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Mouse Anti-EFNB1 Recombinant Antibody (2D3E9) (CBMAB-E0861-FY)


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Summary

Host Animal
Mouse
Specificity
Chicken, Human, Mouse, Rat
Clone
2D3E9
Antibody Isotype
IgG1, κ
Application
ELISA, FC, ICC, IF, IP, WB

Basic Information

Immunogen
Synthetic peptide derived from the ephrin-B sequence
Specificity
Chicken, Human, Mouse, Rat
Antibody Isotype
IgG1, κ
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Buffer
PBS, pH 7.4
Preservative
0.1% sodium azide
Concentration
0.5 mg/mL
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
Ephrin B1
Introduction
The protein encoded by this gene is a type I membrane protein and a ligand of Eph-related receptor tyrosine kinases. It may play a role in cell adhesion and function in the development or maintenance of the nervous system.
Entrez Gene ID
Human1947
Chicken395896
UniProt ID
HumanP98172
ChickenO73612
Alternative Names
Ephrin B1; ELK Ligand; Ephrin-B1; Elk-L; EPLG2; LERK2; EFL3; Craniofrontonasal Syndrome (Craniofrontonasal Dysplasia)
Research Area
Cell surface transmembrane ligand for Eph receptors, a family of receptor tyrosine kinases which are crucial for migration, repulsion and adhesion during neuronal, vascular and epithelial development (PubMed:8070404, PubMed:7973638).

Binding to Eph receptors residing on adjacent cells leads to contact-dependent bidirectional signaling into neighboring cells (PubMed:8070404, PubMed:7973638).

Shows high affinity for the receptor tyrosine kinase EPHB1/ELK (PubMed:8070404, PubMed:7973638).

Can also bind EPHB2 and EPHB3 (PubMed:8070404).

Binds to, and induces collapse of, commissural axons/growth cones in vitro (By similarity).

May play a role in constraining the orientation of longitudinally projecting axons (By similarity).
Biological Process
Axon guidance Source: GO_Central
Cell adhesion Source: ProtInc
Cell-cell signaling Source: ProtInc
Embryonic pattern specification Source: Ensembl
Ephrin receptor signaling pathway Source: GO_Central
Neural crest cell migration Source: Ensembl
Positive regulation of T cell proliferation Source: Ensembl
T cell costimulation Source: Ensembl
Cellular Location
Cell membrane; Membrane raft. May recruit GRIP1 and GRIP2 to membrane raft domains.
Ephrin-B1 C-terminal fragment: Cell membrane
Ephrin-B1 intracellular domain: Nucleus. Colocalizes with ZHX2 in the nucleus.
Involvement in disease
Craniofrontonasal syndrome (CFNS):
X-linked inherited syndrome characterized by hypertelorism, coronal synostosis with brachycephaly, downslanting palpebral fissures, clefting of the nasal tip, joint anomalies, longitudinally grooved fingernails and other digital anomalies.
Topology
Extracellular: 28-237
Helical: 238-258
Cytoplasmic: 259-346
PTM
Inducible phosphorylation of tyrosine residues in the cytoplasmic domain.
Proteolytically processed. The ectodomain is cleaved, probably by a metalloprotease, to produce a membrane-tethered C-terminal fragment. This fragment is then further processed by the gamma-secretase complex to yield a soluble intracellular domain peptide which can translocate to the nucleus. The intracellular domain peptide is highly labile suggesting that it is targeted for degradation by the proteasome.
More Infomation

Gürsoy, S., Hazan, F., Öztürk, T., Çolak, R., & Çalkavur, Ş. (2021). Evaluation of Sporadic and Familial Cases with Craniofrontonasal Syndrome: A Wide Clinical Spectrum and Identification of a Novel EFNB1 Gene Mutation. Molecular Syndromology, 12(5), 269-278.

Zhang, H., Cui, Z., Cheng, D., Du, Y., Guo, X., Gao, R., ... & Wang, C. (2021). RNF186 regulates EFNB1 (ephrin B1)-EPHB2-induced autophagy in the colonic epithelial cells for the maintenance of intestinal homeostasis. Autophagy, 17(10), 3030-3047.

Shi, Y., Sun, Y., Cheng, H., & Wang, C. (2021). EFNB1 Acts as a Novel Prognosis Marker in Glioblastoma through Bioinformatics Methods and Experimental Validation. Journal of oncology, 2021.

Bukowska-Olech, E., Gawliński, P., Jakubiuk-Tomaszuk, A., Jędrzejowska, M., Obersztyn, E., Piechota, M., ... & Jamsheer, A. (2021). Clinical and molecular characterization of craniofrontonasal syndrome: new symptoms and novel pathogenic variants in the EFNB1 gene. Orphanet Journal of Rare Diseases, 16(1), 1-9.

Acosta‐Fernández, E., Zenteno, J. C., Chacón‐Camacho, O. F., Peña‐Padilla, C., Bobadilla‐Morales, L., Corona‐Rivera, A., ... & Corona‐Rivera, J. R. (2020). Extracranial midline defects in a patient with craniofrontonasal syndrome with a novel EFNB1 mutation. American Journal of Medical Genetics Part A, 182(5), 1223-1229.

Shotelersuk, V., Kamolvisit, W., Rojvachiranonda, N., Suphapeetiporn, K., Porntaveetus, T., & Shotelersuk, V. (2020). Severe craniofrontonasal syndrome in a male patient mosaic for a novel nonsense mutation in EFNB1. European Journal of Medical Genetics, 63(6), 103924.

Al Rahim, M., Yoon, Y., Dimovasili, C., Shao, Z., Huang, Q., Zhang, E., ... & Robakis, N. K. (2020). Presenilin1 familial Alzheimer disease mutants inactivate EFNB1-and BDNF-dependent neuroprotection against excitotoxicity by affecting neuroprotective complexes of N-methyl-d-aspartate receptor. Brain communications, 2(2), fcaa100.

Arthur, A., Nguyen, T. M., Paton, S., Zannettino, A. C., & Gronthos, S. (2019). Loss of EfnB1 in the osteogenic lineage compromises their capacity to support hematopoietic stem/progenitor cell maintenance. Experimental Hematology, 69, 43-53.

Jiang, Y., Qian, Y. Q., Yang, M. M., Zhan, Q. T., Chen, Y., Xi, F. F., ... & Luo, Q. (2019). Whole-exome sequencing revealed mutations of MED12 and EFNB1 in fetal agenesis of the corpus callosum. Frontiers in Genetics, 10, 1201.

Wu, T., Zhang, B. Q., Raelson, J., Yao, Y. M., Wu, H. D., Xu, Z. X., ... & Hu, S. J. (2018). Analysis of the association of EPHB6, EFNB1 and EFNB3 variants with hypertension risks in males with hypogonadism. Scientific reports, 8(1), 1-9.

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For research use only. Not intended for any clinical use.

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