AEBP1 Pre-design Chimera RNAi
- Known as:
- AEBP1 Pre-design Chimera RNAi
- Catalog number:
- H00000165-R01
- Product Quantity:
- 10 nmol
- Category:
- -
- Supplier:
- Abno
- Gene target:
- AEBP1 Pre-design Chimera RNAi
Related genes to: AEBP1 Pre-design Chimera RNAi
- Gene:
- AEBP1 NIH gene
- Name:
- AE binding protein 1
- Previous symbol:
- -
- Synonyms:
- ACLP
- Chromosome:
- 7p13
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-06
- Date modifiied:
- 2016-10-05
Related products to: AEBP1 Pre-design Chimera RNAi
Related articles to: AEBP1 Pre-design Chimera RNAi
- The vascular system is the largest organ in the body and underlies most chronic diseases, yet the molecular mechanisms that govern its plasticity remain poorly defined. - Source: PubMed
Publication date: 2026/08/13
Amrute Junedh MJiang LihuaBolar NikhitaHiga KellyZhu ChenchenJian RuiqiKim JenniferDuda MatthewPuaala Anna MarieKlinder AvaniDalal AlexPedroza Albert JReinhardt Dieter PCheng PaulSnyder Michael PFischbein Michael P - Cytokines play an important role in modulating the tumor microenvironment (TME) in glioblastoma multiforme (GBM). However, little work has focused on developing a prognostic model for GBM using cytokine signatures. - Source: PubMed
Publication date: 2026/07/28
Zhang LongxiaoYan XinyangZhou YunfeiYang ZhongboJiang LiangchaoShen YiLi JiaxiSong Jinning - Inflammation and fibrosis can arise as consequences of cardiac injury and further contribute to the progression of heart failure (HF) and arrhythmias. Despite ongoing therapeutic advancements, effective treatments to modulate these pathological processes remain limited. To overcome these limitations, we developed a multifunctional nanotherapeutic system using apoptotic mesenchymal stem cell-derived nanovesicles (ANV) as biocompatible and immunomodulatory delivery platforms for small interfering RNA (siRNA) targeting the adipocyte enhancer binding protein 1 (AEBP1). ANV are constructed via an extrusion method and loaded with AEBP1-targeting siRNA (siAEBP1) through electroporation to form ANV-siAEBP1. The vesicles are then incubated with antibody-conjugated iron oxide magnetic nanoparticles (MNP), forming the ANVP-siAEBP1 complex. For targeted delivery to the injured myocardium, an anti-myosin light chain 3 (MLC3) antibody is incorporated, based on injury-associated MLC3 exposure for localized accumulation of ANVP-siAEBP1 at the injury site. Upon localization, intracellular release of siAEBP1 silences AEBP1 expression, downregulates pro-fibrotic signaling, and mitigates cardiac fibrosis. Simultaneously, the intrinsic anti-inflammatory effects of ANV prevent excessive inflammatory responses. This dual mechanism of action results in synergistic therapeutic effects, significantly attenuating both inflammation and fibrosis with enhanced targeting efficiency. Collectively, this engineered four-in-one nanovesicle platform offers a promising strategy for next-generation precision therapeutics in cardiac injury. STATEMENT OF SIGNIFICANCE: Cardiac injury often leads to heart failure, yet current therapies lack precise targeting and long-term effectiveness. Here, we develop a multifunctional nanocarrier system that enables targeted delivery of siRNA to injured cardiac tissue. This system combines nanoscale engineering with biological functionality, allowing gene regulation that reduces inflammation and fibrosis. By silencing adipocyte enhancer-binding protein 1 (AEBP1) via siRNA, our platform suppresses fibrosis and improves cardiac function in vivo, further supported by the inflammation-regulating properties of the nanovesicle. This work demonstrates how engineered biomaterials can be designed to control cellular responses and disease progression, offering a promising strategy for targeted gene therapy and cardiac repair. - Source: PubMed
Publication date: 2026/08/08
Yoo GyeongseoKang Ji-YoungPark MalgeumLee JaewoongMun DasomYun NuriJoung Boyoung - The occurrence of hepatic fibrosis (HF) is closely related to the activation of hepatic stellate cells (HSCs), but the epitranscriptional regulatory mechanisms involved have not been fully elucidated. This study aims to explore the role and molecular mechanisms of the m6A reader protein IGF2BP2 in HSC activation and HF. - Source: PubMed
Publication date: 2026/07/27
Hu YouwenXiao Yangyang - Persistent activation of cardiac fibroblasts into myofibroblasts drives excessive extracellular matrix deposition, leading to maladaptive myocardial fibrosis, adverse remodeling and heart failure (HF) progression. Adipocyte enhancer binding protein 1 (AEBP1) and Aortic carboxypeptidase-like protein (ACLP, full-length AEBP1 protein coded by ) has been implicated in pathological fibrosis across multiple organs, with tissue-specific knockdown attenuating fibrosis in preclinical models. Although elevated expression has been associated with human HF, its role in myocardial fibrosis progression in vivo remains undefined. Here, we demonstrated that is a critical mediator of myocardial fibrosis and adverse cardiac remodeling. Fibroblast-specific knockout and cardiac-specific knockdown of significantly improved cardiac function and prevented pathological remodeling in murine models of myocardial ischemia and pressure-overload induced injury. In ex vivo human myocardial tissue culture studies, ACLP overexpression in non-failing hearts induced pathological remodeling, whereas knockdown in failing human hearts induced structural reverse remodeling. Mechanistically, we also showed that ACLP regulates key pro-fibrotic transcription factors and genes, including MRTFB, RUNX2, SM22 and COL1A1, thereby orchestrating fibroblast activation. Collectively, these findings establish as a central driver of myocardial fibrosis and highlights its inhibition as a promising therapeutic strategy to mitigate both acute and chronic HF. - Source: PubMed
Publication date: 2026/05/26
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