PTX3 Polyclonal Antibody
- Known as:
- PTX3 Polyclonal Antibody
- Catalog number:
- a-0489-050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Epigentek inc
- Gene target:
- PTX3 Polyclonal Antibody
Ask about this productRelated genes to: PTX3 Polyclonal Antibody
- 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: PTX3 Polyclonal Antibody
Related articles to: PTX3 Polyclonal Antibody
- Osteoarthritis (OA) is a degenerative musculoskeletal disease of multifactorial origin causing chronic disability, despite numerous treatment options for which there are no predictive biomarkers on the different endotypes. We aimed at defining a peripheral blood (PB) profile potentially predictive of early and sustained response to intra-articular injection of autologous platelet-rich plasma (PRP). - Source: PubMed
Publication date: 2026/09/04
Granata ValentinaTonutti AntonioMarrella VeronicaCamisaschi ChiaraPuccio SimoneSconza CristianoMonferini MarziaRani NicolaFilardo GiuseppeDi Matteo BerardoSelmi CarloMorenghi EmanuelaSobacchi CristinaCeribelli Angela - Arbovirus infections are emerging or re-emerging global health threats due to their raised incidence and geographical spread in endemic regions, as well as the increased risk of local transmission in non-endemic areas. When symptomatic, arboviral infections usually manifest as acute febrile illnesses (AFI) accompanied by mild, often non-specific symptoms. This non-specific clinical presentation contributes to their misdiagnosis, leading to adverse effects at both the patient and public health levels. Leveraging the potential of host biomarkers as fever triage tools, we assessed their utility for the early identification of arbovirus-associated AFI. - Source: PubMed
Publication date: 2026/09/03
Tiberti NataliaBertoli GiuliaMazzi CristinaVezzelli ElisabettaSanfilippo LorenzaValerio MatteoAncillotti LeonardoAccordini SilviaPiubelli ChiaraBuonfrate DoraCastilletti ConcettaGobbi Federico Giovanni - Cumulus expansion is important for oocyte maturation, but its molecular regulation in yak remains unclear. This study examined the association of Yes-associated protein 1 (YAP1) with cumulus expansion-related and autophagy-related molecular markers in cumulus cells isolated from yak cumulus-oocyte complexes collected from ovarian follicles. YAP1 was overexpressed or knocked down, and YAP1-overexpressing cultures were additionally treated with 3-methyladenine (3-MA). Transcript abundance was assessed by RT-qPCR and interpreted descriptively, whereas protein abundance was evaluated by Western blotting; representative immunofluorescence and mCherry-GFP-LC3B images were also examined. YAP1 overexpression significantly increased HAS2 and PTGS2 protein abundance, while PTX3 and TNFAIP6 showed non-significant upward trends; YAP1 knockdown significantly reduced all four proteins. YAP1 manipulation was also associated with changes in Beclin-1, ATG5, p62, and the LC3B-II/LC3B-I ratio. Compared with YAP1 overexpression alone, 3-MA co-treatment significantly reduced HAS2, PTGS2, PTX3, TNFAIP6, Beclin-1, and ATG5, increased p62, and numerically reduced the LC3B-II/LC3B-I ratio without statistical significance. These findings support an association between YAP1 and cumulus expansion-related molecular programs and are consistent with partial involvement of 3-MA-sensitive, autophagy-associated signaling. Direct functional assays and pathway-specific validation are required to establish causality. - Source: PubMed
Publication date: 2026/08/22
Zhang TiantianWang MengMa XinLu TingtingZuo QiyongZhang QianWang LibinPan Yangyang - Anthracycline-based chemotherapy improves breast cancer outcomes but may cause cancer therapy-related cardiac dysfunction (CTRCD). Biomarkers reflecting inflammatory and metabolic myocardial stress may complement imaging surveillance, but the combined value of galectin-9 (Gal-9), fatty-acid-binding protein 4 (FABP4) and pentraxin-3 (PTX-3) is unclear. - Source: PubMed
Publication date: 2026/08/26
Ma JinchengMa ZhiqiangCheng YanhuiLi XiaoyunSong HuiqingWang Shuai - Adolescent depression shows marked heterogeneity in symptom severity, yet mechanisms linking early-life adversity to severe depressive presentations remain unclear. Childhood maltreatment may induce persistent alterations in immune and stress-regulatory systems, increasing vulnerability to severe depression. This study examined whether childhood adversity, circulating biomarkers, and recent stress contribute to differences between severe and non-severe adolescent depression. Seventy adolescents with depressive disorder were classified into severe (SD, n = 40, HAMD-17 ≥ 24) and non-severe (NSD, n = 30, HAMD-17 < 24) groups, along with 39 healthy controls (HC). Childhood maltreatment was assessed using the Maltreatment and Abuse Chronology of Exposure (MACE), and recent stress using the Adolescent Life Events Scale. Serum levels of Pentraxin-3 (PTX3), S100B, matrix metalloproteinases (MMP-8, MMP-9), FKBP5, oxytocin, epidermal growth factor, and APCDD1 were measured by enzyme-linked immunosorbent assays. Adolescents with SD reported significantly higher childhood maltreatment than those with NSD. PTX3 and FKBP5 levels were significantly elevated in the severe group compared with both non-severe patients and HC and were positively associated with symptom severity. Receiver operating characteristic analyses showed that childhood maltreatment had good discriminative ability for depressive severity, whereas PTX3 and FKBP5 showed moderate discriminative performance. Multivariable logistic regression identified childhood maltreatment and PTX3 as independent predictors of SD. Hierarchical regression showed that recent life stress explained additional variance in self-reported symptom severity and partly attenuated the associations of early adversity and inflammatory markers. These findings suggest that severe adolescent depression represents a clinically defined severity stratum associated with neuroimmune alterations in the context of childhood adversity and recent life stress, rather than a discrete biological subtype. - Source: PubMed
Publication date: 2026/09/08
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