AMOT
- Known as:
- AMOT
- Catalog number:
- 001534A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- AMOT
Related genes to: AMOT
- Gene:
- AMOT NIH gene
- Name:
- angiomotin
- Previous symbol:
- -
- Synonyms:
- KIAA1071
- Chromosome:
- Xq23
- Locus Type:
- gene with protein product
- Date approved:
- 2002-01-24
- Date modifiied:
- 2014-11-19
Related products to: AMOT
Related articles to: AMOT
- Soluble CD146 (sCD146) is a key circulating biomarker released from vascular endothelial cells via enzymatic cleavage under conditions of stress or activation.sCD146 not only dynamically reflects the integrity of the microvascular endothelial barrier but also profoundly drives the malignant progression of multisystem diseases through targeted interactions with its receptors (such as angiopoietin AMOT and VEGFR2). In malignant solid tumors, it accelerates tumor invasion and immune evasion by inducing epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) phenotypes; In cardiovascular diseases and early-life developmental abnormalities (such as bronchopulmonary dysplasia), it serves as a highly sensitive marker of tissue stasis and microvascular stress. However, the clinical application of sCD146 currently faces substantial translational hurdles: on the one hand, the lack of a standardized, cross-platform detection system and universally accepted clinical-pathological cutoff values hinders data interoperability across centers; on the other hand, its baseline expression exhibits heterogeneity in complex complications, and whether it serves as a "key mediator" of disease progression or a "bystander" of concomitant injury remains inconclusive in certain pathological states. In light of this, this review breaks down disciplinary barriers to systematically summarize the latest medical advances regarding sCD146 across oncology, cardiovascular, neuroimmunology, and reproductive development fields. It clarifies the core pathogenic mechanisms of sCD146 in different microenvironments, addresses practical challenges in clinical translation, and provides a solid theoretical foundation to advance sCD146 from a laboratory biomarker to a clinical precision diagnostic and therapeutic target. - Source: PubMed
Publication date: 2026/07/20
Meng JuanDeng QiXu Shu-QiongChen PingHuang Dan-PingZeng ShengfengHuang Juan - Ischemic heart disease remains a leading cause of mortality worldwide. Although mesenchymal stem cell (MSC) transplantation offers a promising strategy for myocardial infarction, its therapeutic efficacy is limited by poor cell survival and insufficient regenerative capacity. Traditional Chinese medicine has been widely used to promote blood circulation and treat ischemic diseases. Chuanxiong-Chishao ( and ) is a commonly used herb pair for this purpose. This study aimed to investigate whether Chuanxiong-Chishao combined with MSCs could synergistically enhance angiogenesis after myocardial infarction. A rat model of myocardial infarction (MI) was established by permanent ligation of the left anterior descending coronary artery, and the animals were randomly assigned to the sham, model, MSCs, and Chuanxiong-Chishao combined with MSCs (CC-MSCs) groups. MSCs were injected intramyocardially immediately after ligation, and herbal treatment was administered for 28 days. Cardiac function was evaluated by echocardiography, myocardial fibrosis by Masson staining, and angiogenesis by CD31 immunofluorescence. Proteomic profiling was performed using label-free quantitative analysis, and key proteins were validated by Western blot. Compared with MSCs alone, CC-MSCs significantly improved left ventricular ejection fraction, fractional shortening, and cardiac output, reduced infarct size, and enhanced neovascularization in MI rats. Proteomic analysis identified 154 differentially expressed proteins between the model and CC-MSCs groups, and Gene Ontology enrichment analysis indicated significant activation of angiogenesis-related processes. Among these proteins, CDC42, NRP1, and AMOT were markedly altered, which was further confirmed by Western blot analysis. These findings suggest that Chuanxiong-Chishao enhances MSC-mediated angiogenesis and cardiac repair after MI, potentially through modulation of angiogenesis-related protein networks. - Source: PubMed
