RNF34

Last update 08 May 2025

Basic Info

Synonyms

CARP-1, Caspase regulator CARP1, Caspases-8 and -10-associated RING finger protein 1

+ [11]

Introduction

E3 ubiquitin-protein ligase that regulates several biological processes through the ubiquitin-mediated proteasomal degradation of various target proteins. Ubiquitinates the caspases CASP8 and CASP10, promoting their proteasomal degradation, to negatively regulate cell death downstream of death domain receptors in the extrinsic pathway of apoptosis (PubMed:15069192). May mediate 'Lys-48'-linked polyubiquitination of RIPK1 and its subsequent proteasomal degradation thereby indirectly regulating the tumor necrosis factor-mediated signaling pathway (Ref.13). Negatively regulates p53/TP53 through its direct ubiquitination and targeting to proteasomal degradation (PubMed:17121812). Indirectly, may also negatively regulate p53/TP53 through ubiquitination and degradation of SFN (PubMed:18382127). Mediates PPARGC1A proteasomal degradation probably through ubiquitination thereby indirectly regulating the metabolism of brown fat cells (PubMed:22064484). Possibly involved in innate immunity, through 'Lys-48'-linked polyubiquitination of NOD1 and its subsequent proteasomal degradation (PubMed:25012219).

100 Clinical Results associated with RNF34

100 Translational Medicine associated with RNF34

0 Patents (Medical) associated with RNF34

Literatures (Medical) associated with RNF34

15 Dec 2025·Animal Biotechnology

Identification of key factors causing ketosis in dairy cows with low feed intake

Article

Author: Li, Fen ; Feng, Xue ; Ma, Yun ; Abbas Raza, Sayed Haidar ; Feng, Qi

Ketosis is a common metabolic disease in high-yield dairy cows. Key genes affecting ketosis need to be further explored by new methods. The gene expression profiling and clinical data of GSE92398, GSE104079, and GSE4304 were obtained from the gene expression omnibus (GEO) database. Core modules and genes associated with RFI (residual feed intake) and ADF (alternate day fasting) were identified by weighted gene co-expression network analysis (WGCNA). Subsequently, the key genes related to ketosis and RFI were determined by protein-protein interaction (PPI) networks, ROC curves, functional enrichment, and differential expression analysis, respectively. The results showed that the genes of ACACA, ELOVL6 and XPO7 could be used as regulators of ketosis induced by low feed intake in dairy cows. At the same time, three genes (HRFI, STAT3 and IFNAR1) were retained as additional RFI biomarkers that could be considered. We identified three key factors as candidate genes and biomarkers of ketosis and RFI, respectively. These factors may provide a theoretical basis for targeted therapy of ketosis in dairy cows.

01 Mar 2025·Neuroscience

GATA3 modulation of mitochondrial oxidative stress inhibits cerebrovascular remodeling-mediated ischemic stroke by suppressing MBVSMC phenotypic transformation

Article

Author: Fang, Shaokuan ; Wu, Xiaoke

Ischemic stroke (IS) is the most predominant type of stroke, and cerebrovascular remodeling that occurs in response to risk factors facilitates its development. Mouse brain vascular smooth muscle cells (MBVSMCs) undergo phenotypic transformation during cerebrovascular remodeling, and reactive oxygen species (ROS) are a major driver of this process. The transcription factor of GATA binding protein 3 (GATA3) has been shown to enhance the neuroprotective effect induced by ischemic preconditioning. However, its involvement in cerebrovascular remodeling and the underlying mechanism are yet to be elucidated. Our findings showed that the expression of GATA3 was reduced in the cerebrovascular remodeling model constructed using angiotensin II (AngII)-induced MBVSMCs. In addition, the overexpression of GATA3 and the treatment of MBVSMCs with AngII revealed that the activity of NADPH oxidase was decreased, mitochondrial ROS production was reduced, malondialdehyde levels were lowered, glutathione peroxidase activity was increased; the proliferative ability of MBVSMCs was decreased, and the expression levels of molecules related to phenotypic transformation were altered. Furthermore, GATA3 promoted the expression of ring finger protein 34 (RNF34) of ubiquitin ligase, which in turn enhanced the ubiquitinated degradation of oxidative stress-related molecules and inhibited the phenotypic transformation of MBVSMCs, thereby exerting a protective effect on cerebrovascular remodeling. Collectively, these results suggest that GATA3 binds to RNF34 to augment its expression and accelerate the ubiquitinated degradation of oxidative stress-related molecules, thus exerting protective effects in IS.

01 May 2024·Molecular Biotechnology

Multidimensional Transcriptomics Unveils RNF34 as a Prognostic Biomarker and Potential Indicator of Chemotherapy Sensitivity in Wilms’ Tumour

Article

Author: Zheng, Jie ; Su, Cheng ; Ou, Xiuyi ; Ding, Min ; Su, Jinxia ; Shi, Bo ; Liu, Fengling ; Chen, Haoran ; Wang, Congjun ; Chen, Siyu ; Tuo, Jinwei ; Chen, Xun ; Li, Yong

Nephroblastoma, colloquially known as Wilms' tumour (WT), is the predominant malignant renal neoplasm arising in the paediatric population. Modern therapeutic approaches for WT incorporate a synergistic combination of surgical intervention, radiotherapy, and chemotherapy, which substantially ameliorate the overall patient survival rate. Despite this, the optimal sequence of chemotherapy and surgical intervention remains a matter of contention, with each strategy presenting its own strengths and weaknesses that could influence clinical decision-making. To make some headway on this clinical dilemma, we deployed a multidimensional transcriptomics integration approach by analysing bulk RNA sequencing data with 136 samples, as well as single-nucleus RNA sequencing (snRNA-seq) and paired spatial transcriptome sequencing (stRNA) data from 32 WT specimens. Our findings identified a distinct elevation of RNF34 expression within WT samples, which correlated with unfavourable prognostic outcomes. Leveraging the Genomics of Drug Sensitivity in Cancer (GDSC), we simultaneously revealed that patients with high expression of RNF34 have higher sensitivity to commonly used chemotherapy drugs for WT. Furthermore, our analysis of snRNA and stRNA data unveiled a reduced proportion of RNF34 expression in neoplastic cells after chemotherapy. Moreover, stRNA data delineated a significant association between a higher proportion of RNF34 expression in cancer cells and adverse features such as anaplastic histology and tumour recurrence. Intriguingly, we also observed a close association between elevated RNF34 expression and a characteristic exhausted tumour immune microenvironment. Collectively, our findings underscore the pivotal role of RNF34 in the prognostic prediction potential and treatment sensitivity of WT. This comprehensive analysis can potentially inform and refine clinical decision-making for WT patients and guide future studies towards the development of optimized, rational therapeutic strategies.

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RNF34

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