NEUROD6 antibody - N-terminal region (ARP32416_P050)
- Known as:
- NEUROD6 (anti-) - N-terminal region (ARP32416_P050)
- Catalog number:
- arp32416_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- NEUROD6 antibody - N-terminal region (ARP32416_P050)
Related genes to: NEUROD6 antibody - N-terminal region (ARP32416_P050)
- Gene:
- NEUROD6 NIH gene
- Name:
- neuronal differentiation 6
- Previous symbol:
- -
- Synonyms:
- Atoh2, NEX1M, Math-2, bHLHa2, Nex1
- Chromosome:
- 7p14.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-11-28
- Date modifiied:
- 2016-10-05
Related products to: NEUROD6 antibody - N-terminal region (ARP32416_P050)
Related articles to: NEUROD6 antibody - N-terminal region (ARP32416_P050)
- Transgenic mouse strains are essential tools in neuroscience, enabling targeted genetic manipulations to investigate brain function and neurological diseases. The NEX-Cre mouse line, which targets glutamatergic principal neurons in the neocortex and hippocampus by expressing Cre-recombinase under the NEX (NeuroD6) promoter, has been widely used for conditional gene manipulation. Contrary to previous reports suggesting no behavioral and histological abnormalities in NEX-Cre mice, our study reveals distinct behavioral and cellular phenotypes. Behavioral analyses indicate reduced anxiety-like behavior, altered reward-related behavior, and increased locomotor activity in NEX (Cre/Cre) mice. Additionally, Support Vector Machine (SVM) analysis uncovered subtle strain-specific and genotype-specific behavioral traits across all NEX-Cre genotypes relative to the commonly used C57BL/6J mouse strain. While overt behavioral abnormalities were most prominent in NEX (Cre/Cre) mice, SVM-based analysis revealed subtle genotype- and strain-specific behavioral signatures across NEX-Cre genotypes. This underlines the importance of using littermate controls rather than independently maintained or purchased C57BL/6J animals when interpreting genotype-related effects. Histological analyses of Golgi-Cox-stained brain slices revealed alterations in dendritic spine density across key brain regions, including the caudate putamen, hippocampal CA1, nucleus accumbens core region, lateral septum, and medial prefrontal cortex. These findings highlight significant inter- and intra-strain variability, emphasizing the importance of careful characterization of transgenic models and the need for appropriate control groups and experimental designs to ensure the reliability and validity of studies utilizing Cre-Driver lines. - Source: PubMed
Renken KimMasseck Olivia Andrea - Developing precise targeted cell ablation in the axolotl (Ambystoma mexicanum) is crucial for elucidating the roles or interactions of specific cell types in regeneration and modeling diseases. Here we establish a Nitroreductase (NTR)-based inducible cell ablation system in axolotls. Through generation of Sox2:Cherry-NTR knock-in axolotls, we achieve efficient ablation of ependymoglial cells (EGCs) in the central nervous system. Combined spinal cord and brain transplantation and injury models demonstrate regeneration failure upon EGC depletion, suggesting that EGCs are sole source of central nervous system regeneration. Additionally, EGC ablation in the spinal cord resulted in delayed tail regeneration. Moreover, we establish NeuroD6:Cherry-NTR and NeuroD6:Cherry-NTR2.0 knock-in lines to ablate postmitotic cortical neurons, enable the investigation of brain regeneration after large-scale neuronal depletion. We found that NTR2.0 (but not NTR) leads to elimination of >95% of targeted neurons in the dorsal pallium. All lost neuronal subtypes are chronologically regenerated with laminar-like distribution mirroring developmental patterning. Finally, we create Cre-LoxP-based conditional NTR2.0 transgenic axolotls using a constitutive CAGGs promoter, enabling tissue-specific ablation of specific cell types when crossed to existing Cre lines. In summary, our study establishes an efficient and versatile targeted cell ablation system in axolotls, providing a valuable tool for deep dissection of tissue regeneration in axolotls. - Source: PubMed
Publication date: 2026/01/20