Publication date: 2026/07/29
Shi W LLiu S SWang YWang X ZGao H XQin NLu C QLu P F - Targeting the neuro-immune microenvironment to suppress triple-negative breast cancer (TNBC) represents a critical strategy in tumor immunotherapy. - Source: PubMed
Publication date: 2026/07/13
Li Fei-FeiHuang YanGao Chun-FangWu Chun-YuSun Chen-PingQin Yue-NongXie YingLiu ShengWu Huan-Gan - Resistance to 5-fluorouracil (5-FU) and oxaliplatin (OXA) remains an obstacle in colorectal cancer (CRC) therapy, but the upstream mechanisms enabling adaptive survival remain unclear. Angiomotin (AMOT), a Hippo-YAP regulator, is expressed as two major isoforms, p130 and p80, but the contribution of isoform-specific AMOT regulation to chemoresistance is unknown. RNA-seq of OXA-resistant cells identified AMOT as a candidate determinant, and its isoform-specific regulation and functional relevance were then examined in OXA- and 5-FU-resistant CRC sublines. AMOT-p80 was preferentially upregulated, whereas AMOT-p130 remained largely unchanged. Common AMOT pre-mRNA was elevated, whereas p130-specific pre-mRNA was unchanged, consistent with preferential transcriptional activation favoring the p80 isoform. Functionally, AMOT depletion minimally affected basal viability but significantly sensitized resistant cells to 5-FU or OXA, with increased apoptotic responses. AMOT silencing reduced nuclear YAP and lowered c-Myc and Cyclin D1 protein levels, whereas AMOT-p80 re-expression restored nuclear YAP, with recovery of c-Myc/Cyclin D1 levels and drug tolerance. YAP knockdown attenuated these outputs and blunted the additional effect of AMOT depletion. AMOT-p80 overexpression in parental cells increased c-Myc/Cyclin D1 protein levels and enhanced tolerance to 5-FU and OXA. These findings suggest that preferential AMOT-p80 upregulation is linked to YAP-associated chemoresistant phenotypes in CRC cells. - Source: PubMed
Publication date: 2026/05/22
Kim YehoHong Jin-KyungYeom MinaKim Min-JuWoo Jae-HyeonShin Joo-HoWon Tae HyungLee YunjongChoi Jeong-Yun - Sustained attention is often treated as a single, uniform construct, largely interchangeable with vigilance. We propose that sustained attention instead comprises two distinct yet complementary modes of engagement: an active mode, characterized by the need to process continuously changing task information, and a passive mode, defined by monitoring readiness under uncertainty. To test this hypothesis, participants completed two versions of a Multiple Object Tracking (MOT) task. In the Active-MOT (A-MOT), participants continuously tracked moving targets, and in the Passive-MOT (P-MOT), they relied on sustained monitoring until target identities were revealed (unpredictably) late in each trial. Behavioral performance and pupil diameter were recorded as proxies for engagement dynamics and arousal regulation, revealing clear dissociations between the two tasks. Behaviorally, the A-MOT was characterized by lower accuracy and greater sensitivity to task difficulty than P-MOT. These differences were likely driven by attentional engagement: Whereas the A-MOT was accompanied by sustained, load-dependent pupil dilation reflecting continuous cognitive effort, P-MOT yielded smaller phasic pupils punctuated by transient, load-modulated dilations at target assignment, signatures of reactive, event-driven engagement. Pretrial pupil size was larger in P-MOT, indicating heightened anticipatory arousal under uncertainty, but it predicted performance only in A-MOT, suggesting distinct preparatory engagement states. Together, these findings demonstrate that sustained attention operates through two separable modes governed by distinct arousal-control dynamics. Recognizing this dual-mode architecture reframes sustained attention not as a singular capacity to remain alert but as the flexible coordination of processing evolving task information and monitoring readiness across time and context. - Source: PubMed
Publication date: 2026/05/28
Del Sordo Giovanna CPapesh Megan HAlonso Carrillo MayteHout Michael C