ADNP2
- Known as:
- ADNP2
- Catalog number:
- 001226A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ADNP2
Related genes to: ADNP2
- Gene:
- ADNP2 NIH gene
- Name:
- ADNP homeobox 2
- Previous symbol:
- ZNF508
- Synonyms:
- KIAA0863
- Chromosome:
- 18q23
- Locus Type:
- gene with protein product
- Date approved:
- 2006-06-30
- Date modifiied:
- 2019-03-22
Related products to: ADNP2
Related articles to: ADNP2
- In vertebrates, neural induction requires the inhibition of BMP signals by dorsal organizer-derived antagonists. However, the underlying mechanism is not completely understood. Here, using zebrafish as a model, we show that ADNP2 orthologs adnp2a and adnp2b are required for proper neural induction in gastrulating embryos. Deficiency of adnp2 causes deficits in neuroectoderm specification, showing reduced expression of both anterior and posterior neural markers. Adnp2 functions as a transcriptional repressor, and directly occupies and suppresses the BMP-related ved/vent/vox homeobox genes, thereby excluding their expression from dorsal territories, including the dorsal mesoderm and presumptive neural plate. adnp2-deficient larvae display aberrant behavioral alterations, which can be partially rescued by the administration of BMP antagonist Dorsomorphin or dnBmpr1 mRNAs. Our findings in the zebrafish model reveal an indirect role for Adnp2 in neuroectoderm formation by antagonizing the activities of BMP-related ventralizing genes, which will be useful for understanding neural disorders caused by ADNP2 dysfunction in human. - Source: PubMed
Publication date: 2026/04/07
Wang YongxinCao YuqingDuan MingSun Yuhua - Human mutations of and are known to be associated with neural developmental disorders (NDDs), including autism spectrum disorders (ASDs) and schizophrenia (SZ). However, the underlying mechanisms remain elusive. In this study, using CRISPR/Cas9 gene editing technology, we generated and mutant zebrafish models, which exhibited developmental delays, brain deficits, and core behavioral features of NDDs. RNA sequencing analysis of ; and ; larval brains revealed altered gene expression profiles affecting synaptic transmission, autophagy, apoptosis, microtubule dynamics, hormone signaling, and circadian rhythm regulation. Validation using whole-mount in situ hybridization (WISH) and real-time quantitative PCR (qRT-PCR) corroborated these findings, supporting the RNA-seq results. Additionally, loss of and resulted in significant downregulation of pan-neuronal HuC and neuronal fiber network α-Tubulin signals. Importantly, prolonged low-dose exposure to environmental endocrine disruptors (EEDs) aggravated behavioral abnormalities in and mutants. This comprehensive approach enhances our understanding of the complex interplay between genetic mutations and environmental factors in NDDs. Our findings provide novel insights and experimental foundations into the roles of and in neurodevelopment and behavioral regulation, offering a framework for future preclinical drug screening aimed at elucidating the pathogenesis of NDDs and related conditions. - Source: PubMed
Publication date: 2024/08/30
Wang YongxinSun XiaoyunXiong BoDuan MingSun Yuhua - Cocaine use disorder (CUD) is a chronic neuropsychiatric disorder estimated to effect 1-3% of the population. Activity-dependent neuroprotective protein (ADNP) is essential for brain development and functioning, shown to be protective in fetal alcohol syndrome and to regulate alcohol consumption in adult mice. The goal of this study was to characterize the role of ADNP, and its active peptide NAP (NAPVSIPQ), which is also known as davunetide (investigational drug) in mediating cocaine-induced neuroadaptations. Real time PCR was used to test levels of Adnp and Adnp2 in the nucleus accumbens (NAc), ventral tegmental area (VTA), and dorsal hippocampus (DH) of cocaine-treated mice (15 mg/kg). Adnp heterozygous (Adnp )and wild-type (Adnp ) mice were further tagged with excitatory neuronal membrane-expressing green fluorescent protein (GFP) that allowed for in vivo synaptic quantification. The mice were treated with cocaine (5 injections; 15 mg/kg once every other day) with or without NAP daily injections (0.4 µg/0.1 ml) and sacrificed following the last treatment. We analyzed hippocampal CA1 pyramidal cells from 3D confocal images using the Imaris x64.8.1.2 (Oxford Instruments) software to measure changes in dendritic spine density and morphology. In silico ADNP/NAP/cocaine structural modeling was performed as before. Cocaine decreased Adnp and Adnp2 expression 2 h after injection in the NAc and VTA of male mice, with mRNA levels returning to baseline levels after 24 h. Cocaine further reduced hippocampal spine density, particularly synaptically weaker immature thin and stubby spines, in male Adnp) mice while increasing synaptically stronger mature (mushroom) spines in Adnp) male mice and thin and stubby spines in females. Lastly, we showed that cocaine interacts with ADNP on a zinc finger domain identical to ketamine and adjacent to a NAP-zinc finger interaction site. Our results implicate ADNP in cocaine abuse, further placing the ADNP gene as a key regulator in neuropsychiatric disorders. Ketamine/cocaine and NAP treatment may be interchangeable to some degree, implicating an interaction with adjacent zinc finger motifs on ADNP and suggestive of a potential sex-dependent, non-addictive NAP treatment for CUD. - Source: PubMed
Publication date: 2024/09/10
Toren YaelZiv YardenSragovich ShlomoMcKinney R AnneBarak SegevShazman ShulaGozes Illana - Retrotransposon control in mammals is an intricate process that is effectuated by a broad network of chromatin regulatory pathways. We previously discovered ChAHP, a protein complex with repressive activity against short interspersed element (SINE) retrotransposons that is composed of the transcription factor ADNP, chromatin remodeler CHD4, and HP1 proteins. Here we identify ChAHP2, a protein complex homologous to ChAHP, in which ADNP is replaced by ADNP2. ChAHP2 is predominantly targeted to endogenous retroviruses (ERVs) and long interspersed elements (LINEs) via HP1β-mediated binding of H3K9 trimethylated histones. We further demonstrate that ChAHP also binds these elements in a manner mechanistically equivalent to that of ChAHP2 and distinct from DNA sequence-specific recruitment at SINEs. Genetic ablation of ADNP2 alleviates ERV and LINE1 repression, which is synthetically exacerbated by additional depletion of ADNP. Together, our results reveal that the ChAHP and ChAHP2 complexes function to control both nonautonomous and autonomous retrotransposons by complementary activities, further adding to the complexity of mammalian transposon control. - Source: PubMed
Publication date: 2024/07/19
Ahel JosipPandey AparnaSchwaiger MichaelaMohn FabioBasters AnjaKempf GeorgAndriollo AudeKaaij LucasHess DanielBühler Marc - Alzheimer's disease (AD) and age-related macular degeneration (AMD) share similar pathological features, suggesting common genetic aetiologies between the two. Investigating gene associations between AD and AMD may provide useful insights into the underlying pathogenesis and inform integrated prevention and treatment for both diseases. - Source: PubMed
Publication date: 2024/04/15
Zhang XueliZhu ZhuotingHuang YuShang XianwenO'Brien Terence JKwan PatrickHa JasonWang WeiLiu ShunmingZhang XiayinKiburg KaterinaBao YiningWang JingYu HonghuaHe MingguangZhang Lei