Human Polyclonal P4HB Ab
- Known as:
- Human Polyclonal P4HB Antibody
- Catalog number:
- a0692
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ABclonal
- Gene target:
- Human Polyclonal P4HB
Related genes to: Human Polyclonal P4HB Ab
- Gene:
- P4HB NIH gene
- Name:
- prolyl 4-hydroxylase subunit beta
- Previous symbol:
- PO4DB, ERBA2L
- Synonyms:
- PDIA1, PROHB, DSI, GIT, PDI, PO4HB, P4Hbeta
- Chromosome:
- 17q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-10-05
Related products to: Human Polyclonal P4HB Ab
Related articles to: Human Polyclonal P4HB Ab
- Poor repair outcomes of abdominal wall soft tissue defects often lead to hernia recurrence and tissue adhesion, thereby increasing the medical burden. An ideal repair material should simultaneously fulfill the requirements of anti-adhesion properties, wet tissue adhesion capability, biodegradability, and the ability to promote functional tissue regeneration. Herein, inspired by the natural abdominal wall architecture, we designed a biomimetic Janus-structured repair patch, denoted as PS-PDH. This patch integrates a biodegradable poly(4-hydroxybutyrate) (P4HB) electrospun fibrous membrane with a glutathione-responsive degradable poly(sulfobetaine methacrylate) (PSBMA) hydrogel via polydopamine (PDA). It exhibits excellent asymmetric adhesive properties: the fibrous side facilitates cell adhesion and proliferation, while the hydrogel side effectively resists cell and protein adhesion. Furthermore, PS-PDH possesses robust mechanical properties, enabling it to adapt to dynamic tissue deformation. Notably, the patch effectively scavenges free radicals and intracellular reactive oxygen species (ROS), while promoting macrophage polarization from the pro-inflammatory M1 to the pro-regenerative M2 phenotype. In a mouse full-thickness abdominal wall defect model, PS-PDH effectively prevented postoperative adhesion and fibrosis, modulated the inflammatory microenvironment, and promoted functional muscle and vascular regeneration. Therefore, this biomimetic Janus-structured patch offers a reliable and highly clinically translatable strategy for the functional repair of abdominal wall soft tissue defects. - Source: PubMed
Publication date: 2026/06/10
Wang MingPan WenjieLi JiaqiGao YuanChen JiaweiDing ZhenshanZhang YuYu QingsongGan ZhihuaLi ZhiboJiang Ni - Osteosarcoma (OS) is a primary bone malignancy, and its progression can be hindered by inducing programmed cell death (PCD). Protein disulfide-isomerase (PDI) regulates cancer cell death; however, its functional role in OS remains unclear. P4HB expression was assessed in tumor tissues and cells from patients with OS using RT-qPCR. The effects of P4HB on OS cell lines were evaluated. Western blotting was used to assess the impact of P4HB on various forms of PCD (apoptosis, ferroptosis, and pyroptosis). Bioinformatics analysis identified the upstream and downstream mechanisms of P4HB in OS progression. A xenograft tumorigenesis study was performed to elucidate the role and mechanism of P4HB in OS progression. Elevated P4HB expression was observed in OS tissue samples and cell lines. Downregulation of P4HB suppressed OS cell growth, migration, and invasiveness and induced PCD. Functional enrichment analysis and experimental validation revealed that PDI upregulated vascular endothelial growth factor A (VEGFA) vascular endothelial growth factor receptor 2 (VEGFR2) signaling. Methylation analysis showed that the m6A demethylase fat mass and obesity-associated protein (FTO) decreased P4HB m6A levels and enhanced VEGFA-VEGFR2 signaling in OS cells. Moreover, FTO overexpression enhanced the proliferative, migratory, and invasive capabilities of OS cells and decreased PCD. Finally, FTO knockdown inhibited tumor growth and lung metastasis of OS by decreasing the activity of the PDI/VEGFA-VEGFR2 signaling axis. Mechanistically, FTO-mediated m6A modification of P4HB regulates PCD in OS through activation of this axis. © 2026 The Pathological Society of Great Britain and Ireland. - Source: PubMed
Publication date: 2026/06/05