Fu SuleiZeng Yan-YunPeng ChengWang LiqunFeng YuxianWang KunLiu YanmeiFei Ji-Feng - (1) Glioblastoma (GBM) is one of the most aggressive brain tumors with a poor prognosis. Therefore, new insights into GBM diagnosis and treatment are required. In addition to differentially expressed mRNAs, miRNAs may have the potential to be applied as diagnostic biomarkers. (2) In this study, profiling of human miRNAs in combination with mRNAs was performed on total RNA isolated from tissue samples of five control and five GBM patients, using a high-throughput RNA sequencing (RNA-Seq) approach. (3) A total of 35 miRNAs and 365 mRNAs were upregulated, while 82 miRNAs and 1225 mRNAs showed significant downregulation between tissue samples of GBM patients compared to the control samples using the iDEP to analyze RNA-Seq data. To validate our results, the expression of five miRNAs (hsa-miR-196a-5p, hsa-miR-21-3p, hsa-miR-10b-3p, hsa-miR-383-5p, and hsa-miR-490-3p) and fourteen mRNAs (E2F2, HOXD13, VEGFA, CDC45, AURKB, HOXC10, MYBL2, FABP6, PRLHR, NEUROD6, CBLN1, HRH3, HCN1, and RELN) was determined by RT-qPCR assay. The miRNet tool was used to build miRNA-target interaction. Furthermore, a protein-protein interaction (PPI) network was created from the miRNA targets by applying the NetworkAnalyst 3.0 tool. Based on the PPI network, a functional enrichment analysis of the target proteins was also carried out. (4) We identified an miRNA panel and several deregulated mRNAs that could play an important role in tumor development and distinguish GBM patients from healthy controls with high sensitivity and specificity using total RNA isolated from tissue samples. - Source: PubMed
Publication date: 2025/03/19
Géczi DóraKlekner ÁlmosBalogh IstvánPenyige AndrásSzilágyi MelindaVirga JózsefBakó AndreaNagy BálintTorner BernadettBirkó Zsuzsanna - The axolotl is broadly used in regenerative, developmental, and evolutionary biology research. Targeted gene knock-in is crucial for precision transgenesis, enabling disease modeling, visualization, tracking, and functional manipulation of specific cells or genes of interest (GOIs). Existing CRISPR/Cas9-mediated homology-independent method for gene knock-in often causes "scars/indels" at integration junctions. Here, we develop a CRISPR/Cas9-mediated semi-homology-directed recombination (HDR) knock-in method using a donor construct containing a single homology arm for the precise integration of GOIs. This semi-HDR approach achieves seamless single-end integration of the Cherry reporter gene and a large inducible Cre cassette into intronless genes like Sox2 and Neurod6 in axolotls, which are challenging to modify with the homology-independent method. Additionally, we integrate the inducible Cre cassette into intron-containing loci (e.g., Nkx2.2 and FoxA2) without introducing indels via semi-HDR. GOIs are properly expressed in F0 founders, with approximately 5%-10% showing precise integration confirmed by genotyping. Furthermore, using the Nkx2.2:CreER line, we fate-map spinal cord p3 neural progenitor cells, revealing that Nkx2.2 cells adopt different lineages in development and regeneration, preferentially generating motoneurons over oligodendrocytes during regeneration. Overall, this semi-HDR method balances efficiency and precision in the integration of GOIs, providing a valuable tool for generating knock-in axolotls and potentially extending to other species. - Source: PubMed
Publication date: 2025/03/07
Wang LiqunHu YanQiu YuanhuiLin HuitingLi XiangFu SuleiZeng Yan-YunGhouse MariaLong ChengLiu YanmeiFei Ji-Feng - CACNA1C, coding for the α1 subunit of L-type voltage-gated calcium channel (LTCC) Ca1.2, has been associated with multiple psychiatric disorders. Clinical studies have revealed alterations in behavior as well as in brain structure and function in CACNA1C risk allele carriers. These findings are supported by rodent models of Ca1.2 deficiency, which showed increased anxiety, cognitive and social impairments as well as a shift towards active stress-coping strategies. These behavioral alterations were accompanied by functional deficits, such as reduced long-term potentiation (LTP) and an excitation/inhibition (E/I) imbalance. However, these preclinical studies are largely limited to male rodents, with few studies exploring sex-specific effects. Here, we investigated the effects of Ca1.2 deficiency in forebrain glutamatergic neurons in female conditional knockout (CKO) mice. CKO mice exhibited hyperlocomotion in a novel environment, increased anxiety-related behavior, cognitive deficits, and increased active stress-coping behavior. These behavioral alterations were neither influenced by the stage of the estrous cycle nor by the Nex/Neurod6 haploinsufficiency or Cre expression, which are intrinsically tied to the utilization of the Nex-Cre driver line for conditional inactivation of Cacna1c. In the hippocampus, Ca1.2 inactivation enhanced presynaptic paired-pulse facilitation without altering postsynaptic LTP at CA3-CA1 synapses. In addition, CA1 pyramidal neurons of female CKO mice displayed a reduction in dendritic complexity and spine density. Taken together, our findings extend the existing knowledge suggesting Ca1.2-dependent structural and functional alterations as possible mechanisms for the behavioral alterations observed in female Ca1.2-Nex mice. - Source: PubMed
Publication date: 2024/10/06
Loganathan SrivaishnaviMenegaz DanusaDelling Jan PhilippEder MatthiasDeussing Jan M