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Mouse Anti-CNTNAP2 Recombinant Antibody (CBFYC-2022) (V2LY-1206-LY555)


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Summary

Host Animal
Mouse
Specificity
Human
Clone
CBFYC-2022
Antibody Isotype
IgG1
Application
FC

Basic Information

Immunogen
Recombinant human Caspr2 Pro29-Ala1262.
Host Species
Mouse
Specificity
Human
Antibody Isotype
IgG1
Clonality
Monoclonal Antibody
Application Notes
ApplicationNote
FC0.25 µg/10^6 cells

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

Format
Lyophilized
Buffer
PBS, Trehalose
Preservative
None
Purity
>95% as determined by analysis by SDS-PAGE
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.

Target

Full Name
Contactin Associated Protein Like 2
Entrez Gene ID
66797
UniProt ID
Q9CPW0
Function
Required for gap junction formation (Probable). Required, with CNTNAP1, for radial and longitudinal organization of myelinated axons. Plays a role in the formation of functional distinct domains critical for saltatory conduction of nerve impulses in myelinated nerve fibers. Demarcates the juxtaparanodal region of the axo-glial junction.
Biological Process
Adult behavior Source: BHF-UCL
Brain development Source: BHF-UCL
Cell adhesion Source: UniProtKB-KW
Cerebral cortex development Source: BHF-UCL
Clustering of voltage-gated potassium channels Source: BHF-UCL
Learning Source: BHF-UCL
Limbic system development Source: BHF-UCL
Neuron projection development Source: BHF-UCL
Neuron projection morphogenesis Source: UniProtKB
Neuron recognition Source: UniProtKB
Positive regulation of gap junction assembly Source: UniProtKB
Protein localization to juxtaparanode region of axon Source: BHF-UCL
Social behavior Source: BHF-UCL
Striatum development Source: BHF-UCL
Superior temporal gyrus development Source: BHF-UCL
Thalamus development Source: BHF-UCL
Transmission of nerve impulse Source: UniProtKB
Vocalization behavior Source: BHF-UCL
Vocal learning Source: BHF-UCL
Cellular Location
Membrane; Axon; Paranodal septate junction. Expressed in the juxtaparadonal region.
Involvement in disease
Autism 15 (AUTS15):
A complex multifactorial, pervasive developmental disorder characterized by impairments in reciprocal social interaction and communication, restricted and stereotyped patterns of interests and activities, and the presence of developmental abnormalities by 3 years of age. Most individuals with autism also manifest moderate mental retardation.
A chromosomal aberration involving CNTNAP2 is found in a patient with autism spectrum disorder. Paracentric inversion 46,XY,inv(7)(q11.22;q35). The inversion breakpoints disrupt the genes AUTS2 and CNTNAP2.
Pitt-Hopkins-like syndrome 1 (PTHSL1):
A syndrome characterized by severe mental retardation and variable additional symptoms, such as impaired speech development, seizures, autistic behavior, breathing anomalies and a broad mouth, resembling Pitt-Hopkins syndrome. In contrast to patients with Pitt-Hopkins syndrome, PTHSL1 patients present with normal or only mildly to moderately delayed motor milestones.
Topology
Extracellular: 28-1262
Helical: 1263-1283
Cytoplasmic: 1284-1331
More Infomation

Xing, X., Wu, K., Dong, Y., Zhou, Y., Zhang, J., Jiang, F., ... & Li, J. D. (2020). Hyperactive Akt-mTOR pathway as a therapeutic target for pain hypersensitivity in Cntnap2-deficient mice. Neuropharmacology, 165, 107816.

Xing, X., Zhang, J., Wu, K., Cao, B., Li, X., Jiang, F., ... & Li, J. D. (2019). Suppression of Akt-mTOR pathway rescued the social behavior in Cntnap2-deficient mice. Scientific reports, 9(1), 1-9.

Gu, H., Hou, F., Liu, L., Luo, X., Nkomola, P. D., Xie, X., ... & Song, R. (2018). Genetic variants in the CNTNAP2 gene are associated with gender differences among dyslexic children in China. EBioMedicine, 34, 165-170.

Toma, C., Pierce, K. D., Shaw, A. D., Heath, A., Mitchell, P. B., Schofield, P. R., & Fullerton, J. M. (2018). Comprehensive cross-disorder analyses of CNTNAP2 suggest it is unlikely to be a primary risk gene for psychiatric disorders. PLoS genetics, 14(12), e1007535.

Lauber, E., Filice, F., & Schwaller, B. (2018). Dysregulation of parvalbumin expression in the Cntnap2−/− mouse model of autism spectrum disorder. Frontiers in molecular neuroscience, 11, 262.

Gao, R., Piguel, N. H., Melendez-Zaidi, A. E., Martin-de-Saavedra, M. D., Yoon, S., Forrest, M. P., ... & Penzes, P. (2018). CNTNAP2 stabilizes interneuron dendritic arbors through CASK. Molecular psychiatry, 23(9), 1832-1850.

Bridi, M. S., Park, S. M., & Huang, S. (2017). Developmental disruption of GABAAR-meditated inhibition in Cntnap2 KO mice. ENeuro, 4(5).

Zare, S., Mashayekhi, F., & Bidabadi, E. (2017). The association of CNTNAP2 rs7794745 gene polymorphism and autism in Iranian population. Journal of Clinical Neuroscience, 39, 189-192.

Poot, M. (2017). Intragenic CNTNAP2 deletions: a bridge too far. Molecular Syndromology, 8(3), 118-130.

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

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