Human NBEA blocking peptide

Name: Human NBEA blocking peptide
SKU: CDBP2007
Rating: 5 (1 reviews)

Synthetic Human NBEA blocking peptide for Apuri, BL, ELISA

COA

SDS

Datasheet

Summary

Product Overview

Blocking/Immunizing peptide for anti-Neurobeachin antibody

Target

Neurobeachin

Nature

Synthetic

Tag/Conjugate

Unconjugated

Application Notes

For in vitro research use only. Not intended for any diagnostic or therapeutic purpose. Not for human or animal consumption.

Format

Lyophilized powder

Preservative

None

Storage

Shipped at ambient temperature, store at -20°C.

Entrez Gene ID

26960

Antigen Description

This gene encodes a member of a large, diverse group of A-kinase anchor proteins that target the activity of protein kinase A to specific subcellular sites by binding to its type II regulatory subunits. Brain-specific expression and coat protein-like membrane recruitment of a highly similar protein in mouse suggest an involvement in neuronal post-Golgi membrane traffic. Mutations in this gene may be associated with a form of autism. This gene and its expression are frequently disrupted in patients with multiple myeloma. Alternative splicing results in multiple transcript variants encoding distinct isoforms. Additional transcript variants may exist, but their full-length nature has not been determined.[provided by RefSeq, Feb 2011]

Function

protein kinase binding;

Synonyms

NBEA; neurobeachin; BCL8B; LYST2; lysosomal-trafficking regulator 2;

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Neurobeachin and the Kinesin KIF21B Are Critical for Endocytic Recycling of NMDA Receptors and Regulate Social Behavior

CELL REPORTS

Authors: Gromova, Kira, V; Muhia, Mary; Rothammer, Nicola; Gee, Christine E.; Thies, Edda; Schaefer, Irina; Kress, Sabrina; Kilimann, Manfred W.; Shevchuk, Olga; Oertner, Thomas G.; Kneussel, Matthias

Abstract

Autism spectrum disorders (ASDs) are associated with mutations affecting synaptic components, including GluN2B-NMDA receptors (NMDARs) and neurobeachin (NBEA). NBEA participates in biosynthetic pathways to regulate synapse receptor targeting, synaptic function, cognition, and social behavior. However, the role of NBEA-mediated transport in specific trafficking routes is unclear. Here, we highlight an additional function for NBEA in the local delivery and surface re-insertion of synaptic receptors in mouse neurons. NBEA dynamically interacts with Rab4-positive recycling endosomes, transiently enters spines in an activity-dependent manner, and regulates GluN2B-NMDAR recycling. Furthermore, we show that the microtubule growth inhibitor kinesin KIF21B constrains NBEA dynamics and is present in the NBEA-recycling endosome-NMDAR complex. Notably, Kif21b knockout decreases NMDAR surface expression and alters social behavior in mice, consistent with reported social deficits in Nbea mutants. The influence of NBEA-KIF21B interactions on GluN2B-NMDAR local recycling may be relevant to mechanisms underlying ASD etiology.

Neurobeachin regulates neurotransmitter receptor trafficking to synapses

JOURNAL OF CELL BIOLOGY

Authors: Nair, Ramya; Lauks, Juliane; Jung, SangYong; Cooke, Nancy E.; de Wit, Heidi; Brose, Nils; Kilimann, Manfred W.; Verhage, Matthijs; Rhee, JeongSeop

Abstract

The surface density of neurotransmitter receptors at synapses is a key determinant of synaptic efficacy. Synaptic receptor accumulation is regulated by the transport, postsynaptic anchoring, and turnover of receptors, involving multiple trafficking, sorting, motor, and scaffold proteins. We found that neurons lacking the BEACH (beige-Chediak/Higashi) domain protein Neurobeachin (Nbea) had strongly reduced synaptic responses caused by a reduction in surface levels of glutamate and GABA(A) receptors. In the absence of Nbea, immature AMPA receptors accumulated early in the biosynthetic pathway, and mature N-methyl-D-aspartate, kainate, and GABA(A) receptors did not reach the synapse, whereas maturation and surface expression of other membrane proteins, synapse formation, and presynaptic function were unaffected. These data show that Nbea regulates synaptic transmission under basal conditions by targeting neurotransmitter receptors to synapses.