 domain protein, B-cell adapter containing a Src homology 2 domain protein, Cytoplasmic adapter protein, Src homology 2 domain-containing leukocyte protein of 65 kDa, SLP-65 and BLNK, is a cytoplasm and cell membrane protein which contains oneSH2 domain. BLNK is expressed in B-cell lineage and fibroblast cell lines. Highest levels of expression is in the spleen, with lower levels in the liver, kidney, pancreas, small intestines and colon. BLNK functions as a central linker protein that bridges kinases associated with the B-cell receptor (BCR) with a multitude of signaling pathways, regulating biological outcomes of B-cell function and development. BLNK plays a role in the activation of ERK EPHB2, MAP kinase p38 and JNK. BLNK modulates AP1 activation. It is important for the activation of NF-kappa-B and NFAT. BLNK plays an important role in BCR-mediated PLCG1 and PLCG2 activation and Ca2+mobilization and is required for trafficking of the BCR to late endosomes. BLNK may be required for the RAC1-JNK pathway. It plays a critical role in orchestrating the pro-B cell to pre-B cell transition. BLNK also plays an important role in BCR-induced B-cell apoptosis.Defects in BLNK are the cause of agammaglobulinemia type 4 (AGM4) which is a primary immunodeficiency characterized by profoundly low or absent serum antibodies and low or absent circulating B cells due to an early block of B-cell development.