LRRC59

Last update 08 May 2025

Basic Info

Synonyms

FLJ21675, leucine rich repeat containing 59, Leucine-rich repeat-containing protein 59

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Introduction

Required for nuclear import of FGF1, but not that of FGF2. Might regulate nuclear import of exogenous FGF1 by facilitating interaction with the nuclear import machinery and by transporting cytosolic FGF1 to, and possibly through, the nuclear pores.

100 Clinical Results associated with LRRC59

100 Translational Medicine associated with LRRC59

0 Patents (Medical) associated with LRRC59

Literatures (Medical) associated with LRRC59

01 Oct 2024·Phytomedicine

Exoticin as a selective agonist of 6TM μ opioid receptors identifies endogenous chaperones essential for its activity

Article

Author: Lu, Zhigang ; Mu, Xinru ; Wang, Yuxuan ; Qin, Fenfen ; Wang, Qian ; Liu, Xingjun ; Liu, Qingyang ; Lin, Weixin ; Wang, Qisheng ; Li, Zhonghao ; Liu, Anlong

BACKGROUNDClassical opioids are effective analgesics but carry various side effects, necessitating safer alternatives. Truncated six-transmembrane mu opioid receptors (6TM-μORs) mediate potent analgesia with fewer side effects and are a promising therapeutic target. However, few ligands known selectively target 6TM-μORs. Moreover, endogenous chaperones are believed essential for 6TM-μOR ligand binding and function.PURPOSETo identify a 6TM-μOR selective agonist and elucidate requisite endogenous chaperones.METHODSVirtual screening was used to identify promising selective 6TM-μOR agonists from traditional Chinese medicines. The role of 6TM-μOR in Exoticin analgesia was validated in loss- and gain-of-function models. APEX2 proteomics profiled proximal proteins under Exoticin or IBNtxA. Interactions were further characterized in vivo and in vitro.RESULTSExoticin was shortlisted for its selective binding to 6TM-μOR and ability to induce 6TM-μOR-dependent signal transduction. Exoticin analgesia was sensitive to β-FNA and absent in E11 KO mice, but restored in mice infected with AAV-μOR1G. Slc3a2, Lrrc59, and Ppp1cb co-interacted with 6TM-μOR1G and were equally essential for Exoticin binding and 6TM-μOR1G activity.CONCLUSIONExoticin is a promising selective agonist of 6TM μ opioid receptors with broad-spectrum analgesic efficacy but few side effects. Slc3a2, Lrrc59, Ppp1cb are endogenous chaperones essential for 6TM-μOR ligand binding and function.

01 Oct 2024·Journal of Proteomics

Construction of a prognostic model for colon cancer by combining endoplasmic reticulum stress responsive genes

Article

Author: Zhang, Meng ; Yuan, Zhibin ; Xu, Song ; Wang, Yi ; Tang, Jianjun

Endoplasmic reticulum stress may affect the occurrence and development of cancer. However, its effect on the prognosis of colon cancer (CC) patients is not clear yet. Herein, based on TCGA database, we screened 15 endoplasmic reticulum stress responsive genes (ERSRGs) associated with the prognosis of CC patients by Cox regression. By LASSO and multivariate Cox regression analyses, a prognostic risk assessment model involving 12 genes (DNAJB2, EIF4A1, YPEL4, COQ10A, IRX3, ASPHD1, NTRK2, TRIM39, XBP1, GRIN2B, LRRC59, and RORC) was built. The survival curves indicated that patients in the low-risk group had good prognosis. ROC curves demonstrated a good performance of this 12-gene prognostic model, and the Riskscore could be considered as an independent prognostic factor. Patients in low-risk group benefit more from immune checkpoint inhibitor and immune checkpoint blockade (ICB) treatment. Besides, the enrichment analysis suggested a remarkable difference in Ca²⁺ signaling in both groups. Finally, based on the cMAP database, we identified several potential drugs that could target high-risk groups, such as Dasatinib, GNF-2, Saracatinib, and WZ-1-84. To sum up, our research constructed an ERSRGs-characteristic prognostic model. The model is a promising biomarker for prediction of clinical outcomes and immune therapy response of CC patients. SIGNIFICANCE: Based on the transcriptomic data of colon cancer in the TCGA database, this study screens 12 endoplasmic reticulum stress-related genes (ERSRGs), including DNAJB2, EIF4A1, YPEL4, COQ10A, IRX3, ASPHD1, NTRK2, TRIM39, XBP1, asphD1, NTRK2. GRIN2B, LRRC59, and RORC, and a prognostic model was constructed. This model can be used as a predictor of prognosis and immunotherapy response in colon cancer patients. At the same time, model-based prediction of drugs can also be a potential option for colon cancer treatment in the future.

01 Sep 2024·International Journal of Hematology

Comprehensive analysis of microRNAs modulated by histone deacetylase inhibitors identifies microRNA-7-5p with anti-myeloma effect

Article

Author: Kitadate, Akihiro ; Tagawa, Hiroyuki ; Takahashi, Naoto ; Yamada, Masahiro ; Takahashi, Yuto ; Iwama, Sayaka ; Ikeda, Sho ; Kuroki, Wataru

Basic research to expand treatment options for multiple myeloma is greatly needed due to the refractory nature of the disease. Histone deacetylase (HDAC) inhibitors, which are epigenetic regulators, are attractive but have limited applications. MicroRNAs (miRNAs), which are also epigenetic regulators, are important molecules that may lead to future therapeutic breakthroughs. In this study, we comprehensively searched for miRNAs that are altered by HDAC inhibitors in myeloma cells. We identified miR-7-5p (miR-7) as a miRNA downregulated by HDAC inhibitors. Transfection of myeloma cell lines with miR-7 suppressed cell proliferation, induced apoptosis, and enhanced the effects of the HDAC inhibitor panobinostat. Expression of miR-7 was downregulated by c-Myc inhibition, but upregulated by bortezomib. Comprehensive examination of miR-7 targets revealed four candidates: SLC6A9, LRRC59, EXOSC2, and PSME3. Among these, we focused on PSME3, an oncogene involved in proteasome capacity in myeloma cells. PSME3 knockdown increases myeloma cell death and panobinostat sensitivity. In conclusion, miR-7, which is downregulated by HDAC inhibitors, is a tumor suppressor that targets PSME3. This miR-7 downregulation may be involved in HDAC inhibitor resistance. In addition, combinations of anti-myeloma drugs that complement changes in miRNA expression should be considered.

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LRRC59

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