Avil antibody - N-terminal region (ARP31494_P050)
- Known as:
- Avil (anti-) - N-terminal region (ARP31494_P050)
- Catalog number:
- arp31494_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- Avil antibody - N-terminal region (ARP31494_P050)
Related genes to: Avil antibody - N-terminal region (ARP31494_P050)
- Gene:
- AVIL NIH gene
- Name:
- advillin
- Previous symbol:
- -
- Synonyms:
- p92, FLJ12386, ADVIL, DOC6
- Chromosome:
- 12q14.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-09-02
- Date modifiied:
- 2015-09-11
Related products to: Avil antibody - N-terminal region (ARP31494_P050)
Related articles to: Avil antibody - N-terminal region (ARP31494_P050)
- Deer antler polypeptides (DAPs), one of the most bioactive components of deer antler, have been reported to possess multiple biological functions. However, the role of DAPs in fracture healing remains unclear. This study aims to investigate the therapeutic effects of DAPs on fracture healing and elucidate their potential pharmacological mechanism. - Source: PubMed
Publication date: 2026/05/08
He YunfanXi JihaoDai HaoqiangFang LiangYu YiheYing YongganLi JinFu DanqingXia Chenjie - Hiccups (singultus) are generally benign and self-limiting conditions; however, in some patients, they may become persistent and require treatment. Although proton pump inhibitors (PPIs), chlorpromazine, and various centrally acting agents are commonly used, evidence for alternative treatment options remains limited. While PPIs are frequently utilized for hiccups that develop secondary to dyspepsia, there is limited data in the literature to support antihistamines as an effective treatment modality, and clinical data supporting their use are also limited. This case series aimed to evaluate the clinical utility and safety of the combination of intravenous pantoprazole and pheniramine, an H1 antihistamine with anticholinergic properties, in the treatment of persistent hiccups. - Source: PubMed
Publication date: 2026/04/16
Sahin Yusuf S - The liver plays a central role in energy balance, glucose homeostasis, and lipid metabolism through neural and humoral pathways. Intriguingly, impaired hepatic lipid metabolism has been also associated with an increased risk of anxiety and depression in rodents and humans. However, the mechanisms by which it affects mood behaviors via neural pathways remain poorly understood. This study investigated whether activation of the liver-brain axis can modulate anxiety-like behavior in mice. Advillin (Avil); channelrhodopsin-tdTomato mice and wireless optogenetics were used to selectively stimulate Avil-positive vagal sensory neurons that innervate the liver in freely moving mice. Acute optogenetic stimulation of their nerves in the liver activated neurons in the nodose ganglia, the dorsal motor nucleus of the vagus, and the nucleus of the solitary tract (NTS). Behavioral assessments revealed that acute optogenetic stimulation of these liver-innervating vagal sensory nerves increased anxiety-like behavior in male and female mice during open field, elevated plus maze, and light/dark box tests. Retrograde viral tracing revealed that neurons in the NTS sent projections to the locus coeruleus (LC), and optogenetic stimulation of liver-innervating vagal sensory nerves resulted in significant activation of norepinephrine-expressing neurons in the LC. Chemogenetic inhibition of LC norepinephrine (NE) neurons completely abolished the anxiogenic effect of stimulating Slc6a2‑positive vagal sensory neurons, demonstrating that LC NE neuron activity is essential for this behavioral response. Therefore, these findings reveal a novel liver - NTS - LC circuit that plays a role in the regulation of anxiety-like behavior through vagal sensory neurons. Unlike the traditional top-down neuronal circuits associated with the liver, this newly identified liver-brain axis is essential for regulating not only systemic energy homeostasis but also emotional behaviors. - Source: PubMed
Publication date: 2026/05/11
Lee SangbhinHwang JiyeonJo Young-Hwan - Glioblastoma multiforme (GBM) is the most prevalent and aggressive malignant primary brain tumor, marked by rapid growth, extensive invasiveness, and a median survival of only ∼15 months despite current multimodal therapy. To identify new therapeutic vulnerabilities, we investigated the actin-regulatory protein , previously implicated through a gene fusion in rhabdomyosarcoma. Comprehensive genomic and transcriptomic analyses across REMBRANDT, TCGA, and CGGA datasets revealed recurrent amplification and consistently elevated AVIL expression in GBM compared with normal brain tissue. was overexpressed across all GBM molecular subtypes and glioma stem cell (GSC) states but was nearly undetectable in normal astrocytes, neural stem cells, and brain tissues. Functional studies demonstrated that is both necessary and sufficient for glioma genesis: silencing eradicated GBM cells and suppressed xenograft growth , while overexpression enhanced proliferation, migration, and transformation. Mechanistically, drives tumor progression through actin cytoskeleton remodeling and activation of the FOXM1-LIN28B oncogenic pathway. Using a small molecule microarray screen, we identified a selective -binding compound (compound A) that potently inhibited GBM cell growth with minimal toxicity to normal astrocytes. Gene expression changes induced by compound A mirrored those following knockdown, indicating on-target activity. Compound A demonstrated robust antitumor efficacy in multiple preclinical GBM models, including orthotopic xenografts, GSC-derived tumors, patient-derived xenografts, and temozolomide-resistant GBM with favorable pharmacokinetics and blood-brain barrier penetration. The minimal expression in normal tissues and lack of phenotype in -deficient mice underscore its potential as a low-toxicity therapeutic target. Together, these findings establish as a critical oncogenic driver in GBM and introduce a first-in-class inhibitor with strong translational promise for precision neuro-oncology. - Source: PubMed
Publication date: 2026/03/10
Xie ZhongqiuXie SophiaLi Hui - Photo-thermal stability is a key factor in pharmaceutical development, as light and heat can compromise drug safety and efficacy. Conventional methods such as HPLC, DSC, and GC-MS are slow, require complex pretreatment, and often treat photolysis and thermolysis separately. Here, we demonstrate microwave plasma torch mass spectrometry (MPT-MS) as a rapid, pretreatment-free approach for simultaneous analysis of photo-thermal stability and degradation pathways. Using direct desorption/ionization of intact tablets, six pharmaceuticals: chlorpheniramine, ornidazole, metronidazole, tinidazole, acetaminophen, and theophylline, were analyzed on average in 2 min with milligram-level sample consumption. Their stability order matched reported thermal decomposition data, validating the method. MPT-MS revealed unique photo-thermal fragmentation patterns, including nitroimidazole-specific [M + H-29] ions not accessible by electrospray ionization. The more MPT power the pharmaceutical molecules require to reach 80% abundance of the precursor ion, the more stable the pharmaceuticals are. The technique also resolved stability differences among isomers such as xylenes and nitrobenzenes. These results highlight MPT-MS as a powerful high-throughput tool for rapid screening of drug candidates, providing both stability ranking and mechanistic insight. - Source: PubMed
Publication date: 2026/02/24
Wang ShuanglongXie HuaxueLiu FengLobinski RyszardSzpunar JoannaDuan JizeWang BinDong XiaofengQiu ZidongZhang Xinglei