PRPF3

Last update 08 May 2025

Basic Info

Synonyms

hPrp3, pre-mRNA processing factor 3, Pre-mRNA-splicing factor 3

+ [6]

Introduction

Plays a role in pre-mRNA splicing as component of the U4/U6-U5 tri-snRNP complex that is involved in spliceosome assembly, and as component of the precatalytic spliceosome (spliceosome B complex).

100 Clinical Results associated with PRPF3

100 Translational Medicine associated with PRPF3

0 Patents (Medical) associated with PRPF3

146

Literatures (Medical) associated with PRPF3

31 Mar 2025·Plant And Cell Physiology

The Arabidopsis basic–helix–loop–helix transcription factor LRL1 activates cell wall-related genes during root hair development

Article

Author: Yamada, Koh ; Aoyama, Takashi ; Kato, Mariko ; Haghir, Shahrzad ; Wada, Takuji ; Tsuge, Tomohiko ; Tominaga, Rumi ; Ohashi, Yohei

AbstractLotus japonicus-ROOT HAIR LESS1-LIKE-1 (LRL1) of Arabidopsis thaliana encodes a basic helix–loop–helix (bHLH) transcription factor (TF) involved in root hair development. Root hair development is regulated by an elaborate transcriptional network, in which GLABRA2 (GL2), a key negative regulator, directly represses bHLH TF genes, including LRL1 and ROOT HAIR DEFECTIVE6 (RHD6). Although RHD6 and its paralogous TFs have been shown to connect downstream to genes involved in cell morphological events, such as endomembrane and cell wall modification, the downstream network of LRL1 remains elusive. We found that a mutation of LRL1 causes a short-root hair phenotype and that this phenotype can be partially rescued by a transgene encoding a glucocorticoid receptor (GR) domain-fused LRL1, LRL1-GR, in the presence of glucocorticoids. Using this conditional rescue system, we identified 46 genes that are activated downstream of LRL1. Among these, the cell wall-related genes were significantly enriched and many of them were found to be immediately downstream of LRL1 without de novo protein synthesis in between. We further analyzed three representative genes, PROLINE-RICH PROTEIN1 (PRP1), PRP3, and XYLOGLUCAN ENDOTRANSGLUCOSYLASE/HYDOLASE12 (XTH12). Reporter gene analyses showed that these genes are specifically transcribed in root hair cells including those in the root–hypocotyl junction, and that their proteins were localized to the cell wall of elongating root hairs, root hair bulges, and root hair bulge-expecting loci. A T-DNA insertion mutant of PRP3 showed a moderate short-root hair phenotype. Based on these results, LRL1 is likely to promote root hair development throughout the morphogenetic process by activating cell wall-related genes.

01 Feb 2025·Anticancer Research

PRPF4 Knockdown Suppresses Glioblastoma Progressionviathe p38 MAPK and ERK Signaling Pathways

Article

Author: Han, Se-Hyeon ; Park, Jin-Kyu ; Kim, Daehwan ; Kim, Hee-Yeon ; Ryoo, Zae Young ; Lee, Seoung-Woo ; Kim, Wansoo ; Cho, Jaelim ; Choi, Seong-Kyoon ; Han, Jee Eun ; Lee, Jiyeon ; Kim, Choonok ; Jang, Soyoung ; Park, Song ; Seah, Ethan

BACKGROUND/AIMPre-mRNA processing factor 4 (PRPF4), a core protein of U4/U6 small nuclear ribonucleoproteins (snRNPs), is crucial for maintaining their structure by interacting with PRPF3 and Cyclophilin H. Beyond its role in splicing, PRPF4 has been implicated in cell survival, apoptosis, and oncogenesis. Although PRPF4 mutations have been associated with retinitis pigmentosa, its role in glioblastoma (GBM) remains unclear. This study aimed to investigate the function of PRPF4 in GBM progression and its potential as a therapeutic target.MATERIALS AND METHODSGene expression profiling was conducted to compare PRPF4 levels between GBM tumors and normal tissues. PRPF4 expression was also evaluated in various cancer and GBM cell lines. Stable PRPF4 knockdown cell lines were established using A172 and T98G GBM cell lines. Cellular proliferation, apoptosis, migration, and invasion were assessed through gene expression and functional assays. Additionally, molecular pathways affected by PRPF4 knockdown were examined, focusing on the p38 MAPK signaling pathway. Finally, metabolic processes in PRPF4 knockdown cells were estimated through proteomic analysis.RESULTSPRPF4 expression was elevated in GBM. Knockdown of PRPF4 reduced cell proliferation, induced apoptosis, and suppressed migration and invasion in GBM cells. PRPF4 knockdown also suppressed MKK3/6-p38-ATF2 and RAS-MEK-ERK1/2 signaling pathways. Proteome analysis revealed disruptions in metabolic pathways, including glutathione and carbon metabolisms, which are associated with GBM progression.CONCLUSIONPRPF4 knockdown inhibits GBM progression by reducing p38 MAPK and ERK signaling cascade with metabolic alterations. Targeting PRPF4 may offer novel therapeutic strategies for GBM treatment.

01 Jun 2023·MedComm

TXNL4B regulates radioresistance by controlling the PRP3‐mediated alternative splicing of FANCI

Article

Author: Wang, Yin ; Xiang, Jing ; Zhang, Le ; He, Yan ; Xiao, Liang ; Miszczyk, Justyna ; Nie, Yunfeng ; Huang, Ruixue ; Yang, Long ; Zhou, Pingkun ; Ju, Zhao ; Lei, Ridan

AbstractIonizing radiation (IR) has been extensively used for cancer therapy, but the radioresistance hinders and undermines the radiotherapy efficacy in clinics greatly. Here, we reported that the spliceosomal protein thioredoxin‐like 4B (TXNL4B) is highly expressed in lung tissues from lung cancer patients with radiotherapy. Lung cancer cells with TXNL4B knockdown illustrate increased sensitivity to IR. Mechanistically, TXNL4B interacts with RNA processing factor 3 (PRP3) and co‐localizes in the nucleus post‐IR. Nuclear localization of PRP3 promotes the alternative splicing of the Fanconi anemia group I protein (FANCI) transcript variants, FANCI‐12 and FANCI‐13. PRP3 regulates alternative splicing of FANCI toward the two variants, FANCI‐12 and FANCI‐13. Radioresistance was greatly enhanced through the combination of PRP31 and PRP8, the critical components of core spliceosome promoted by PRP3. Notably, the inhibition of PRP3 to suppress the production of FANCI‐12 would deprive PRP31 and PRP8 of such interaction. As a result, cell cycle G2/M arrest was induced, DNA damage repair was delayed, and radiosensitivity was improved. Collectively, our study highlights potential novel underlying mechanisms of the involvement of TXNL4B and alternative splicing in radioresistance. The results would benefit potential cancer radiotherapy.

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PRPF3

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