ADCYAP1R1
- Known as:
- ADCYAP1R1
- Catalog number:
- 001203A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ADCYAP1R1
Related genes to: ADCYAP1R1
- Gene:
- ADCYAP1R1 NIH gene
- Name:
- ADCYAP receptor type I
- Previous symbol:
- -
- Synonyms:
- PAC1, PACAPR, PAC1R
- Chromosome:
- 7p14.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-05-18
- Date modifiied:
- 2017-07-07
Related products to: ADCYAP1R1
Related articles to: ADCYAP1R1
- Pituitary adenylate cyclase-activating polypeptide (PACAP) is a neuropeptide which was shown to be released in the hypothalamo-hypophyseal system but subsequently demonstrated in the entire nervous system and nearly all peripheral organs, including skeletal elements. PACAP has an important function in the regulation of chondrogenic differentiation, protecting in vitro chondrogenesis during various stresses and in osteogenesis. PACAP knockout (KO) mice show early signs of aging. Its most potent receptor is PAC1-R, the activation of which leads to enhanced Sox9 expression and subsequently, increase in the expression of collagen type II, glycosaminoglycans, and aggrecan. In the present experiments, we investigated the effect of the absence of PAC1 receptor in PAC1 KO homozygous and heterozygous mice focusing on joints of hind limb in young and aged animals. Thickness and extracellular matrix content of articular cartilage of joints increased in the absence of PAC1 receptor with aging. A thicker cartilage was detected in aged animals in mechanically affected joints. Interestingly, the disturbance of PACAP signaling pathways increased the nuclear translocation of P-Sox9 transcription factor in various joints. In summary, the alteration of PAC1 receptor regulated signalization elevated cartilage formation and protected cartilage architecture during aging suggesting a balancing effect of the receptor in chondrogenesis. - Source: PubMed
Publication date: 2026/04/20
Fillér CsabaKovács Lili SaroltaRácz KálmánSegal YonatanVágó JuditTóth AnnaSzegeczki VinceJüngling AdélGergely PéterZákány RózaReglődi DóraJuhász Tamás - The context-dependent behavior serves as a core behavioral manifestation of intrusive traumatic memory flashbacks in PTSD, its neural circuit and underlying brain regions remain incompletely understood. Although pituitary adenylate cyclase-activating polypeptide (PACAP) has been implicated as a key pathological factor in PTSD pathogenesis, its role in PTSD-like contextual behavioral responses has not yet been elucidated. In this study, we demonstrated that chronic social defeat stress (CSDS) induced locomotor hyperactivity in male mice, but only when they were re-exposed to the stress-associated chamber. Notably, neurons in the paraventricular thalamus (PVT) showed significant activation following the expression of above context-dependent behavior. Chronic optogenetic activation of PVT neurons was sufficient to recapitulate PTSD-like contextual behavior in naïve mice. Furthermore, anterograde and retrograde tracing revealed that the ventral hippocampus (vHip) sends monosynaptic and glutamatergic projections to the PVT. Chronic inhibition of PVT-projecting vHip neurons selectively suppressed PTSD-like context-dependent locomotion hyperactivity without affecting other stress-induced behavioral alterations. In contrast, chronic inhibition of vHip recipient PVT neurons attenuated most CSDS-induced PTSD-like behaviors. Moreover, CSDS led to upregulated expression of the PAC1 receptor in PVT neurons. Local pharmacological blockade of the PAC1 receptor in the PVT during the CSDS paradigm prevented the development of both context-dependent hyperactivity and other PTSD-like behavioral phenotypes. Collectively, our findings identify a vHip-PVT circuit and PVT PACAP/PAC1 signaling in the pathophysiology of PTSD-like contextual behavior and highlight the PVT as a potential therapeutic target for treating PTSD-related context-dependent symptoms. - Source: PubMed
Publication date: 2026/03/17
Cao ZhipingGao HaiyanTang BinliangXu Yong - - Source: PubMed
Publication date: 2026/03/07
Wang JunWang MinshenDong QiufengHuo JunliYan ZhifengLi JuanChen XiaoyanLi LiwenZhen Haining - Photoperiodic regulation is a key technique in modern poultry farming. In geese, however, the molecular pathways by which the pituitary gland transduces photoperiodic signals remain incompletely understood. Therefore, this study aimed to identify key factors by analyzing the pituitary transcriptome of female Yangzhou geese subjected to a short photoperiod and a long photoperiod. RNA-seq analysis showed that the prolactin (PRL) gene was the most highly expressed among all DEGs in the pituitary, and its dynamic expression pattern was closely associated with reproductive status. Furthermore, the neuroactive ligand-receptor interaction pathway was significantly enriched. Within this pathway, we identified key receptor genes, including neurotransmitter receptors (e.g., Gamma-Aminobutyric Acid Type A Receptor Subunit Gamma1 (GABRG1), Gamma-Aminobutyric Acid Type B Receptor Subunit 2 (GABBR2), Glutamate Ionotropic Receptor NMDA Type Subunit 1 (GRIN1), Opioid Receptor Mu 1 (OPRM1)) as well as neuropeptides and their receptors (e.g., Adenylate Cyclase Activating Polypeptide 1 Receptor 1 (ADCYAP1R1), Galanin Receptor 1 (GALR1)). Our results established the pituitary transcriptomic profile of geese under photoperiod-mediated reproduction, underscoring its role as a critical neuroendocrine center. It regulates reproductive activity primarily through PRL signaling and through specific neural pathways that receive and integrate diverse neural signals. - Source: PubMed
Publication date: 2025/12/17
Chen XiaojingMei HaiyueLiu JieFeng YuyanDai ZichunGuo BinbinZhu HuanxiHe Bin - Stress-related disorders, including PTSD, acute stress disorders, adjustment disorder, and attachment disorders, arise from complex interactions between genetic susceptibility and environmental stressors. While early environmental factors play a central role in the development of these disorders, there is growing evidence that genetic predisposition also contributes to individual differences in vulnerability and resilience. This narrative review examines current evidence on genetic predisposition and resilience mechanisms in stress-related psychopathology during developmental age. A literature search was performed using PubMed, Cochrane, MedRxiv, and Medline databases, focusing on studies published between 2010 and 2025, written in English, in the pediatric and adolescent population. Priority was given to original research articles and high-impact reviews. Studies were selected based on relevance to the genetic mechanisms underlying vulnerability and resilience to stress. 71 of 317 were selected. Two hundred forty-six articles were excluded due to a lack of relevance to the topic or because they included an adult population. Polymorphisms and epigenetic modifications in genes involved in hypothalamus-pituitary-adrenal axis (, , and ), serotoninergic ( and ), noradrenergic and dopaminergic system ( and ), , estrogen receptor and excitatory amino acid transporters are associated with increased risk of psychopathology following early trauma, but are also implicated in the development of resilience. Genetic factors influence both vulnerability and resilience to stress-related disorders. However, further studies based on the role of genetics are needed to advance precision and personalized medicine, which is still largely underexplored to this day in the field of stress-induced disorders. - Source: PubMed
Publication date: 2025/11/10
Raffagnato AlessiaRaicich AriannaPaiusco LisaCoser GiuliaBonemazzi IlariaGazzin AndreaPelizza Maria FedericaAncora CaterinaToldo Irene