Ask about this productRelated genes to: NTNG2 Blocking Peptide
- Gene:
- NTNG2 NIH gene
- Name:
- netrin G2
- Previous symbol:
- NTNG1
- Synonyms:
- KIAA1857, Lmnt2
- Chromosome:
- 9q34.13
- Locus Type:
- gene with protein product
- Date approved:
- 2001-01-02
- Date modifiied:
- 2016-10-05
Related products to: NTNG2 Blocking Peptide
Related articles to: NTNG2 Blocking Peptide
- Peripheral nerve injury (PNI) frequently causes persistent sensory and motor deficits with limited therapeutic options. While Ptbp1-mediated astrocyte reprogramming shows promise in central nervous system repair, its role in PNI-particularly regarding spinal cord astrocytes and dorsal root ganglia (DRG) satellite glial cells (SGCs)-remains unexplored. - Source: PubMed
Song HonghaoPeng LeiChen DashuangFan XiaoyiHua TongDing RuifengDeng MengqiuChen QianboYang MeiYuan Hongbin - Netrin-G2 is a membrane-anchored protein known to play critical roles in neuronal circuit development and synaptic organization. In this study, we identify compound heterozygous mutations of c.547delC, p.(Arg183Alafs∗186) and c.605G>A, p.(Trp202X) in NTNG2 causing a syndrome exhibiting developmental delay, intellectual disability, hypotonia, and facial dysmorphism. To elucidate the underlying cellular and molecular mechanisms, CRISPR-Cas9 technology is employed to generate a knock-in mouse model expressing the R183Afs and W202X mutations. We report that the Ntng2 mice exhibit hypotonia and impaired learning and memory. We find that the levels of CaMKII and p-GluA1 are decreased, and excitatory postsynaptic transmission and long-term potentiation are impaired. To increase the activity of CaMKII, the mutant mice receive intraperitoneal injections of DCP-LA, a CaMKII agonist, and show improved cognitive function. Together, our findings reveal molecular mechanisms of how NTNG2 deficiency leads to impairments of cognitive ability and synaptic plasticity. - Source: PubMed
Publication date: 2024/08/14
Chen YaotingChen JiangLiang LiliDai WeiqianLi NanDong ShuangshuangZhan YongkunChen GuiquanYu Yongguo - Dysregulated liquid-liquid phase separation (LLPS) instigates tumorigenesis through biomolecular condensate dysfunction. However, the association between LLPS-associated genes and glioma remains underexplored. - Source: PubMed
Publication date: 2024/04/22
Lv LingZhang XinLiu YajunZhu XutongPan RuihanHuang Lifa - The inner ear sensory neurons play a pivotal role in auditory processing and balance control. Though significant progresses have been made, the underlying mechanisms controlling the differentiation and survival of the inner ear sensory neurons remain largely unknown. During development, ISL1 and POU4F transcription factors are co-expressed and are required for terminal differentiation, pathfinding, axon outgrowth and the survival of neurons in the central and peripheral nervous systems. However, little is understood about their functional relationship and regulatory mechanism in neural development. Here, we have knocked out or or both in mice of both sexes. In the absence of , the differentiation of cochleovestibular ganglion (CVG) neurons is disturbed and with that -deficient CVG neurons display defects in migration and axon pathfinding. Compound deletion of and causes a delay in CVG differentiation and results in a more severe CVG defect with a loss of nearly all of spiral ganglion neurons (SGNs). Moreover, ISL1 and POU4F1 interact directly in developing CVG neurons and act cooperatively as well as independently in regulating the expression of unique sets of CVG-specific genes crucial for CVG development and survival by binding to the -regulatory elements including the promoters of , , and and enhancers of and These findings demonstrate that and are indispensable for CVG development and maintenance by acting epistatically to regulate genes essential for CVG development. - Source: PubMed
Publication date: 2024/02/21
Xu MeiLi ShuchunXie XiaolingGuo LumingYu DongliangZhuo JiapingLin JaceyKol LotemGan Lin - The cyanotoxin cylindrospermopsin (CYN) has been postulated to cause neurotoxicity, although the studies in this concern are very few. In addition, some studies in vitro indicate its possible effects on development. Furthermore, pesticides can be present in the same environmental samples as cyanotoxins. Therefore, chlorpyrifos (CPF) has been one of the most common pesticides used worldwide. The aim of this report was to study the effects of CYN, isolated and in combination with CPF, in a developmental neurotoxicity in vitro model. The human neuroblastoma SH-SY5Y cell line was exposed during 6 days of differentiation to both toxics to study their effects on cell viability and neurite outgrowth. To further evaluate effects of both toxicants on cholinergic signaling, their agonistic and antagonistic activities on the α7 homomeric nicotinic acetylcholine receptor (nAChR) were studied upon acute exposure. Moreover, a transcriptomic analysis by qPCR was performed after 6 days of CYN-exposure during differentiation. The results showed a concentration-dependent decrease on both cell viability and neurite outgrowth for both toxics isolated, leading to effective concentration 20 (EC) values of 0.35 µM and 0.097 µM for CYN on cell viability and neurite outgrowth, respectively, and 100 µM and 58 µM for CPF, while the combination demonstrated no significant variations. In addition, 95 µM and 285 µM CPF demonstrated to act as an antagonist to nicotine on the nAChR, although CYN up to 2.4 µM had no effect on the efficacy of these receptors. Additionally, the EC for CYN (0.097 µM) on neurite outgrowth downregulated expression of the 5 genes NTNG2 (netrin G2), KCNJ11 (potassium channel), SLC18A3 (vesicular acetylcholine transporter), APOE (apolipoprotein E), and SEMA6B (semaphorin 6B), that are all important for neuronal development. Thus, this study points out the importance of studying the effects of CYN in terms of neurotoxicity and developmental neurotoxicity. - Source: PubMed
Publication date: 2023/12/12
Hinojosa M GJohansson YJos ACameán A MForsby A