OSR2

Last update 08 May 2025

Basic Info

Synonyms

FLJ90037, odd-skipped related transciption factor 2, OSR2

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Introduction

May be involved in the development of the mandibular molar tooth germ at the bud stage.

100 Clinical Results associated with OSR2

100 Translational Medicine associated with OSR2

0 Patents (Medical) associated with OSR2

Literatures (Medical) associated with OSR2

11 Mar 2025·Investigative Ophthalmology & Visual Science

Long Non-Coding RNA Osr2 Promotes Fusarium solani Keratitis Inflammation via the miR-30a-3p/ Xcr1 Axis

Article

Author: Tang, Hanfeng ; Hu, Jianzhang ; Lin, Yi

PurposeFungal keratitis (FK) is a challenging and sight-threatening corneal disease caused by fungal infections. Although long noncoding RNAs (lncRNAs) have been explored in various infectious diseases, their specific roles in FK remain largely unexplored.MethodsA mouse model of FK was created by infecting corneal stromal cells with Fusarium solani. High-throughput lncRNA expression profiling was conducted on FK-affected corneal tissues to identify differentially expressed lncRNAs. Reverse transcription quantitative PCR (RT-qPCR) was used to validate the results. A competing endogenous RNA (ceRNA) network was constructed. Additionally, a specific antisense oligonucleotide (ASO) targeting lncRNA ENSMUST00000226838/Osr2 (Osr2) was developed for therapeutic evaluation. Inflammatory markers IL-1β, IL-6, and TNF-α were measured, and corneal inflammation was assessed through histological analysis and slit-lamp examination. Fluorescent in situ hybridization (FISH) was used to confirm Osr2 localization, whereas a dual-luciferase reporter assay verified interactions between Osr2 and miR-30a-3p.ResultsWe identified 1143 differentially expressed lncRNAs in FK, with 701 upregulated and 442 downregulated. The ceRNA network analysis indicated that lncRNA Osr2 regulates Xcr1 expression through miR-30a-3p. Treatment with ASO-Osr2 significantly reduced corneal inflammation, and FISH confirmed lncRNA Osr2 distribution in both the nucleus and cytoplasm. Dual-luciferase assays demonstrated the interaction between Osr2 and miR-30a-3p, highlighting their potential roles in the progression of FK.ConclusionsThis study outlined the lncRNA expression profile in FK and established a ceRNA regulatory network, identifying lncRNA Osr2 as a crucial modulator of FK pathogenesis through its interaction with miR-30a-3p. These findings highlighted lncRNA Osr2 as a promising therapeutic target for the treatment of FK.

01 Jun 2024·Cell

Osr2 functions as a biomechanical checkpoint to aggravate CD8+ T cell exhaustion in tumor

Article

Author: Song, Zengfang ; Huang, Hongling ; Chen, Yixin ; Gao, Huan ; Shi, Yiran ; Zhao, Hao ; Peng, Zhihai ; Sun, Min ; Chen, Qinghua ; Zhou, Dawang ; Li, Wengang ; Ye, Lilin ; Chen, Kaiyun ; Li, Zifeng ; Tang, Jiayu ; Liu, Yue ; Hou, Yongqiang ; Li, Junhong ; Su, Dongxue ; Liu, Pingguo ; Cheng, Yao ; Xiao, Bailong ; Li, Jiaxin ; Chen, Wei ; Lai, Zhangjian ; Yang, Bingying ; Lin, Yao ; Pan, Lei ; Chen, Lanfen ; Zhang, Jinjia ; Nian, Cheng ; Xing, Yunzhi ; Sun, Xiufeng ; Zhou, Zhien ; Huang, Haitao ; Linghu, Yueyue

Alterations in extracellular matrix (ECM) architecture and stiffness represent hallmarks of cancer. Whether the biomechanical property of ECM impacts the functionality of tumor-reactive CD8⁺ T cells remains largely unknown. Here, we reveal that the transcription factor (TF) Osr2 integrates biomechanical signaling and facilitates the terminal exhaustion of tumor-reactive CD8⁺ T cells. Osr2 expression is selectively induced in the terminally exhausted tumor-specific CD8⁺ T cell subset by coupled T cell receptor (TCR) signaling and biomechanical stress mediated by the Piezo1/calcium/CREB axis. Consistently, depletion of Osr2 alleviates the exhaustion of tumor-specific CD8⁺ T cells or CAR-T cells, whereas forced Osr2 expression aggravates their exhaustion in solid tumor models. Mechanistically, Osr2 recruits HDAC3 to rewire the epigenetic program for suppressing cytotoxic gene expression and promoting CD8⁺ T cell exhaustion. Thus, our results unravel Osr2 functions as a biomechanical checkpoint to exacerbate CD8⁺ T cell exhaustion and could be targeted to potentiate cancer immunotherapy.

01 Mar 2024·Heliyon

odd skipped-related 2 as a novel mark for labeling the proximal convoluted tubule within the zebrafish kidney

Article

Author: Liu, Chi ; Zhang, Yunfeng ; Yang, Wenmin ; Liu, Xiaoliang ; Tan, Xiaoqin ; He, Zhongwei

The proximal convoluted tubule (PCT) of the kidney is a crucial functional segment responsible for reabsorption, secretion, and the maintenance of electrolyte and water balance within the renal tubule. However, there is a lack of a well-defined endogenous transgenic line for studying PCT morphogenesis. By analyzing single-cell transcriptome data from the adult zebrafish kidney, we have identified the expression of odd-skipped-related 2 (osr2, which encodes an odd-skipped zinc-finger transcription factor) in the PCT. To gain insight into the role of osr2 in PCT morphogenesis, we have generated a transgenic zebrafish line Tg(osr2:EGFP), expressing enhanced green fluorescent protein (EGFP). The EGFP expression pattern closely mirrors that of endogenous Osr2, faithfully recapitulating its native expression profile. During kidney development, we can use EGFP to track PCT development, which is also preserved in adult zebrafish. Additionally, osr2:EGFP-labeled zebrafish PCT fragments displayed short lengths with infrequent overlap, rendering them conducive for nephrons counting. The generation of Tg(osr2:EGFP) transgenic line is accompanied by simultaneous disruption of osr2 activity. Importantly, our findings demonstrate that osr2 inactivation had no discernible impact on the development and regeneration of Tg(osr2:EGFP) zebrafish nephrons. Overall, the establishment of this transgenic zebrafish line offers a valuable tool for both genetic and chemical analysis of PCT.

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