AMIGO2
- Known as:
- AMIGO2
- Catalog number:
- 001527A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- AMIGO2
Related genes to: AMIGO2
- 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
Related articles to: AMIGO2
- A variant in the patatin-like phospholipase domain-containing protein 3 (PNPLA3) was reported to be related to metabolic-associated fatty liver disease. However, the mechanism by which this variant leads to liver fibrosis has not been unveiled yet. Using induced pluripotent stem cell (iPSC)-derived hepatic stellate cells (iHSC) containing a single nucleotide polymorphism (SNP) within PNPLA3, this study sought to clarify the mechanism through which this PNPLA3 SNP induces liver fibrosis. - Source: PubMed
Toshida KatsuyaTakeishi KazukiItoh ShinjiKurihara TakeshiMotomura TakashiIshikawa TakumaIwasaki HitoshiMita JunyaNakayama YukiTomiyama TakahiroIseda NorifumiFlorentino Rodrigo MToshima TakeoSoto-Gutierrez AlejandroYoshizumi Tomoharu - Pancreatic ductal adenocarcinoma (PDAC) carries an extremely poor prognosis. Excessive lactate accumulation occurs in the hypoxic tumor microenvironment, yet the roles of lactate receptor GPR81 and adhesion molecule AMIGO2 and their crosstalk in PDAC remain unclear. This study applied PDAC data from TCGA/GTEx databases, 83 clinical samples from Zhongda Hospital, CFPAC1/CAPAN2/CAPAN1 cell lines, and BALB/c-nu nude mouse models. Lactate levels were detected; Expression of GPR81, AMIGO2 and related molecules were measured by qPCR, IHC and Western Blot. GPR81/AMIGO2 were regulated via lentivirus, siRNA or plasmid transfection. Cell functions and tumorigenesis were evaluated by CCK-8, wound-healing, Transwell and in vivo assays. RNA-seq and enrichment analyses screened differential genes; Cox regression and nomogram assessed the prognostic value of AMIGO2. Lactate concentration and GPR81 expression were significantly increased in PDAC and correlated with poor prognosis. High-lactate conditions upregulated GPR81 expression under both energy deficiency and normal energy supply conditions. GPR81 knockdown inhibited PDAC cell proliferation, migration and tumorigenicity, whereas overexpression showed the opposite effects independently of lactylation. GPR81 activated the TGFβ2-pSMAD2/3-ZEB1 pathway by upregulating AMIGO2, and AMIGO2 rescued the inhibitory effects caused by GPR81 knockdown. AMIGO2 was highly expressed in PDAC and acted as an independent prognostic factor. The prognostic model combining AMIGO2 and TNM staging system showed superior predictive accuracy. Our results elucidate that AMIGO2 mediates lactate-GPR81-driven PDAC progression through the TGFβ2-pSMAD2/3-ZEB1 signaling cascade. AMIGO2 is an independent prognostic factor for PDAC, and its integration with the TNM staging system yields a preliminary prognostic model with improved predictive performance in our single-center cohort. - Source: PubMed
Publication date: 2026/05/27
Zhang QiannanWang LishanYu ZeqianXu TongleiTang JiapingZhu ZhuZhou Jiahua - 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