TNFAIP5 antibody Polyclonal Antibodies Primary antibodies
- Known as:
- TNFAIP5 (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb100676
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- TNFAIP5 antibody Polyclonal Antibodies Primary antibodies
Related genes to: TNFAIP5 antibody Polyclonal Antibodies Primary antibodies
- Gene:
- PTX3 NIH gene
- Name:
- pentraxin 3
- Previous symbol:
- TNFAIP5
- Synonyms:
- TSG-14
- Chromosome:
- 3q25.32
- Locus Type:
- gene with protein product
- Date approved:
- 1993-11-08
- Date modifiied:
- 2016-10-05
Related products to: TNFAIP5 antibody Polyclonal Antibodies Primary antibodies
Related articles to: TNFAIP5 antibody Polyclonal Antibodies Primary antibodies
- In ischemic heart failure, the biological mechanisms underlying the benefits of mesenchymal stromal cells (MSCs) and c-kit-positive cardiac progenitor cells (CPCs) remain incompletely understood. - Source: PubMed
Publication date: 2026/04/20
Chacon-Alberty LourdesTan XinLi MengTang Xian-LiangHochman-Mendez CamilaBolli Roberto - Alpha-fetoprotein (AFP) is the most widely used biomarker for hepatocellular carcinoma (HCC) diagnosis; however, its sensitivity is limited, especially for early-stage disease and in AFP-negative HCC cases. Pentraxin-3 (PTX3), a marker of local inflammation and angiogenesis, may outperform AFP in detection by reflecting distinct biological pathways involved in hepatocarcinogenesis. - Source: PubMed
Publication date: 2026/04/14
Amdetsion Gedion YilmaMurali Arvind RPan Chun-WeiMiranda CliveSueldo AlexandraTebeje Hiwot GebeyehuGuifarro DanielKwei-Nsoro RobertKotwal Vikram - DRG adhesion is a key pathological feature of failed back surgery syndrome and a major cause of neuropathic pain. DRG, or epidural adhesion, commonly results from spinal surgery, leakage of disk material into the epidural space, or inflammation. To better mimic this clinical condition, we developed a novel and reliable animal model of DRG adhesion-induced neuropathic pain. Using this model, we investigated the therapeutic potential and underlying mechanisms of CLARIX FLO, a sterile, particulate human amniotic membrane and umbilical cord tissue product. Our results demonstrate that CLARIX FLO exerts significant analgesic and anti-inflammatory effects in the DRG adhesion model. The application of CLARIX FLO to the injured DRG markedly attenuated mechanical allodynia. CLARIX FLO treatment also reduced outer sheath thickening, suppressed the inflammatory microenvironment, and decreased hypersensitivity of isolectin B4-positive neurons. Mechanistically, CD44 was identified as a potential downstream mediator of CLARIX FLO. Furthermore, a high dose of HC-HA/PTX3, the key bioactive component of CLARIX FLO, effectively reversed mechanical allodynia and inflammation. Notably, CLARIX FLO inhibited the overexpression of TNF-α and TRPV1 adhering to the DRG. In this study, we demonstrated that CLARIX FLO effectively alleviates DRG adhesion-induced neuropathic pain through a CD44-TRPV1-dependent mechanism. - Source: PubMed
Publication date: 2026/03/28
Kung Chia-ChiDai Shih-PingTu Chao-ChiangTsai Tsung-AnChen Po-HengSung Chao-HsienFu Chun-HsienLiu Jen-HaoChen Chih-Li - Epithelial-mesenchymal transition (EMT) plays a critical role in tumor progression; however, the underlying molecular mechanisms of EMT in papillary thyroid carcinoma (PTC) remain incompletely understood. This study aimed to investigate EMT-related mechanisms in PTC using an integrative approach combining single-cell RNA sequencing and machine learning. - Source: PubMed
Xu TianfengSun RuonanZhang YujieZheng Xun - Acquired cognitive impairments occur in diverse neurological and psychiatric conditions, yet the mechanisms linking neural circuit activity to neurovascular function remain poorly understood. Using a mouse model of nicotine withdrawal (WD), we identified an activity-dependent NEPAS-pentraxin-3 (PTX3) axis in mPFC neurons that couples circuit hypoactivity to cognitive deficits. In this model, NEPAS expression is significantly upregulated in mPFC neurons, accompanied by reduced myelin formation. Neuronal activity in mPFC and PVA is suppressed and chemogenetic activation of the PVA-mPFC neural circuit downregulates NEPAS. Elevated neuronal NEPAS suppresses the secretion of PTX3, thereby impairing angiogenesis. Conversely, knockdown of neuronal NEPAS restores PTX3 expression and angiogenesis, alleviates myelin formation deficits, and improves cognitive memory following nicotine WD. Notably, activation of the PVA-mPFC neural circuit produces similar therapeutic effects. Human transcriptomic data reveal a consistently elevated HIF-3α expression in ex-smokers versus controls. Our findings demonstrate that the NEPAS-PTX3 axis in mPFC neurons links neural circuit hypoactivity to neurovascular and myelin deficits, providing a mechanistic framework for acquired cognitive impairment. This pathway represents a potential target for neuromodulation-based therapies in prefrontal circuit dysfunction associated cognitive disorders. - Source: PubMed
Publication date: 2026/04/07
Hu BoyaChen ZifeiSun BingmeiGao JialeXu JialeGuo XiaochunGao FenfeiWang ZhongsiWu JieJi XiaoyuLiu PeipeiHuang Bing