AVPR1B Antibody
- Known as:
- AVPR1B Antibody
- Catalog number:
- AF1129b
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- AVPR1B Antibody
Ask about this productRelated genes to: AVPR1B Antibody
- Gene:
- AVPR1B NIH gene
- Name:
- arginine vasopressin receptor 1B
- Previous symbol:
- AVPR3
- Synonyms:
- -
- Chromosome:
- 1q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1995-07-06
- Date modifiied:
- 2016-10-05
Related products to: AVPR1B Antibody
Related articles to: AVPR1B Antibody
- Nitrogen-containing heterocyclic compounds with multiple fused rings have gained significant interest in medicinal chemistry due to their structural versatility and wide range of pharmacological applications. Within this category, pyrazolopyrrolopyrazines stand out as scaffolds featuring a tricyclic fused core composed of pyrazole, pyrrole, and pyrazine rings. These molecules have demonstrated promising biological activities, including potent antibacterial and antifungal properties, significant inhibition of phosphodiesterase type 5 (PDE5), and other activities. Moreover, analogous molecules have shown potential applications as antioxidants, anti-inflammatory agents, antitumor compounds, regulators of the vasopressin receptor AVPR1b, among others. Despite their potential, the development of unified and efficient synthetic methodologies for specific isomers- particularly less explored structural variants-remains limited and fragmented across the literature. This mini-review provides a comprehensive analysis of the synthetic strategies and biological potential of pyrazolo[4,3-e]pyrrolo[1,2-a]pyrazine isomers and related tricyclic systems. This study discusses selected synthetic methodologies reported in the literature, ranging from classical synthetic methods to modern catalytic approaches, aiming to facilitate access to these heterocyclic analogs. Furthermore, this work identifies an existing research gap through the lack of systematic studies on the pyrazolo[3,4-e] isomer. To address this limitation, this study proposes a novel retrosynthetic strategy based on the stepwise construction of the tricyclic core from readily available 5- aminopyrazoles. This approach integrates well-established transformations, including nitrosations, reductions, Clauson-Kaas pyrrole formation, and Pictet-Spengler-type cyclization, for strategically construct this isomer of interest. This study presents precise and detailed breakdowns of each step, with the expressed priority of identifying common ground in analogous structures and reactivity between the literature and the proposal. By consolidating current knowledge, this review seeks to open new avenues for research on the design and functionalization of pyrazolopyrrolopyrazine derivatives, providing medicinal chemists with a valuable toolkit for developing new bioactive entities. - Source: PubMed
Publication date: 2026/09/14
Becerra R Christian AAlarcón F Juan DCuervo P Paola AFabian L Orozco - Alcohol use disorder (AUD) remains a significant global health challenge, necessitating the exploration of novel pharmacotherapeutics. Our recent study observed that intranasal (IN) administration of arginine vasopressin (AVP) decreases voluntary consumption of sweetened ethanol (EtOH) in mice, a promising development, given that IN AVP does not affect the blood pressure or stress responses associated with systemic AVP administration. To characterize AVP's potential to regulate alcohol drinking, here we investigated the effects of IN AVP on voluntary intake of unsweetened ethanol (EtOH) in single- and group-housed mice, the involvement of AVP and Oxytocin (Oxt) receptors, and the potential neural substrates of these effects. - Source: PubMed
