| 2002 |
JDP2 recruits the histone deacetylase 3 (HDAC3) complex to the differentiation response element (DRE) of the c-jun promoter, thereby repressing ATF-2/p300-mediated transactivation and inhibiting retinoic acid-induced differentiation of F9 cells. ChIP assays showed that the JDP2/HDAC3 complex is replaced by the p300 complex in response to RA, accompanied by changes in histone acetylation status. |
Chromatin immunoprecipitation (ChIP), transient transfection/reporter assays, Co-IP, overexpression in F9 cells |
Molecular and cellular biology |
High |
12052888
|
| 2006 |
JDP2 directly inhibits p300-mediated acetylation of core histones both in vitro and in vivo, requiring its N-terminal 35 residues and the DNA-binding region. JDP2 also possesses histone-chaperone activity in vitro, enabling nucleosome assembly. |
In vitro histone acetylation assay with recombinant proteins, deletion mutagenesis, in vivo acetylation assays, nucleosome assembly assay |
Nature structural & molecular biology |
High |
16518400
|
| 2001 |
JDP2 represses p53 transcription via a conserved atypical AP-1 site in the p53 promoter, thereby increasing cell survival following UV irradiation. |
Reporter assays, UV survival assays, overexpression in mammalian cells |
Molecular and cellular biology |
Medium |
11287607
|
| 2001 |
JDP2 is phosphorylated by JNK (c-Jun N-terminal kinase) both in vitro and in vivo at threonine-148; substitution of T148 with alanine blocks JNK-dependent phosphorylation. JDP2 contains a consensus JNK docking site. |
In vitro kinase assay, site-directed mutagenesis (T148A), in vivo phosphorylation assay |
FEBS letters |
High |
11602244
|
| 2003 |
JDP2 expression is induced by RANKL in macrophage/osteoclast progenitor cells; overexpression of JDP2 activates TRAP and cathepsin K gene promoters and facilitates TRAP-positive multinuclear osteoclast formation; antisense oligonucleotides to JDP2 suppress osteoclast formation. |
Retroviral overexpression, transient transfection/reporter assay, antisense oligonucleotide knockdown, osteoclastogenesis assay in primary bone marrow cells |
The Journal of experimental medicine |
High |
12707301
|
| 2012 |
JDP2 is required in vivo for osteoclastogenesis (Jdp2-/- mice show osteopetrosis) and for neutrophil bactericidal function. JDP2 directly suppresses ATF3 expression via inhibition of histone acetylation at the ATF3 promoter, and ATF3 acts as an inhibitor of neutrophil differentiation. |
Jdp2 knockout mice, skeletal phenotyping, ChIP assay, in vitro differentiation assay, bacterial/fungal infection challenge |
Immunity |
High |
23200825
|
| 2002 |
JDP2 expression is induced during myoblast differentiation; ectopic JDP2 expression in C2C12 cells inhibits cell cycle progression, induces spontaneous muscle differentiation, and activates p38 kinase. JDP2 restores myogenic program in rhabdomyosarcoma (RD) cells. |
Overexpression in C2C12 and RD cells, cell cycle analysis, p38 kinase activity assay, differentiation markers |
The Journal of biological chemistry |
Medium |
12171923
|
| 2007 |
JDP2 suppresses adipocyte differentiation by inhibiting histone H3 acetylation at the C/EBPdelta gene promoter; Jdp2 KO mouse embryonic fibroblasts show elevated C/EBP family gene expression and increased adipogenesis. |
Jdp2 knockout MEFs, hormonal adipocyte induction assay, ChIP for histone acetylation at C/EBPdelta promoter, histological analysis |
Cell death and differentiation |
High |
17464331
|
| 2009 |
JDP2 is directly recruited to an AP-1 site in the cyclin-A2 (Ccna2) promoter to repress its transcription; Jdp2 KO cells have elevated cyclin-A2 mRNA and proliferate faster; reintroduction of JDP2 represses Ccna2 transcription and cell-cycle progression. |
Jdp2 KO mice/MEFs, ChIP, reporter assay, proliferation assays, reintroduction experiments |
Oncogene |
High |
20802531
|
| 2009 |
JDP2 represses ATF3 promoter activity through binding to both a consensus ATF/CRE site and a non-consensus ATF3 auto-repression element; JDP2 KO MEFs show elevated ATF3 expression and potentiated ATF3 induction upon serum or ER stress stimulation. |
Jdp2 KO MEFs, reporter assays, EMSA (implied by promoter binding analysis), Western blotting, in vivo mouse models |
