PEBP4

Last update 08 May 2025

Basic Info

Synonyms

CORK1, hPEBP4, MGC22776

+ [5]

Introduction

Promotes AKT phosphorylation, suggesting a possible role in the PI3K-AKT signaling pathway.

100 Clinical Results associated with PEBP4

100 Translational Medicine associated with PEBP4

0 Patents (Medical) associated with PEBP4

Literatures (Medical) associated with PEBP4

01 Jun 2025·Progress in Biophysics and Molecular Biology

The role of phosphatidylethanolamine-binding protein (PEBP) family in various diseases: Mechanisms and therapeutic potential

Review

Author: Xue, Haiping ; Wu, Tao ; Luo, Yanqun ; Deng, Xiaoliang ; Teng, Yeying

This article focuses on the phosphatidylethanolamine-binding protein (PEBP) family proteins, detailing PEBP1 and PEBP4 due to limited information on PEBP2 and PEBP3, in cellular signaling pathways and research in a spectrum of pathologies, including diverse cancers, metabolic disorders, immunological diseases and a subset of organ-specific diseases. It outlines the mechanisms through which PEBP1 and PEBP4 regulate essential signaling pathways that are critical for cellular processes such as proliferation, apoptosis, and metastasis. Recent advancements have shown further understanding of these proteins' roles in pathophysiology and their potential as future therapeutic targets. The findings suggest that the impact of PEBP1 and PEBP4 on the course of different diseases has underscored their potential for more in-depth medical research and novel clinically targeted therapies.

01 Mar 2025·Cell and Tissue Research

In situ spatial transcriptomic analysis of human skeletal muscle using the Xenium platform

Article

Author: Prosenc Zmrzljak, Uršula ; Horvat, Simon ; Šink, Žiga ; Blagotinšek Cokan, Kaja ; Umek, Nejc ; Meznarič, Marija

Traditional transcriptomic studies often overlook the complex heterogeneity of skeletal muscle, as they typically isolate RNA from mixed muscle fibre and cell populations, resulting in an averaged transcriptomic profile that obscures fibre type-specific differences. This study assessed the potential of the recently developed Xenium platform for high-resolution spatial transcriptomic analysis of human skeletal muscle histological sections. Human vastus lateralis muscle samples from two individuals were analysed using the Xenium platform and Human Multi-Tissue and Cancer Panel targeting 377 genes complemented by staining of successive sections for Myosin Heavy Chain isoforms to differentiate between type 1 and type 2 muscle fibres. Manual segmentation of muscle fibres allowed accurate comparisons of transcript densities across fibre types and subcellular regions, overcoming limitations in the platform's automated segmentation. The analysis revealed higher transcript density in type 1 fibres, particularly in nuclear and perinuclear areas, and identified 191 out of 377 genes with differential expression between muscle fibres and perimysium. Genes such as PROX1, S100A1, LGR5, ACTA2, and LPL exhibited higher expression in type 1 fibres, whereas PEBP4, CAVIN1, GATM, and PVALB in type 2 fibres. We demonstrated that the Xenium platform is capable of high-resolution spatial in situ transcriptomic analysis of skeletal muscle histological sections. This study demonstrates that, with manual segmentation, the Xenium platform effectively performs fibre type-specific transcriptomic analysis, providing new insights into skeletal muscle biology.

01 Feb 2025·Andrology

Knockout of phosphatidylethanolamine binding protein4 (PEBP4) promotes chronic non‐bacterial prostatitis by mediating the activation of NF‐κB signaling

Article

Author: Zou, Xiaofeng ; Hu, Xing ; Luo, Hui ; Qian, Biao ; He, Hailan ; Zou, Junrong ; Xiao, Guancheng ; Zhang, Guoxi ; Liao, Yunfeng

AbstractBackgroundThe etiology of chronic prostatitis remains unclear; consequently, this disease is associated with recurrence and ineffective clinical therapy. Therefore, there is an urgent need to investigate the underlying pathogenesis of chronic prostatitis in order to develop more efficacious treatments.ObjectiveThe previous study found that knocking out of PEBP4 leads to chronic prostatitis in the male mice. This research aimed to identify the role of PEBP4 in prostatitis, determine the molecular pathogenic mechanisms associated with chronic prostatitis, and provide guidelines for the development of new treatment strategies for chronic prostatitis.Materials and methodsA PEBP4 exon knockout strain (PEBP4−/−) was established in C57BL/6 mice via the Cre‐loxP system. Hematoxylin‐eosin (H&E) staining was used to investigate histological changes. RNA‐sequencing was used to investigate the gene expression signature of the prostate and the levels of inflammatory cytokines were determined by real‐time polymerase chain reaction (RT‐PCR). The expression of PEBP4 protein in prostate tissue was determined by immunohistochemistry in specimens from patients with BPH and BPH combined with chronic prostatitis. Finally, we used a CRISPR‐Cas9 plasmid to knockout PEBP4 in RWPE‐1 cells; western blotting was subsequently used to measure the level of activation in the NF‐κB signaling pathway after activating with TNF‐α.ResultsHemorrhage and inflammatory cell infiltration were incidentally observed in the seminal vesicles and prostate glands of PEBP4−/− mice after being fed with a normal diet for 1 year. In addition, we found significantly lower (p < 0.001) expression levels of PEBP4 protein in prostate tissues from patients with benign prostate hyperplasia (BPH) and chronic and non‐bacterial prostatitis (CNP) when compared to those with BPH only. The reduced expression of PEBP4 led to a higher risk of prostatitis recurrence in patients after 2 years of follow‐up. Increased levels of NF‐κB and IκB phosphorylation were observed in PEBP4‐knockout RWPE‐1 cells and prostate glands from PEBP4−/− mice.ConclusionThe knockout of PEBP4 in experimental mice led to chronic prostatitis and the reduced expression of PEBP4 in patients with higher risk of chronic and non‐bacterial prostatitis suggested that PEBP4 might act as a protective factor against chronic prostatitis. The knockout of PEBP4 in RWPE‐1 cells led to the increased activation of NF‐κB and IκB, thus indicating that inhibition of PEBP4 faciliated the NF‐κB signaling cascade. Our findings provide a new etiology and therapeutic target for chronic prostatitis.

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PEBP4

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