RAE1

Last update 08 May 2025

Basic Info

Synonyms

Gle2, Mnrp41, mRNA export factor RAE1

+ [5]

Introduction

Acts as a mRNA export factor involved in nucleocytoplasmic transport (PubMed:20498086, PubMed:33849972). Plays a role in mitotic bipolar spindle formation (PubMed:17172455). May function in attaching cytoplasmic mRNPs to the cytoskeleton both directly or indirectly (PubMed:17172455).

100 Clinical Results associated with RAE1

100 Translational Medicine associated with RAE1

0 Patents (Medical) associated with RAE1

284

Literatures (Medical) associated with RAE1

01 Apr 2025·iScience

M-Motif, a potential non-conventional NLS in YAP/TAZ and other cellular and viral proteins that inhibits classic protein import

Article

Author: Di Ciano-Oliveira, Caterina ; Venugopal, Shruthi ; Kapus, András ; Gill, Gary ; Kofler, Michael

Multiple mechanisms were proposed to mediate the nuclear import of TAZ/YAP, transcriptional co-activators regulating organ growth and regeneration. Our earlier observations showed that TAZ/YAP harbor a C-terminal, unconventional nuclear localization signal (NLS). Here, we show that this sequence, necessary and sufficient for basal, ATP-independent nuclear import, contains an indispensable central methionine flanked by negatively charged residues. Based on these features, we define the M-motif and propose that it is a new class of NLS, also present and import-competent in other cellular (STAT1 and cyclin B1) and viral (ORF6 of SARS-CoV2, VSV-M) proteins. Accordingly, ORF6 SARS-Cov2 competitively inhibits TAZ/YAP uptake, while TAZ abrogates STAT1 import. Similar to viral M-motif proteins, TAZ binds RAE1 and inhibits classic nuclear protein import, including that of antiviral factors (IRF3 and NF-κB). However, RAE1 is dispensable for TAZ import itself. Thus, the TAZ/YAP NLS has a dual function: it mediates unconventional nuclear import and inhibits classic import, contributing to the suppression of antiviral responses.

01 Mar 2025·Biophysical Chemistry

Met58 and di-acidic motif located at C-terminal region of SARS-CoV-2 ORF6 plays a crucial role in its structural conformations

Article

Author: Bhardwaj, Taniya ; Saumya, Kumar Udit ; Kumar, Prateek ; Giri, Rajanish

Despite being mostly neglected in structural biology, the C-terminal Regions (CTRs) are studied to be multifunctional in humans as well as in viruses. Previously, SARS-CoV-2 Spike and NSP1 proteins' CTRs are observed to be disordered, and experimental evidence showed a gain of structure properties in different physiological environments. In this line, we have investigated the structural dynamics of CTR (residues 38-61) of SARS-CoV-2 ORF6 protein, disrupting bidirectional transport between the nucleus and cytoplasm. ORF6-CTR is disordered in nature but doesn't gain any structure in most conditions. As per studies, residue such as Methionine at 58th position in ORF6 is critical for interaction with Rae1-Nup98. Therefore, along with M58, we have identified a few other mutations from the literature and performed extensive structure modelling and dynamics studies using computational simulations. The exciting revelations in CTR models provide evidence of its structural flexibility and possible capabilities to perform multifunctionality inside the host.

01 Jan 2025·Cancer Science

Targeting CLK2 and serine/arginine‐rich splicing factors inhibits multiple myeloma through downregulating RAE1 by nonsense‐mediated mRNA decay mechanism

Article

Author: Liao, Yaping ; Lai, Shuping ; Chen, Yan ; Wei, Rongfang ; Liang, Laoqi ; Zhang, Yihao ; Wu, Xiaoyan ; Liu, Yang

AbstractMultiple myeloma (MM) is closely related to abnormal RNA splicing in its pathogenesis. CDC2‐like kinase‐2 (CLK2) regulates RNA splicing by phosphorylating serine/arginine‐rich splicing factors (SRSFs), but the role of CLK2 in MM remains undefined. This study was to explore the role and mechanism of CLK2 in MM. Analyzing GEO datasets of MM patients found that high CLK2 expression predicted poor prognosis. Overexpression of CLK2 promoted the cell proliferation and cell cycle progression of MM cell ARP1 and H929. Knockdown or inhibition of CLK2 suppressed cell proliferation and induced cell apoptosis and cell cycle arrest in ARP1 and H929 cells in vitro. An MM xenograft tumor experiment showed that CLK2 overexpression promoted tumor growth, while CLK2 inhibition suppressed tumor growth in vivo. Mechanistic studies revealed that interfering CLK2 inhibited SRSF phosphorylation, and induced exon 9 skipping of RAE1, resulting in nonsense‐mediated mRNA decay (NMD) of RAE1. In addition, RAE1 knockdown inhibited cell proliferation in ARP1 and H929 cells. Moreover, RAE1 overexpression promoted cell proliferation and cell cycle progression of ARP1 and H929 cells, and partially reversed the antitumor effect of CLK2 knockdown. Targeting CLK2 shows antitumor effects on MM partially through inhibiting SRSF phosphorylation and inducing NMD of RAE1. Therefore, targeting the CLK2/SRSFs/RAE1 axis could be a potential therapeutic strategy for MM.

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RAE1

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