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Mouse Anti-NEUROD2 Antibody (1G1) (CBMAB-0713-YC)

Provided herein are mouse monoclonal antibodies against Human NEUROD2. The antibody clone 1G1 can be used for immunoassay techniques, such as ELISA and IP.
See all NEUROD2 antibodies

Summary

Host Animal
Mouse
Specificity
Human
Clone
1G1
Antibody Isotype
IgG2b
Application
ELISA, IP

Basic Information

Immunogen
Recombinant protein
Specificity
Human
Antibody Isotype
IgG2b
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
Supernatant
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
NEUROD2
Introduction
NEUROD2 (neuronal differentiation factor 2) is a member of the neuroD family of neurogenic basic helix-loop-helix (bHLH) proteins. NEUROD2 can induce transcription from neuron-specific promoters, such as the GAP-43 promoter, which contain a specific DNA sequence known as an E-box. In human, NEUROD2 can induce neurogenic differentiation in non-neuronal cells in Xenopus embryos, and is thought to play a role in the determination and maintenance of neuronal cell fates.
Entrez Gene ID
4761
UniProt ID
Q15784
Alternative Names
NDRF; bHLHa1
Function
Transcriptional regulator implicated in neuronal determination. Mediates calcium-dependent transcription activation by binding to E box-containing promoter. Critical factor essential for the repression of the genetic program for neuronal differentiation; prevents the formation of synaptic vesicle clustering at active zone to the presynaptic membrane in postmitotic neurons. Induces transcription of ZEB1, which in turn represses neuronal differentiation by down-regulating REST expression. Plays a role in the establishment and maturation of thalamocortical connections; involved in the segregation of thalamic afferents into distinct barrel domains within layer VI of the somatosensory cortex. Involved in the development of the cerebellar and hippocampal granular neurons, neurons in the basolateral nucleus of amygdala and the hypothalamic-pituitary axis. Associates with chromatin to the DPYSL3 E box-containing promoter (By similarity).
Biological Process
Associative learning Source: Ensembl
Behavioral fear response Source: Ensembl
Cellular response to calcium ion Source: UniProtKB
Cellular response to electrical stimulus Source: UniProtKB
Cerebellar cortex development Source: UniProtKB
Negative regulation of synapse maturation Source: UniProtKB
Nervous system development Source: ProtInc
Neuron development Source: Ensembl
Neuron differentiation Source: GO_Central
Positive regulation of calcium-mediated signaling Source: UniProtKB
Positive regulation of DNA-binding transcription factor activity Source: UniProtKB
Positive regulation of neuron differentiation Source: UniProtKB
Positive regulation of synapse maturation Source: UniProtKB
Positive regulation of synaptic plasticity Source: UniProtKB
Protein ubiquitination Source: UniProtKB
Regulation of transcription by RNA polymerase II Source: GO_Central
Cellular Location
Nucleus
Involvement in disease
Developmental and epileptic encephalopathy 72 (DEE72):
A form of epileptic encephalopathy, a heterogeneous group of severe early-onset epilepsies characterized by refractory seizures, neurodevelopmental impairment, and poor prognosis. Development is normal prior to seizure onset, after which cognitive and motor delays become apparent. DEE72 is an autosomal dominant form with variable severity and onset in infancy.

Cota, P., Saber, L., Jing, C., Shahryari, A., & Bakhti, M. (2023). NEUROD2 function is dispensable for human pancreatic β cell specification. Frontiers in Endocrinology, 14, 1286590.

Yan, K., Bormuth, I., Bormuth, O., Tutukova, S., Renner, A., Bessa, P., ... & Tarabykin, V. (2023). TrkB-dependent EphrinA reverse signaling regulates callosal axon fasciculate growth downstream of Neurod2/6. Cerebral Cortex, 33(5), 1752-1767.

Pang, Y., & Shi, M. (2021). Repetitive transcranial magnetic stimulation improves mild cognitive impairment associated with Alzheimer’s disease in mice by modulating the miR-567/NEUROD2/PSD95 axis. Neuropsychiatric Disease and Treatment, 2151-2161.

Runge, K., Mathieu, R., Bugeon, S., Lafi, S., Beurrier, C., Sahu, S., ... & de Chevigny, A. (2021). Disruption of NEUROD2 causes a neurodevelopmental syndrome with autistic features via cell-autonomous defects in forebrain glutamatergic neurons. Molecular psychiatry, 26(11), 6125-6148.

Mis, E. K., Sega, A. G., Signer, R. H., Cartwright, T., Ji, W., Martinez‐Agosto, J. A., ... & Lakhani, S. A. (2021). Expansion of NEUROD2 phenotypes to include developmental delay without seizures. American Journal of Medical Genetics Part A, 185(4), 1076-1080.

Guzelsoy, G., Akkaya, C., Atak, D., Dunn, C. D., Kabakcioglu, A., Ozlu, N., & Ince-Dunn, G. (2019). Terminal neuron localization to the upper cortical plate is controlled by the transcription factor NEUROD2. Scientific Reports, 9(1), 19697.

Pieper, A., Rudolph, S., Wieser, G. L., Götze, T., Mießner, H., Yonemasu, T., ... & Goebbels, S. (2019). NeuroD2 controls inhibitory circuit formation in the molecular layer of the cerebellum. Scientific reports, 9(1), 1448.

Hahn, M. A., Jin, S. G., Li, A. X., Liu, J., Huang, Z., Wu, X., ... & Pfeifer, G. P. (2019). Reprogramming of DNA methylation at NEUROD2-bound sequences during cortical neuron differentiation. Science Advances, 5(10), eaax0080.

Sega, A. G., Mis, E. K., Lindstrom, K., Mercimek-Andrews, S., Ji, W., Cho, M. T., ... & Lakhani, S. A. (2019). De novo pathogenic variants in neuronal differentiation factor 2 (NEUROD2) cause a form of early infantile epileptic encephalopathy. Journal of Medical Genetics, 56(2), 113-122.

Zhu, Y., Xu, Q., Sha, W. P., Zhao, K. P., & Wang, L. M. (2019). MiR-219-5p promotes spinal cord injury recovery by inhibiting NEUROD2-regulated inflammation and oxidative stress. European Review for Medical & Pharmacological Sciences, 23(1).

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

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