PCBP1

Last update 08 May 2025

Basic Info

Synonyms

Alpha-CP1, Heterogeneous nuclear ribonucleoprotein E1, hnRNP E1

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Introduction

Single-stranded nucleic acid binding protein that binds preferentially to oligo dC (PubMed:15731341, PubMed:7556077, PubMed:7607214, PubMed:8152927). Together with PCBP2, required for erythropoiesis, possibly by regulating mRNA splicing (By similarity). (Microbial infection) In case of infection by poliovirus, plays a role in initiation of viral RNA replication in concert with the viral protein 3CD.

100 Clinical Results associated with PCBP1

100 Translational Medicine associated with PCBP1

0 Patents (Medical) associated with PCBP1

319

Literatures (Medical) associated with PCBP1

01 Jun 2025·Environmental Pollution

PFOS exposure impairs porcine oocyte maturation and embryo development via mitochondria-dependent ferroptosis

Article

Author: Zhang, Enbo ; Sun, Yutong ; Chen, Xingfu ; Teng, Ran ; Guo, Qing ; Xu, Ning ; Li, Suo ; Sun, Xiaoqing

Perfluorooctane sulfonate (PFOS) is a widely utilized chemical known for its exceptional environmental stability over extended periods, its significant potential to bioaccumulate in living organisms, and its considerable risks to both health and the environment. Several studies have suggested that PFOS may pose reproductive risks in mammals; however, the exact mechanisms driving these effects are not well understood. In this study, we explored the possible mechanisms by which PFOS toxicity affects the maturation of mammalian oocytes and the embryonic development employing porcine oocytes as a model system. SMART-seq results suggested that PFOS may affect oocyte maturation through mechanisms involving ferroptosis, autophagy, and alterations in membrane structure. Our results suggest that PFOS exposure adversely affects mitochondrial function and structure, thereby influencing peroxisome biogenesis and contributing to oxidative stress. Most importantly, we found that exposure to PFOS significantly elevated Fe²⁺ levels, an indicator associated with ferroptosis in oocytes. Furthermore, malondialdehyde (MDA) levels in the PFOS group were significantly higher than those in the control group. Additionally, the mRNA expression levels of PCBP1 and PCBP2, which are related to ferroptosis, as well as the expression level of P53, were significantly reduced in the PFOS group. Overall, exposure to PFOS in vitro results in mitochondrial damage in porcine oocytes, which induces lipid peroxidation and subsequently leads to the occurrence of ferroptosis.

01 Jun 2025·Life Sciences

The role of RAB12 in inhibiting osteogenic differentiation and driving metabolic dysregulation in osteoporosis

Article

Author: Liu, Wenjie ; Jin, Jiahao ; Wu, Yanfeng ; Zhang, Yibin ; Shen, Guozhen ; Cao, Qian ; Zhang, Yunhui ; Li, Quanfeng ; Wang, Peng ; Ji, Pengfei ; Yuan, Zihao

AIMSThe osteogenic differentiation of mesenchymal stem cells (MSCs) is crucial in osteoporosis, and the metabolic level of the bone microenvironment directly affects metabolic dysregulation in postmenopausal women. RAB12 is a member of the small GTPase Rab family proteins, known to play an important role in autophagy. However, the role of RAB12 in the osteogenic differentiation of osteoporotic hMSCs remains unclear.MATERIALS AND METHODImmunohistochemical staining was used to validate the high expression of RAB12 in aged osteoporotic mouse models and ovariectomized (OVX) mouse models. Co-immunoprecipitation (Co-IP) and LC-MS/MS were employed to explore downstream proteins that may interact with RAB12. Adenovirus containing RAB12 siRNA sequences was injected into the tail vein of OVX osteoporotic mice to analyze the impact of the RAB12/PCBP1/GLUT1 axis on MSC osteogenic differentiation.KEY FINDINGSWe found that RAB12 expression is upregulated in elderly osteoporotic patients and in osteoporotic mouse models. RAB12 negatively regulates the osteogenic differentiation of hMSCs both in vivo and in vitro. RAB12 interacts with the PCBP1 protein, affecting its autophagic degradation when its expression levels change. RAB12 regulates the transcriptional level of GLUT1 by influencing the autophagic degradation of PCBP1, thereby affecting MSC's regulation of glucose uptake, which in turn impacts MSC osteogenic differentiation and metabolic changes.SIGNIFICANCERAB12 negatively regulates osteogenic differentiation through the PCBP1/GLUT1 axis, affecting glucose metabolism levels in the bone microenvironment. RAB12 may serve as a potential target for the treatment of osteoporosis and postmenopausal metabolic dysregulation.

01 Apr 2025·American Journal of Physiology-Lung Cellular and Molecular Physiology

Therapeutic strategies to reverse cigarette smoke-induced ion channel and mucociliary dysfunction in COPD airway epithelial cells

Article

Author: Baumlin, Nathalie ; Silswal, Neerupma ; Yoshida, Makoto ; Dennis, John S. ; Yerrathota, Sireesha ; Haworth, Steven ; Salathe, Matthias ; Montgomery, Robert N. ; Kim, Michael D.

Cigarette smoke (CS) increases transforming growth factor-beta1 (TGF-β1) expression that causes mucociliary dysfunction by decreasing ion channel function. In our study, a CFTR amplifier (nesolicaftor) and angiotensin II receptor blockers (losartan and telmisartan) improve CS-induced ion channel dysfunction, by increasing binding of PCBP1 to CFTR and LRRC26 mRNAs. Therefore, nesolicaftor and ARBs, acting on the same target, may provide therapeutic benefits for treating smoking-related diseases.

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PCBP1

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