Nucleic acids research |
Medium |
19233874
|
| 2009 |
JDP2-deficient MEFs are resistant to replicative senescence due to increased H3K27 methylation at the p16(Ink4a) promoter; in the absence of JDP2, Polycomb repressive complexes (PRC-1 and PRC-2) bind efficiently to the p16(Ink4a) promoter and silence it. Conversely, JDP2 overexpression induces p16(Ink4a) and p19(Arf) expression. |
Jdp2 KO MEFs, ChIP for H3K27 methylation and PRC binding, overexpression, senescence assays (β-galactosidase) |
The Journal of biological chemistry |
High |
19233846
|
| 2008 |
JDP2 associates with CHOP10 (DDIT3) through leucine zipper interactions; the JDP2-CHOP10 complex strongly activates transcription from promoters containing TPA response elements (TRE) but not CRE elements, with CHOP10's basic domain contributing to DNA binding of the complex. |
Co-IP, reporter assays, EMSA (in vitro and in vivo DNA binding), luciferase assay, overexpression |
Nucleic acids research |
Medium |
18463134
|
| 2008 |
JDP2 binds to the CHOP AARE (amino acid response element) in unstimulated cells and represses CHOP transcription in association with HDAC3; upon amino acid starvation, JDP2 binding decreases and CHOP transcription is derepressed. |
EMSA, reporter assays, ChIP, amino acid deprivation experiments |
FEBS letters |
Medium |
18396163
|
| 2008 |
IRF2-BP1 (IRF2-binding protein-1) interacts with JDP2 and functions as a ubiquitin E3 ligase for JDP2, enhancing its polyubiquitination. IRF2-BP1 also represses ATF2-mediated transcriptional activation from CRE-containing promoters. |
Epitope-tagging co-purification, ubiquitination assay, reporter assay |
FEBS letters |
Medium |
18671972
|
| 2011 |
JDP2 phosphorylation at Thr148 by JNK targets it for proteasomal degradation; T148A substitution stabilizes JDP2, T148E destabilizes it; JNK inhibitor (SP600125) abolishes serum-induced JDP2 degradation; proteasome inhibitor MG132 rescues JDP2 from degradation. |
Site-directed mutagenesis, kinase inhibitor treatment, proteasome inhibitor (MG132), cycloheximide chase, Western blotting |
The Biochemical journal |
High |
21463260
|
| 2011 |
JDP2 suppresses Epstein-Barr virus BZLF1 promoter (Zp) activity by binding the ZII cis-element (CREB/ATF/AP-1 site) in association with HDAC3, reducing histone acetylation. Silencing JDP2 by RNAi increased viral early gene products and viral DNA replication. |
Reporter assay, EMSA, ChIP, mutant virus analysis, siRNA knockdown |
The Journal of biological chemistry |
High |
21525011
|
| 2009 |
JDP2 acts as a co-activator of the progesterone receptor (PR) by interacting with the carboxyl-terminal extension (CTE) of the PR DNA-binding domain; NMR chemical shift analysis mapped binding to CTE residues; mutations in the CTE reduce JDP2-enhanced PR transcriptional activity. The bZIP domain of JDP2 mediates this interaction. |
NMR spectroscopy, peptide competition, point mutagenesis, domain swapping, reporter/transactivation assay |
The Journal of biological chemistry |
High |
19553667
|
| 2012 |
JDP2 transcriptionally represses the Trp53 (p53) promoter via an atypical AP-1 site; JDP2 expression negatively regulates Trp53 expression levels in the context of leukaemogenesis. |
Transposon insertional mutagenesis screen, reporter assay, expression analysis in KO/OE contexts |
Oncogene |
Medium |
22370638
|
| 2019 |
Upon genotoxic stress, ATM phosphorylates JDP2, enabling formation of a β-catenin/JDP2/PRMT5 chromatin complex that elicits H3R2me1/H3R2me2s-induced transcriptional activation via WDR5/MLL methyltransferase recruitment and H3K4 methylation at promoters of GSH-metabolic cascade genes to reestablish glutathione/redox homeostasis. |
Co-IP, chromatin fractionation, ChIP, histone methylation assays, pharmacological inhibition (OICR-9429), genotoxic stress models |
Nature communications |
High |
31434880
|
| 2018 |
JDP2 directly regulates MCL1 transcription to promote T-ALL cell survival; JDP2 depletion by shRNA leads to apoptosis; JDP2 is capable of initiating T-ALL in transgenic zebrafish (rag2:jdp2) with elevated mcl1 expression and steroid resistance. |
shRNA knockdown, reporter/ChIP assay, zebrafish transgenic T-ALL model, in vivo steroid treatment |
The Journal of experimental medicine |