Nipper Michelle AZweig Jonathan AJohnson Michael CRyabinin Andrey E - Much attention has been devoted to exploring the similarities between schizophrenia and autism spectrum disorder (ASD). Autistic traits in schizophrenia have recently been assessed using the Positive and Negative Syndrome Scale for Schizophrenia Autism Severity Scale (PAUSS). Although studies on arginine-vasopressin (AVP) systems have focused on the etiology of ASD, there are no reports regarding AVP systems and autistic traits in schizophrenia. This study aimed to assess autistic traits in schizophrenia using the PAUSS and examine their associations with the PAUSS and AVP-related biological measures. This is a cross-sectional study. We recruited patients with schizophrenia (n = 80) and healthy controls (HCs; n = 27). Patients with schizophrenia were classified as having either an autistic phenotype schizophrenia (AU) or a non-autistic phenotype (NAU). All patients with schizophrenia underwent clinical assessments focusing on symptom severity, autistic traits, neurocognition, and social cognition. HCs were examined for neurocognition and social cognition. We also evaluated AVP-related biomarkers, including serum AVP levels, single-nucleotide polymorphisms, and promoter-region microsatellites. The AU group showed worse symptom severity and social cognition than the NAU group. The T allele of rs28632197 in the AVP receptor (AVPR)1b was associated with more severe autistic traits in patients with schizophrenia, while the short allele of RS1 in AVPR1a was associated with less severe autistic traits. Our results suggest that autistic traits in schizophrenia are linked to more severe symptoms and poorer social cognition and that AVP system dysfunction may contribute to their etiology. Clinicians should carefully evaluate autistic traits. - Source: PubMed
Publication date: 2026/04/28
Yamasaki FumiakiNakata YusukeKanahara NobuhisaMiyazawa AtsuhiroMashimo YoichiHirose YukiOda YasunoriNiitsu TomihisaOnouchi YoshihiroIyo Masaomi - BACKGROUND: The Hypothalamic-pituitary-adrenal axis (HPA) and its single nucleotide polymorphisms (SNPs) potentially influence depressive symptoms and non-suicidal self-injury (NSSI) among adolescents. Adverse childhood experiences (ACEs) may dysregulate HPA axis functioning, with these complex gene-environment interactions showing significant heterogeneity across individuals. This study examined whether depressive symptoms mediate the relationship between ACEs and adolescent NSSI, and whether HPA axis genetic polymorphisms moderate this indirect pathway. METHODS: For this study, 172 adolescents aged 12 to 18 years were recruited from Xuzhou Oriental Hospital affiliated with Xuzhou Medical University as the NSSI group. Additionally, 58 age-, sex-, residence-, and health-matched volunteers were recruited from the local area as the healthy control group. Demographic information was collected through questionnaires, and adverse childhood experiences, depressive symptoms, and non-suicidal self-injury behaviors were assessed using the Adverse Childhood Experiences Scale (ACEs Scale), the Beck Depression Inventory-II (BDI-II), and the Non-Suicidal Self-Injury Behavior Scale (NSSI-BS). Blood samples were collected for HPA axis genotyping targeting the following loci: SKA2 (rs7208505, rs9911583), SLC1A3 (rs2269272), FKBP5 (rs9470080), and AVPR1B (rs28373064), which were analyzed using TaqMan-PCR. All statistical analyses were performed in SPSS 27.0, including Hardy-Weinberg equilibrium (HWE), χ² test, and Pearson’s correlation coefficient, as well as PROCESS macro-model mediation analysis and simple slope analysis. RESULTS: Depressive symptoms were found to mediate the association between ACEs and NSSI. The SKA2-rs7208505 polymorphism significantly moderated the relationship between ACEs and depressive symptoms, influencing the indirect pathway from ACEs to depressive symptoms to NSSI. Adolescents with the AA genotype of the SKA2-rs7208505 polymorphism were more susceptible to ACEs and more likely to develop depressive symptoms compared to those with GA and GG genotypes. CONCLUSION: Timely identification and interventions targeting depressive symptoms, especially among individuals with AA genotypes of SKA2-rs7208505 who have experienced ACEs, may be crucial for preventing or reducing the risk of NSSI in adolescents. - Source: PubMed
Publication date: 2026/04/20
Wang YihanLiang QingqingZhou WeiWang YingxueTian SusuHu XinyiTian JiayiLiu YuxuanFang HaiyanWang Wei - To investigate the interaction between HPA-axis gene polymorphisms (FKBP5, NR3C1, AVPR1B, SLC1A3, SKA2) and brain functional alterations in adolescent depression. - Source: PubMed
Publication date: 2026/04/02
Tian SusuLiang QingqingZhou WeiHu XinyiLiu YuxuanTian JiayiLuo YunjiaoFang HaiyanWang Wei