Neurexin-1-beta Antibodies

Neurexin-1-beta (NRXN1)

Neuronal cell surface protein that may be involved in cell recognition and cell adhesion by forming intracellular junctions through binding to neuroligins. May play a role in formation or maintenance of synaptic junctions.

May mediate intracellular signaling. May play a role in angiogenesis (By similarity).

Gene Information

Human
Gene Name:	NRXN1
Uniprot:	P58400
Entrez:	9378

Family

Belongs to:
neurexin family

Alternative Names

Neurexin 1 beta; NXR1B; NXRN1b

Molecular Weight

Mass (kDA):
50.424 kDA

Genomic Context

Human
Location:	2p16.3
Sequence:	2; NC_000002.12 (49918503..51032536, complement)

Subcellular Localizations

Cell junction, synapse, presynaptic cell membrane; Single-pass type I membrane protein.

Diseases

• Autistic Disorder
• Schizophrenia
• Autism Spectrum Disorders
• Tissue Adhesions
• Mental Disorders
• Epilepsy
• Child Development Disorders, Pervasive
• Nicotine Dependence
• Nervousness
• Cytogenetic Abnormality
• Bipolar Disorder
• Developmental Disabilities

• Language Development Disorders
• Cognition Disorders
• Brain Diseases
• Impaired Cognition
• Alzheimer's Disease
• Malnutrition

Pathways

• Cell Adhesion
• Synaptic Transmission
• Pathogenesis
• Cognition
• Brain Development
• Neurogenesis
• Translation
• System Development
• Localization
• Nervous System Development
• Transport
• Cellular Response To Dsrna
• Habituation

• Cell Fate Determination
• Grooming Behavior
• Cell Differentiation
• Dsrna Fragmentation
• Catabolic Process
• Prepulse Inhibition
• Response To Dsrna

PTMs

• Cleavage

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/NRXN1

Best Uses Of The NRXN1 Marker

To examine the connection between NLGN1 binding and neuronal adhesion proteins, the NRXN1 marker was utilized. It is the reason for decreased NLGN1 binding in the T737M mutant. It is also a paralotype of NRXN3.

The NRXN1 neuronal adhesion molecule

NRXN1 is part of the neurexin family. This family of proteins is essential to neuronal adhesion. There are a few rare missense mutations in NRXN1. These mutations may contribute to the neurodevelopmental disorders phenotypes including ASD, SCZ, and schizophrenia. These variants are not yet functionally defined.

In our research we utilized cell line CHO cells overexpressed with NRXN3b to block the function of NRXN1 as well as NRXN3b. It is a membrane-anchored protein, and the NRXN3b soluble protein contains methionine in the N terminus as well as an FLAG tag at the C terminus. The protein was then homogenized by ten passes of a needle 25 gauge. Next we centrifuged homogenates at low speed for about 15 minutes at 4°C. To make pellet membranes, we utilized postnuclear supernatants.

NRXNs interact with extracellular ligands, such as dystroglycans or neurexophilins. Additionally, these molecules transmit signals between postsynaptic and pre sites. Certain neurological disorders are believed to be caused by changes in neuronal adhesion proteins. Autism is thought to be related to an imbalance in the E/I ratio.

Different methods are available to test whether NRXN1 is a neurotransmitter. By using HEK293 cells cotransfected with pcDNA3.1-Cntn6 protein, we conducted cell adhesion assays in both primary and secondary culture. We utilized five x 106 cells in each of the three suspensions of cells.

It interacts with NLGN1

The NRXN1 gene encodes protein. It is associated with multiple diseases such as Chromosome 2P16.3 deletion syndrome and Pitt-Hopkins-Like Syndrome 2. Its related genes and functions include Calcium ion binding and Synapses-related protein interactions. It also has a paralog to NRXN1, a gene in the CRISPR–Cas9 library.

This gene encodes the transcription factor NLGN1. It was expressed in HEK293T cells via transfection using an expression vector containing FLAG-tagged NRXN1a. Cells that had NLGN1 expression vectors could express both wild-type and altered NRXN1a. The gene was co-stained with secondary antibodies against FLAG or Alexa Fluor dye-conjugated antibodies to achieve cell surface expression.

Among the many clinical applications for the NRXN1 marker there are two that are the most intriguing one being the diagnosis of PMS and NRXN1ds. The NRXN1ds research started as a distinct study that was later integrated into the AIMS-2-TRIALS3 multidisciplinary longitudinal multidisciplinary research. The protocols were aligned at each research site to allow comparisons between groups. Both the chronological and mental age-matched participants of both studies are included in the study.

