RANBP17

Last update 08 May 2025

Basic Info

Synonyms

RAN binding protein 17, Ran-binding protein 17, RANBP17

Introduction

May function as a nuclear transport receptor.

100 Clinical Results associated with RANBP17

100 Translational Medicine associated with RANBP17

0 Patents (Medical) associated with RANBP17

Literatures (Medical) associated with RANBP17

01 May 2024·Cell Genomics

NRDE2 deficiency impairs homologous recombination repair and sensitizes hepatocellular carcinoma to PARP inhibitors

Article

Author: Chen, Hongxia ; Li, Yuanfeng ; Zuo, Xianbo ; Wang, Cuiling ; Jia, Weihua ; Wang, Yahui ; Wu, Tianzhun ; Zhang, Hongxin ; Liu, Mengyu ; Chen, Shunqi ; Li, Qi ; Zhang, Zheng ; Yang, Chenning ; Le, Yi ; Xing, Jinliang ; Xie, Hui ; Zeng, Tao ; An, Jiaze ; Zhang, Haitao ; He, Fuchu ; Zhou, Gangqiao ; Zhang, Hongxing ; Song, Qingfeng ; Kang, Longli ; Zhang, Xuejun ; Liu, Xinyi ; Ye, Jiazhou

To identify novel susceptibility genes for hepatocellular carcinoma (HCC), we performed a rare-variant association study in Chinese populations consisting of 2,750 cases and 4,153 controls. We identified four HCC-associated genes, including NRDE2, RANBP17, RTEL1, and STEAP3. Using NRDE2 (index rs199890497 [p.N377I], p = 1.19 × 10^-9) as an exemplary candidate, we demonstrated that it promotes homologous recombination (HR) repair and suppresses HCC. Mechanistically, NRDE2 binds to the subunits of casein kinase 2 (CK2) and facilitates the assembly and activity of the CK2 holoenzyme. This NRDE2-mediated enhancement of CK2 activity increases the phosphorylation of MDC1 and then facilitates the HR repair. These functions are eliminated almost completely by the NRDE2-p.N377I variant, which sensitizes the HCC cells to poly(ADP-ribose) polymerase (PARP) inhibitors, especially when combined with chemotherapy. Collectively, our findings highlight the relevance of the rare variants to genetic susceptibility to HCC, which would be helpful for the precise treatment of this malignancy.

10 Apr 2024·The Journal of Neuroscience

RANBP17 Overexpression Restores Nucleocytoplasmic Transport and Ameliorates Neurodevelopment in Induced DYT1 Dystonia Motor Neurons

Article

Author: Akter, Masuma ; Ding, Baojin ; Hosain, Md Abir ; Duan, Yuntian ; Cui, Haochen ; Liu, Jinmei

DYT1 dystonia is a debilitating neurological movement disorder, and it represents the most frequent and severe form of hereditary primary dystonia. There is currently no cure for this disease due to its unclear pathogenesis. In our previous study utilizing patient-specific motor neurons (MNs), we identified distinct cellular deficits associated with the disease, including a deformed nucleus, disrupted neurodevelopment, and compromised nucleocytoplasmic transport (NCT) functions. However, the precise molecular mechanisms underlying these cellular impairments have remained elusive. In this study, we revealed the genome-wide changes in gene expression in DYT1 MNs through transcriptomic analysis. We found that those dysregulated genes are intricately involved in neurodevelopment and various biological processes. Interestingly, we identified that the expression level of RANBP17, a RAN-binding protein crucial for NCT regulation, exhibited a significant reduction in DYT1 MNs. By manipulating RANBP17 expression, we further demonstrated that RANBP17 plays an important role in facilitating the nuclear transport of both protein and transcript cargos in induced human neurons. Excitingly, the overexpression of RANBP17 emerged as a substantial mitigating factor, effectively restoring impaired NCT activity and rescuing neurodevelopmental deficits observed in DYT1 MNs. These findings shed light on the intricate molecular underpinnings of impaired NCT in DYT1 neurons and provide novel insights into the pathophysiology of DYT1 dystonia, potentially leading to the development of innovative treatment strategies.

07 Sep 2023·The oncologist

The Mutational, Prognostic, and Therapeutic Landscape of Neuroendocrine Neoplasms.

Article

Author: Li, Na ; Tang, Hongzhen ; Lin, Yuan ; Wei, Shaozhen ; Zhang, Ning ; Chen, Jie ; Liu, Xuemei ; Luo, Yanji ; Chen, Minhu ; Wang, Jiaqian ; Liu, Man ; Wang, Yu ; Wen, Wenli ; Chen, Luohai

BACKGROUNDNeuroendocrine neoplasms (NENs) represent clinically and genetically heterogeneous malignancies, thus a comprehensive understanding of underlying molecular characteristics, prognostic signatures, and potential therapeutic targets is urgently needed.METHODSNext-generation sequencing (NGS) and immunohistochemistry were applied to acquire genomic and immune profiles of NENs from 47 patients.RESULTSDifference was distinguished based on differentiation grade and primary localization. Poorly differentiated neuroendocrine carcinomas (NECs) and well-differentiated neuroendocrine tumors (NETs) harbored distinct molecular features; we observed that tumor mutational burden (TMB) and tumor neoantigen burden (TNB) were significantly higher in NECs versus NETs. Notably, we identified a 7-gene panel (MLH3, NACA, NOTCH1, NPAP1, RANBP17, TSC2, and ZFHX4) as a novel prognostic signature in NENs; patients who carried mutations in any of the 7 genes exhibited significantly poorer survival. Furthermore, loss of heterozygosity (LOH) and germline homogeneity in human leukocyte antigen (HLA) are common in NENs, accounting for 39% and 36%, respectively. Notably, HLA LOH was an important prognostic biomarker for a subgroup of NEN patients. Finally, we analyzed clinically actionable targets in NENs, revealing that TMB high (TMB-H) or gene mutations in TP53, KRAS, and HRAS were the most frequently observed therapeutic indicators, which granted eligibility to immune checkpoint blockade (ICB) and targeted therapy.CONCLUSIONOur study revealed heterogeneity of NENs, and identified novel prognostic signatures and potential therapeutic targets, which directing improvements of clinical management for NEN patients in the foreseeable future.

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RANBP17

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