High |
29941549
|
| 2016 |
JDP2 acts as a transcriptional repressor of the FSHβ (Fshb) subunit gene; JDP2 binds the Fshb promoter at an AP-1 site in a complex with c-JUN; GnRH treatment induces c-FOS to replace JDP2 as the c-JUN binding partner, forming transcriptionally active AP-1. JDP2 null female mice show elevated FSH, early puberty, and premature reproductive senescence. |
ChIP, reporter assays, Co-IP, Jdp2 KO mouse phenotyping, hormone measurements |
The Journal of biological chemistry |
High |
28007961
|
| 2014 |
Doublecortin-like protein kinase (DCLK) kinase domain interacts with JDP2 (identified by yeast two-hybrid) and phosphorylates JDP2 efficiently only when histone is present; nuclear translocation of DCLK kinase domain occurs under hyperosmotic stress conditions. |
Yeast two-hybrid, in vitro kinase assay, nuclear translocation imaging |
Biochemical and biophysical research communications |
Low |
24582561
|
| 2019 |
JDP2 directly regulates ATF3 expression; in ATF3/JDP2 double-KO fibroblasts, SDF-1 secretion is elevated and drives tumor growth and vascular perfusion; ATF3 and JDP2 jointly regulate SDF-1 transcription in fibroblasts. |
Double KO mouse model, conditioned medium assay, tumor implantation, SDF-1 depletion rescue |
Oncogene |
Medium |
30670778
|
| 2021 |
JDP2 forms a transcriptional complex with AhR-ARNT and Nrf2-sMAF at DRE and ARE cis-elements of the AhR promoter; Jdp2 is required for AhR promoter activation in response to DMSO; Co-IP and ChIP showed Jdp2 integrates into these phase I/II transcription factor complexes. |
Co-immunoprecipitation, ChIP, reporter assays, Jdp2 KO MEFs, ROS measurement |
Cell biology and toxicology |
Medium |
33723743
|
| 2020 |
In Jdp2-deficient granule cell progenitors (GCPs), a complex of p21Cip1 and Nrf2 binds to antioxidant response elements of the Slc7a11 promoter, increasing xCT/Slc7a11 expression and glutathione levels, thereby conferring resistance to ROS-mediated apoptosis. |
Jdp2 KO mice, primary GCP cultures, ChIP, glutathione measurement, ROS assay, apoptosis assay |
Scientific reports |
Medium |
32188872
|
| 2017 |
CGRP suppresses β-glucan-induced inflammation and osteoclast multinucleation via direct suppression of NF-κB p65 by JDP2 (a transcriptional repressor) and inhibition of actin polymerization; Dectin-1/TRP channel signaling in Nav1.8+ nociceptors drives this pathway. |
Nociceptor ablation, TRPV1/TRPA1 KO mice, β-glucan injection model, CGRP treatment, osteoclast multinucleation assay |
Cell reports |
Medium |
28658621
|
| 2024 |
JDP2 interacts directly with p53 via its C-terminal domain and enhances p53 transactivation; JDP2 decreases MDM2 levels, thereby reversing MDM2-induced p53 repression. JDP2 also slightly enhances p53 protein stability in CHX chase experiments. |
Co-IP, reporter assay (p53-responsive luciferase), CHX chase, overexpression/knockdown, domain mapping |
Cancers |
Medium |
38473360
|
| 2024 |
IRF2BP2 interacts with the AP-1 heterodimer ATF7/JDP2 and is recruited to chromatin by this dimer; IRF2BP2 counteracts the gene-activating function of ATF7/JDP2, and its loss leads to inflammatory pathway overactivation and reduced proliferation in AML cells. |
Co-IP, ChIP, siRNA/KO loss-of-function, proliferation assay, gene expression analysis |
Nucleic acids research |
Medium |
38801077
|
| 2020 |
JDP2 directly activates PDE4B transcription; ChIP and dual-luciferase reporter assays confirmed JDP2 binding to the PDE4B promoter; JDP2 overexpression upregulates PDE4B and exacerbates hypoxia/reoxygenation-induced cardiomyocyte injury. |
Dual-luciferase reporter assay, ChIP, overexpression/knockdown in H9c2 cells, H/R model |
Experimental and therapeutic medicine |
Medium |
35401806
|
| 2009 |
Retroviral insertion into Jdp2 intron 2 in T-cell lymphomas activates non-canonical Jdp2 RNA subspecies generating protein isoforms lacking the INHAT (inhibitor of histone acetyltransferase) domain; these shorter isoforms localize to the nucleus and, when co-expressed with oncogenic NRAS, increase anchorage-independent growth. |
Northern blot, qRT-PCR, promoter analysis, nuclear localization imaging, anchorage-independent growth assay |
Nucleic acids research |
Medium |
19502497
|