AGTRAP antibody Polyclonal Antibodies Primary antibodies
- Known as:
- AGTRAP (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb100423
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- AGTRAP antibody Polyclonal Antibodies Primary antibodies
Related genes to: AGTRAP antibody Polyclonal Antibodies Primary antibodies
- Gene:
- AGTRAP NIH gene
- Name:
- angiotensin II receptor associated protein
- Previous symbol:
- -
- Synonyms:
- ATRAP
- Chromosome:
- 1p36.22
- Locus Type:
- gene with protein product
- Date approved:
- 2002-09-12
- Date modifiied:
- 2018-02-19
Related products to: AGTRAP antibody Polyclonal Antibodies Primary antibodies
Related articles to: AGTRAP antibody Polyclonal Antibodies Primary antibodies
- Angiotensin II Receptor-Associated Protein (AGTRAP) is markedly overexpressed in hepatocellular carcinoma (HCC) cases associated with poor prognosis; however, its precise functional role remains inadequately elucidated. - Source: PubMed
Publication date: 2026/04/23
Liu ShanshanLi ZhenghangLiu HongqingChen XinyuLiu YilinTang JunChen YanlinZeng Dan - Multiple complex mechanisms link type 2 diabetes mellitus (T2DM) with the pathogenesis, development, and progression of pancreatic cancer (PC). This study aims to elucidate these complex relationships using cross-disease co-expression analysis of PC and T2DM. Transcriptomic data from peripheral blood samples of patients with pancreatic ductal adenocarcinoma (PDAC), PDAC patients with diabetes (DP), patients with diabetes mellitus (DM), and healthy controls were analyzed. Following differential expression analysis (DEA), four disease-specific gene co-expression networks were constructed using weighted gene co-expression network analysis (WGCNA). Pearson correlation analysis was then applied to identify modules significantly associated with each clinical trait. In the experimental phase, peripheral blood samples from 20 PDAC patients, 20 DP patients, 20 DM patients, and 20 healthy controls were included. The co-expression network analysis identified modules highly associated with PDAC, DP, and DM. Among the 11 overlapping genes shared between these modules, the high-confidence hub genes , , and were selected for quantitative real-time PCR (qPCR) validation. Comparative analysis of expression among the four study groups showed significantly higher expression in the PDAC group than in the DM group (p < 0.01) and healthy controls (p < 0.0001). Similarly, expression was significantly elevated in the DP group compared with the DM group (p < 0.01) and healthy controls (p < 0.0001). The survival analysis also suggests that high expression is a favorable prognostic biomarker. - Source: PubMed
Publication date: 2026/03/31
Dehghanian FaribaKhalilian SheydaMousavian ZaynabAlavi ShahryarBahreini Amin - There is an urgent need for actionable therapeutic targets for glioma. Angiotensin II receptor-associated protein (AGTRAP) is upregulated in glioma, but its functional role and downstream programs remain insufficiently defined. This study aimed to clarify the clinical relevance, biological function, and mechanism of AGTRAP in glioma. - Source: PubMed
Chen SiyuLi YuntaoNie XiaohuZhang YonggangChen QianxueXiong XiaoxingSu ZhongzhouQiu Sheng - Arterial aging is associated with enhanced angiotensin II (Ang II) signaling via Ang II type 1 receptor (AT1R) and with microRNA-34a (miR-34a) increased expression. AT1R-associated protein (ATRAP/Agtrap) binds to AT1R, promotes its internalization, and inhibits Ang II signaling. This study addresses the hypothesis that miR-34a targets ATRAP/Agtrap and enhances Ang II pro-inflammatory signaling via AT1R in arterial vascular smooth muscle cells (VSMC). Our results show that miR-34a exhibits an age-associated increase in Rhesus monkey's common carotid artery and rat aorta. Further, AGTRAP protein expression is lower in old rat VSMC and in old mice aorta. Ang II enhances miR-34a in old rat VSMC and human aortic smooth muscle cells (HASMC), and inhibits AGTRAP and sirtuin 1 (SIRT1) mRNA/protein expression. In miR-34a-overexpressing HASMC, AGTRAP and SIRT1 mRNA/protein decrease, and these effects are rescued by AGTRAP forced expression. Moreover, miR-34a directly targets AGTRAP and AGTRAP downmodulation further enhances miR-34a expression decreasing SIRT1 in HASMC. Finally, Ang II and miR-34a induce the upregulation of pro-inflammatory genes, interleukin (IL)-6, cyclooxygenase 2 (COX2), monocyte chemoattractant protein-1 (MCP-1), and milk fat globule-epidermal growth factor 8 (MFGE8) in HASMC, and this effect is abolished by AGTRAP forced expression. In conclusion, Ang II upregulates miR-34a, activating a negative feedback loop on AGTRAP that reinforces Ang II signaling. The age-associated AGTRAP downmodulation in central arteries and VSMC underlies a potential miR-34a/AGTRAP role in vascular aging. - Source: PubMed
Publication date: 2025/11/26
Florio Maria CristinaSileno SaraJiang LiqunD'Agostino MarcoSyed Sunayana BegumMonteonofrio LauraBaranzini MirkoPrampolini ChiaraMacrì FedericaCasaburo ManuelFanotti NadiaCastiglione StefaniaMonticone Robert EZiman BruceTelljohann RichardWang MingyiMattison Julie AMorrell Christopher HRaucci AngelaLakatta Edward GMagenta AlessandraColognesi-Capogrossi Maurizio - Chronic kidney disease generally progresses to irreversible fibrosis through chronic inflammation and age-related changes. We had previously reported that genetic knockdown of angiotensin II type 1 receptor (AT1R)-associated protein (ATRAP) exacerbates aging-associated kidney tubulointerstitial fibrosis in mice. However, whether enhanced ATRAP expression can suppress renal fibrosis and senescence in vivo remains unknown. Recently, we proposed that aristolochic acid nephropathy (AAN) could be used for modeling kidney aging with fibrosis. The present study aimed to investigate the functional role of ATRAP in aging-associated kidney fibrosis and inflammation using ATRAP transgenic (Tg19) mice subjected to AAN. AA administration caused histological renal fibrosis and enhanced ATRAP expression had no apparent effect on AA-induced renal fibrosis. However, enhanced ATRAP expression significantly suppressed AA-induced macrophage infiltration concomitant with reductions in inflammation-related, macrophage-related and senescence-related gene expression in the kidneys. Furthermore, the renal expression of anti-aging gene (Klotho, Sirtuin1) was significantly reduced in control mice in response to AA administration, whereas AA-mediated downregulation of Sirtuin1 expression was tendentially less prominent in Tg19 mice. Collectively, the enhancement of ATRAP expression failed to ameliorate renal fibrosis but partially attenuated renal inflammation and cellular senescence in AAN. Thus, ATRAP is a potential therapeutic target against renal inflammation and senescence. - Source: PubMed
Publication date: 2025/07/31
Furuta RikaUrate ShingoWakui HiromichiUehara TatsukiTsukamoto ShunichiroTaguchi ShinyaMorita RyutaroOkami NaohitoYamashita AkioAzushima KengoTamura Kouichi