Wang JiashiHao YingyingHe MingZhou Weizheng - Surgical meshes have transformed the repair of hernias and pelvic organ prolapse, advancing from conventional suture methods, which demonstrated elevated recurrence rates, to efficient, tension-free prosthetic alternatives. This review examines the fabrication methods of various mesh types, their classification, and their efficacy in clinical environments. This discussion encompasses novel composites, biological scaffolds, and synthetic polymers such as polypropylene, polyester, and ePTFE. Most repairs utilize synthetic meshes, such as polypropylene, due to their efficacy and infrequent failure. However, they can result in significant long-term complications, including chronic inflammation, foreign body reactions, and pain. Lightweight, large-pore configurations and bioactive coatings are intended to enhance biocompatibility and facilitate tissue integration, thereby mitigating adverse effects. Biological and biosynthetic meshes, such as P4HB, demonstrate efficacy in contaminated environments; however, they are linked to higher recurrence rates and increased expenses. Surgical techniques, fixation methods, and individual patient variability significantly influence outcomes in the complex clinical environment. The field has experienced extensive regulatory oversight, particularly concerning transvaginal implants. This instance shows how important it is to have a lot of long-term data. Future trends point to a move toward smart, personalized solutions like 3D-printed scaffolds, drug-eluting meshes, and prosthetics with built-in biosensors. The best mesh must strike a balance between mechanical strength and biological compatibility. This is a goal that drives progress in both material science and surgery. - Source: PubMed
Publication date: 2026/05/25
Rezvani MiladZamani SepehrShahrami Rad SoheilNaeiji MahdiMaghsoodifar HasanVataniman MohammadRezaJahanbazi RoyaSalehi Majid - Triple-negative breast cancer (TNBC) is characterized by aggressive clinical behaviour and frequent resistance to chemotherapy. While ferroptosis-an iron-dependent form of cell death driven by lipid peroxidation-holds promise as a therapeutic strategy, its efficacy is often limited by adaptive resistance mechanisms that remain incompletely understood. C-terminal binding protein (CtBP) is an oncogene associated with poor prognosis in TNBC; however, whether CtBP confers resistance to oxidative stress and ferroptosis, thereby contributing to its oncogenic function, remains unknown. - Source: PubMed
Publication date: 2026/05/16
Wang LifenXu HongxiaLiu TianyuZhu DongliangChen LipingLiu Tzu-MingLin ShuhaiLiu XueyiFeng HaoWang LiDi Li-Jun - Bladder cancer (BLCA) poses a significant clinical challenge due to its high mortality rates and the inadequacy of current prognostic biomarkers. Programmed cell death (PCD) is crucial in BLCA initiation, progression, and treatment, yet the interplay and specific roles of different PCD pathways in BLCA prognosis remain elusive. This study aimed to develop and validate predictive models by integrating 14 PCD patterns using comprehensive analyses of bulk RNA and single-cell RNA transcriptomic data from TCGA-BLCA and six GEO datasets. Through weighted gene co-expression network (WGCNA) analyses, 24 hub PCD-related genes (PCDGs) were identified in BLCA. Subsequently, we implemented a computational framework that integrated 10 machine learning algorithms along with 101 of their combined permutations. This framework was used to develop a programmed cell death-related signature (PCDRS). The final PCDRS consisted of 12 prognostic genes: P4HB, CHEK2, PTPN2, ATP13A2, CCT6A, TFRC, RRP12, TRAF7, POLR1B, B4GALT3, SIVA1, and TP73.The PCDRS was validated in training and external validation sets, with multivariate analysis confirming its independent prognostic value in BLCA. The PCDRS-integrated nomogram was also developed as a quantitative clinical tool. Furthermore, differences in reactive oxygen species (ROS) levels were observed in the tumor microenvironment between high- and low-risk groups based on PCDRS risk scores. Additionally, the elevated expression and tumorigenic role of P4HB in BLCA were validated through in vitro assays. In summary, P4HB may serve as a candidate gene with potential relevance to BLCA prognosis that could enhance personalized treatment strategies for patients with BLCA. - Source: PubMed
Publication date: 2026/04/02
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