Ask about this productRelated genes to: Amigo2 Blocking Peptide
- Gene:
- AMIGO2 NIH gene
- Name:
- adhesion molecule with Ig like domain 2
- Previous symbol:
- -
- Synonyms:
- ALI1, DEGA
- Chromosome:
- 12q13.11
- Locus Type:
- gene with protein product
- Date approved:
- 2005-06-23
- Date modifiied:
- 2016-07-04
Related products to: Amigo2 Blocking Peptide
Related articles to: Amigo2 Blocking Peptide
- Pancreatic adenocarcinoma (PAAD), the predominant form of pancreatic cancer, is highly aggressive and refractory to current therapies. The Amphoterin-Induced Gene and ORF (AMIGO) family encodes three structurally related type I transmembrane proteins (AMIGO1-3) containing leucine-rich repeat and immunoglobulin-like domains, which mediate cell adhesion and signaling. Although AMIGO proteins have been implicated in neural development and tumor progression, their functional relevance in PAAD remains unclear. Here we identify AMIGO2 as a key driver of PAAD progression through integrated transcriptomic, proteomic, and functional analyses. Multi-cohort datasets (ONCOMINE, TCGA) and immunohistochemistry revealed marked AMIGO2 overexpression in PAAD tissues, with recurrent genetic alterations (~11%) and strong association with poor relapse-free and overall survival. Functional enrichment of AMIGO2-correlated genes indicated activation of focal adhesion and PI3K/AKT signaling. Consistently, inhibition of AMIGO2 expression in pancreatic cancer cells reduced migration and invasion while restoring E-cadherin expression, indicating inhibition of epithelial mesenchymal transition. Protein profiling from the Human Protein Atlas further confirmed elevated AMIGO2 expression in tumors. Together, these findings demonstrate that AMIGO2 promotes PAAD aggressiveness by enhancing adhesion- and EMT-associated pathways, establishing it as a potential prognostic biomarker and therapeutic target in pancreatic cancer. - Source: PubMed
Publication date: 2026/01/14
Chen Ze-SyuanChang Tsung-ShunShen Wan-JouLiu Shan-JuWang Chih-YangLee Yung-KuoHsu Wen-HsinWang Wei-Jan - Pyramidal cells (PCs) of hippocampal area CA2 exhibit increased excitability in temporal lobe epilepsy (TLE) and in mouse models of TLE. In epileptic mice, selective inhibition of CA2 PCs reduces chronic seizures. Here we asked if activating CA2 PCs increases seizures. Mice expressing Cre recombinase in CA2 PCs (-Cre mice) were injected with the convulsant pilocarpine to induce a period of severe seizures (, SE), which leads to chronic seizures after 3-4 weeks (epilepsy). Epileptic mice were injected with a Cre-dependent adeno-associated virus (AAV) to express an excitatory designer receptor exclusively activated by designer drug (eDREADD; hM3Dq) in dorsal CA2 bilaterally and implanted with subdural EEG electrodes. After recovery, mice were recorded continuously using video and EEG for 6 weeks, 3 weeks with drinking water containing the eDREADD activator clozapine-N-oxide (CNO) and 3 weeks without CNO. CA2 activation with CNO caused a significant increase in seizure frequency and duration. Seizures occurred in clusters (many seizures per day over several consecutive days) and mice given water with CNO had a greater maximum number of seizures per day during a cluster compared to water without CNO. CNO had no significant effect in control mice. In naïve -Cre mice expressing hM3Dq, pre-treatment with CNO before pilocarpine administration shortened the latency to SE and increased EEG power at the start of SE. Taken together with prior findings, the results suggest that CA2 is a control point for regulating seizures in the pilocarpine mouse model of TLE. - Source: PubMed
Publication date: 2025/12/29
LaFrancois John JKennedy MeghanRathod MonarchsinhSantoro BinaLisgaras Christos PanagiotisSiegelbaum Steven AScharfman Helen E - Pyramidal cells (PCs) of hippocampal area CA2 exhibit increased excitability in temporal lobe epilepsy (TLE) and in mouse models of TLE. In epileptic mice, selective inhibition of CA2 PCs reduces chronic seizures. Here we asked if activating CA2 PCs increases seizures. Mice expressing Cre recombinase in CA2 PCs (Amigo2-Cre mice) were injected with the convulsant pilocarpine to induce a period of severe seizures (status epilepticus, SE), which leads to chronic seizures after 3-4 weeks (epilepsy). Epileptic mice were injected with a Cre-dependent adeno-associated virus (AAV) to express an excitatory designer receptor exclusively activated by designer drug (eDREADD; hM3Dq) in dorsal CA2 bilaterally and implanted with subdural EEG electrodes. After recovery, mice were recorded continuously using video and EEG for 6 weeks, 3 weeks with drinking water containing the eDREADD activator clozapine-N-oxide (CNO) and 3 weeks without CNO. CA2 activation with CNO caused a significant increase in seizure frequency and duration. Seizures occurred in clusters (many seizures per day over several consecutive days) and mice given water with CNO had a greater maximum number of seizures per day during a cluster compared to water without CNO. CNO had no significant effect in control mice. In naïve Amigo2-Cre mice expressing hM3Dq, pre-treatment with CNO before pilocarpine administration shortened the latency to SE and increased EEG power at the start of SE. Taken together with prior findings, the results suggest that CA2 is a control point for regulating seizures in the pilocarpine mouse model of TLE. - Source: PubMed
Publication date: 2026/01/03
LaFrancois John JKennedy MeghanRathod MonarchsinhSantoro BinaLisgaras Christos PanagiotisSiegelbaum Steven AScharfman Helen E - Extensive studies have demonstrated the relationship between metabolic reprogramming and the tumor microenvironment. Here, we characterized the head and neck squamous cell carcinoma (HNSCC) evolutionary landscape using spatial metabolomics/transcriptomics, single-cell transcriptomics, and bulk multi-omics. Metabolic heterogeneity during HNSCC malignant transformation was identified, with significant enrichment in the purine metabolism. Integrating single-cell and bulk data, we developed a robust ligand-receptor-based signature (LRS) linked to NT5E, a key upstream regulator of purine metabolism, which served as an independent prognostic indicator. The low LRS subtype was associated with a high proportion of immune cell infiltration and improved response to immunotherapy. Notably, in vitro and in vivo experiments demonstrated that AMIGO2, a core molecule within the LRS, regulates tumor-associated purine metabolism, and that its downregulation suppresses tumor cell invasion and migration, inhibits myofibroblast differentiation, and promotes immune effector cell infiltration. Moreover, combining AMIGO2 targeting with anti-PD-1 therapy yielded superior efficacy. Consistent validation was also obtained in a clinical cohort of HNSCC and premalignancy patients. - Source: PubMed
Publication date: 2025/11/18
Liu GanYao XinfengHou YuchenDeng WentaoZhang LiyuLi ShutongHuang PanpanChang WenjiaoHuang HaiyanShi LanZhou QianqianWang YanqingChen JiaGu WenchaoMa XiaolingZhou YuLiu HonghongZhang ShanshanYang Zongcheng - - Source: PubMed
Publication date: 2025/10/23
Nasti AlessandroAyers DuncanSeki Akihiro