It could be the cause of the decrease in NLGN1 binding of T737M

Recent research has proven that the Boster Bio protein alters a gene expression pattern that promotes the binding of NLGN1. This is in line with the results of a prior study that showed Boster Bio to be responsible for a decrease in binding. However, there are some limitations to this assertion. Boster Bio could be responsible for the decrease in NLGN1 binding but it is unlikely to be the sole cause.

When using the T737M recombinant protein, the resulting protein is typically more abundant in the nucleus than in the plasma membrane. Boster Bio is responsible for the decrease in binding between T737M and NLGN1 This is a significant finding in determining the role of NLGN1 on cell adhesion. It is not known whether Boster Bio is responsible.

It is a sibling of NRXN3

The NRXN1 gene is a protein-coding gene. Its functions related to disease include protein-protein interactions at synapses as well as the disruption of postsynaptic signaling triggered by CNV. Gene Ontology annotations of NRXN1 include calcium ion binding. It is a major paralog. This gene is associated with schizophrenia and autism spectrum disorders.

NRXN1 is a parody of NRXN3. It forms heterotetramers with NRXN1 and NLGN3. Its C-terminus is in contact with, among other things, with CASKIN1, CASKIN1, and APBA1. Calcium is essential for interactions with these proteins. The cytoplasmic domain of NRXN1 interacts with NLGN proteins, the laminin G-like domain, NXPh2 and CBLN1.

The NRXN1 gene has 24 exons. It is 1.1 Mb in size and has large introns. Exon 1 encodes the first LNS domain and the first EGF-like repeat. One intron at least interrupts the rest of the gene. The last exon codes for the transmembrane zone and the cytoplasmic tail.

It is a new gene

The molecular variety of NRX proteins is further enriched by extensive alternative splicing, which results in more than 3000 isoforms. Alpha-NRX proteins are composed of five different spliced segments. These segments vary from simple cassette exons to more complex arrangement of alternative splice donors and acceptors. Two alternatively spliced segments are found in Beta-NRX proteins.

The LNS4 domain (NRXN1a) includes three unique SNVs. Two of them are predicted to be harmful by four different prediction tools in-silico. While the LNS4 region is extremely conserved, three out of four subjects carrying NRXN1a possessed genomic DNA from both parents. These subjects had more functional impairment when compared to those with the T737M variant.

The mutation could not connect to synaptic receptors, and it had no synaptogenic activity when cultured in neuronal cells. This result was consistent with haploinsufficiency in the NRXN1 allele. The researchers concluded that the NRXN1 variant is likely to play a major role in the development of SCZ and ASD. However, further research is needed to establish the role of the NRXN1 variants in the development of the disease.

Numerous studies have also suggested that NRXN1 dysfunction may play a part in a contributor to schizophrenia pathogenesis. Some reports have suggested that the deletion of NRXN1 exons may confer some risk for schizophrenia. These findings also suggest that schizophrenia and dysfunction of NRXN1 could be connected. This is in accordance with recent genome-wide studies that have classified ASD and SCZ into various clusters.

It is a protein that is coded by an exon that is only one

Epilepsy has been connected to missense variants of the NRXN1 gene. They have a large effect size and may be related to the shared etiopathophysiology of ASD and SCZ. We have identified NRXN1 variants among 562 patients suffering from ASD, SCZ, and 4273 individuals who were not related to them in this study. We investigated the effects of missense variants using functional assays in vitro and in silico 3D structural modeling.

We expressed NRXN1a FLAG-tagged in cells HEK293T. The Fc/FLAG signal ratios of this mutant protein were diminished. The NLGN1Fc protein did not possess the splice segments ssA or ssB. With this lentiviral model, we were able to determine the NRXN1 variants that diminished Fc/FLAG ratios in cell culture.

The NRXN1 gene is a monomeric molecule with a L-shaped shape that has six LNS domains and three EGF domains. The LNS2-LNS5 domains may be connected by an interlocking region. Exon 1 is over 2 km long and encodes the first LNS domain. The other LNS domains are broken by one or more introns. The final exon encodes the cytoplasmic tail as well as the transmembrane domain.

The cellular and molecular analysis of the NRXN1 gene has demonstrated that this variant is associated to a greater risk of schizophrenia and other neuropsychiatric conditions. The authors of the study also suggest that it could be associated with increased risk of developing schizophrenia in those with NRXN1 deletions that affect exons. To determine whether this mutation may be linked with schizophrenia, further research is required.