JDP2

Last update 08 May 2025

Basic Info

Synonyms

JDP2, Jun dimerization protein 2, JUNDM2

Introduction

Component of the AP-1 transcription factor that represses transactivation mediated by the Jun family of proteins. Involved in a variety of transcriptional responses associated with AP-1 such as UV-induced apoptosis, cell differentiation, tumorigenesis and antitumogeneris. Can also function as a repressor by recruiting histone deacetylase 3/HDAC3 to the promoter region of JUN. May control transcription via direct regulation of the modification of histones and the assembly of chromatin.

100 Clinical Results associated with JDP2

100 Translational Medicine associated with JDP2

0 Patents (Medical) associated with JDP2

178

Literatures (Medical) associated with JDP2

01 Mar 2025·Biochemical Pharmacology

The AHR–NRF2–JDP2 gene battery: Ligand–induced AHR transcriptional activation

Review

Author: Yu, Fang-Jung ; Hsu, Wen-Hung ; Wu, Deng-Chyang ; Kuo, Kung-Kai ; Nagata, Kyosuke ; Yu, Hsin-Su ; Yang, Ya-Han ; Wuputra, Kenly ; Yokoyama, Kazunari K ; Ku, Chia-Chen ; Kuo, Chao-Hung

Aryl hydrocarbon receptor (AHR) and nuclear factor-erythroid 2-related factor 2 (NRF2) can regulate a series of genes encoding the detoxifying phase I and II enzymes, via a signaling crosstalk known as the "AHR-NRF2 gene battery". The chromatin transcriptional regulator Jun dimerization protein 2 (JDP2) plays a central role in thetranscription of AHR gene in response to the phase I enzyme ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin. It forms a transcriptional complex with AHR-AHR nuclear translocator (ARNT) and NRF2-small musculoaponeurotic fibrosarcoma proteins (sMAF), which are then recruited to the respective cis-elements, such as dioxin response elements and antioxidant response elements, respectively, in the AHR promoter. Here, we present a revised description of the AHR-NRF2 gene battery as the AHR-NRF2-JDP2 gene battery for transactivating the AHR promoter by phase I enzyme ligands. The chromatin regulator JDP2 was found to be involved in the movement of AHR-NRF2 complexes from the dioxin response element to the antioxidant response element in the AHR promoter, during its activation in a spatiotemporal manner. This new epigenetic and chromatin remodeling role of AHR-NRF2-JDP2 axis is useful for identifying new therapeutic targets for various diseases, including immunological response, detoxification, development, and cancer-related diseases.

01 Feb 2025·Current Protein & Peptide Science

Down-Regulated JDP2 Attenuated Trophoblast Invasion and Migration in Preeclampsia by Inhibiting Epithelial-Mesenchymal Transition through the Wnt/β-Catenin Pathway

Article

Author: Feng, Runrun ; Liu, Lenan ; Han, Yufei ; Ying, Tingting ; Cao, Ceng ; Huang, Shiyun ; Ge, Zhiping ; Jiang, Ziyan ; Sun, Haiyan ; Zuo, Qing

Introduction:Preeclampsia (PE) is an immensely prevalent condition that poses a significant risk to both maternal and fetal health. It is recognized as a primary cause of perinatal morbidity and mortality. Despite extensive research efforts, the precise impact of JDP2 on trophoblast invasion and migration in the context of preeclampsia remains unclear.Materials and Methods:The present study aimed to investigate the differential expression of JDP2 between normal control and preeclampsia placentas through the use of quantitative polymerase chain reaction (qPCR), western blotting, and immunostaining techniques. Furthermore, the effects of JDP2 overexpression and silencing on the migration, invasion, and wound healing capabilities of HTR-8/SVneo cells were evaluated. In addition, this study also examined the impact of JDP2 on epithelial-mesenchymal transition (EMT)-associated biomarkers and the Wnt/β-catenin pathway.Results:In the present investigation, it was ascertained that Jun dimerization protein 2 (JDP2) exhibited a substantial decrease in expression levels in placentae afflicted with preeclampsia in comparison to those of normal placentae. Impairment in migration and invasion was noted upon JDP2 down-regulation, whereas augmentation of migration and invasion was observed upon JDP2 overexpression in HTR-8/SVneo cells. Subsequently, western blot and immunofluorescence assays were conducted, revealing marked alterations in EMT-associated biomarkers, such as E-cadherin, N-cadherin, and β-catenin, thereby indicating that JDP2 can facilitate cell invasion by modulating the EMT process in HTR-8/SVneo cells. Finally, activation of Wnt/β-catenin signaling was observed as a result of JDP2. After that, IWR-1, a Wnt inhibitor, was used in the recovery study. IWR-1 could inhibit the role of JDP2 in promoting migration and invasion in HTR-8/SVneo cells.Conclusion:Our findings elucidated the impact of JDP2 on trophoblast invasion and migration in preeclampsia by suppressing the EMT through the Wnt/β-catenin signaling pathway, thereby offering a potential prognostic and therapeutic biomarker for this condition.

01 Jan 2025·Genome Research

High-quality sika deer omics data and integrative analysis reveal genic and cellular regulation of antler regeneration

Article

Author: Zhou, Botong ; Zhang, Guokun ; Qiu, Qiang ; Li, Chunyi ; Yue, Huishan ; Jia, Shuaijun ; Guan, Qing ; Wang, Yong ; Li, Zihe ; Wang, Wen ; Ma, Jinrui ; Qin, Tao ; Zhu, Lei ; Hao, Dingjun ; Han, Ge ; Xu, Ziyu ; Feng, Zhanying

The antler is the only organ that can fully regenerate annually in mammals. However, the regulatory pattern and mechanism of gene expression and cell differentiation during this process remain largely unknown. Here, we obtain comprehensive assembly and gene annotation of the sika deer (Cervus nippon) genome. We construct, together with large-scale chromatin accessibility and gene expression data, gene regulatory networks involved in antler regeneration, identifying four transcription factors,MYC,KLF4,NFE2L2,andJDP2, with high regulatory activity across the whole regeneration process. Comparative studies and luciferase reporter assay suggest theMYCexpression driven by a cervid-specific regulatory element might be important for antler regenerative ability. We further develop a model called combinatorial TF Oriented Program (cTOP), which integrates single-cell data with bulk regulatory networks and findPRDM1,FOSL1,BACH1, andNFATC1as potential pivotal factors in antler stem cell activation and osteogenic differentiation. Additionally, we uncover interactions within and between cell programs and pathways during the regeneration process. These findings provide insights into the gene and cell regulatory mechanisms of antler regeneration, particularly in stem cell activation and differentiation.

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JDP2

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