| 2002 |
RANKL selectively induces NFATc1 expression via TRAF6 and c-Fos signaling pathways, evokes Ca2+ oscillations leading to calcineurin-mediated NFATc1 activation, and triggers a sustained NFATc1-dependent transcriptional program during osteoclast differentiation. NFATc1-deficient embryonic stem cells fail to differentiate into osteoclasts in response to RANKL, and ectopic NFATc1 expression causes precursor cells to differentiate without RANKL, establishing NFATc1 as a master transcriptional switch downstream of RANKL for terminal osteoclast differentiation. |
NFATc1-deficient ES cell differentiation assay, ectopic NFATc1 expression, Ca2+ oscillation imaging, genetic epistasis (TRAF6/c-Fos pathways) |
Developmental cell |
High |
12479813
|
| 1997 |
Glycogen synthase kinase-3 (GSK-3) is a component of the NF-ATc kinase that phosphorylates conserved serines in the NF-ATc N-terminus, promotes nuclear export, and thereby opposes Ca2+-calcineurin signaling that drives nuclear import. |
Biochemical purification of NF-AT kinase, in vitro phosphorylation assay, nuclear localization assays |
Science |
High |
9072970
|
| 2000 |
GSK-3 phosphorylation of the conserved Ser-Pro repeat motifs in NFATc negatively regulates its intrinsic DNA binding activity, in addition to controlling its subcellular localization; calcineurin-mediated dephosphorylation enhances DNA binding. |
Gel mobility shift assay, in vitro phosphorylation, NFATc mutant analysis |
The Journal of biological chemistry |
High |
11063740
|
| 2000 |
JNK, ERK, p38, and CK2 physically associate with the NFATc N-terminal regulatory domain and directly phosphorylate Ser172 and conserved Ser-Pro repeats, blocking ionomycin-induced nuclear translocation; CK2 additionally phosphorylates a conserved motif downstream of the Ser-Pro repeats important for nuclear export. |
Co-immunoprecipitation, in vitro kinase assay, overexpression/inhibitor studies, subcellular localization assay |
The Journal of biological chemistry |
High |
10652349
|
| 1997 |
The DNA-binding domain (DBD) of NFATc has an unusual Rel-like fold that is both necessary and sufficient for DNA binding and cooperative transcriptional activation; despite overall structural homology to NF-κB p50, the two proteins use significantly different strategies for DNA recognition. A model was proposed for cooperative complex formation with AP-1 on the IL-2 enhancer. |
NMR solution structure determination, DNA binding assays, transcriptional activation assays |
Nature |
High |
8990122
|
| 2001 |
NFATc1 (NFATc) undergoes activity-dependent nuclear translocation in adult skeletal muscle fibers: slow-twitch electrical stimulation patterns (10 Hz continuous or 5-s trains) drive cyclosporin A-sensitive nuclear accumulation of NFATc-GFP foci, whereas fast-twitch patterns (50 Hz) or low-frequency (1 Hz) stimulation do not, indicating NFATc1 nuclear import contributes to slow fiber-type gene regulation. |
Live-cell GFP imaging in adult muscle fibers, electrical stimulation, pharmacological inhibition (cyclosporin A), kinase inhibitors |
The Journal of cell biology |
High |
11581284
|
| 2008 |
NFATc1 is preferentially expressed by hair follicle stem cells in their niche downstream of BMP signaling, where it transcriptionally represses CDK4 to maintain stem cell quiescence; pharmacological or genetic ablation of calcineurin/NFATc1 signaling causes premature stem cell activation and precocious follicular growth. |
Conditional and complete NFATc1 gene ablation, pharmacological calcineurin inhibition, reporter/ChIP assays for CDK4 repression |
Cell |
High |
18243104
|
| 2008 |
NFATc1 binds a novel regulatory element at the pdcd1 (PD-1) locus and is required for PD-1 gene transcription upon T cell stimulation; mutation of the NFATc1 binding site abolishes promoter activity. |
Chromatin immunoprecipitation, reporter gene assay with binding site mutagenesis, calcineurin inhibitor and NFAT-specific inhibitor treatment |
Journal of immunology |
High |
18802087
|
| 1999 |
NFATc1 isoforms B and C contain long C-terminal extensions beyond the previously described isoform A; isoform C possesses a second transactivation domain (TAD-B) in its C-terminal peptide that responds to T cell stimuli similarly to TAD-A but remains unphosphorylated, while isoform B exerts suppressive transcriptional effects through its shorter C-terminal peptide. |
Alternative splicing analysis, transactivation domain mapping, reporter assays, phosphorylation analysis in stimulated T cells |
Journal of immunology |
Medium |
10358178
|
| 2002 |
NFATc1 and NFATc2 are both positive regulators of IL-4 gene transcription with intrinsically similar DNA-binding and transcriptional activities at the IL-4 gene, suggesting that the disparate IL-4 phenotypes in NFAT1−/− vs. NFAT2−/− T cells arise from differential regulation of the two proteins rather than intrinsic differences in their transcriptional activities. |
Constitutively active NFATc mutants (alanine substitutions), IL-4 transcription assays in T cells |
European journal of immunology |
Medium |
12355451
|
| 2014 |
NFAT2 (NFATc1) is required in follicular regulatory T cells (TFR) to upregulate CXCR5 expression, enabling their homing to B cell follicles; T cell-specific NFAT2 ablation reduces TFR cells in follicular populations and exacerbates lupus-like autoimmune disease. |
T cell-specific Nfat2 conditional knockout mice, immunization experiments, flow cytometry, disease scoring |
The Journal of experimental medicine |
High |
24590764
|
| 2003 |
NFATc1 is required cell-intrinsically for normal B-1a cell development; NFATc1-deficient mice lack peritoneal and splenic B-1a cells, while NFATc2-deficient mice have a normal B-1a compartment; NFATc1 protein is elevated ~5-fold in B-1a versus B-2 cells. |
NFATc1-deficient and NFATc2-deficient mouse analysis, mixed-allotype chimeras, retroviral gene transduction, flow cytometry |
Proceedings of the National Academy of Sciences |
High |
14595020
|
| 2006 |
The calcineurin-NFATc pathway directly regulates AQP2 (aquaporin-2) expression in renal collecting duct cells through functional NFAT binding sites in the AQP2 proximal promoter; hypertonicity promotes nuclear translocation of NFATc proteins (in addition to TonEBP/NFAT5) to induce AQP2, and calcineurin activity is involved in TonEBP/NFAT5 induction by hypertonicity. |
Promoter mutational analysis, chromatin immunoprecipitation, nuclear translocation assays, calcineurin inhibitor studies |
American journal of physiology. Cell physiology |
High |
17166937
|
| 2011 |
NFATC1 is expressed in epicardium-derived cells and is required for their invasion into myocardium; RANKL/calcineurin signaling activates NFATC1 to induce cathepsin K (CTSK) expression, enabling ECM degradation and cell invasion; loss of NFATC1 in EPDCs causes reduced coronary vessel and fibrous matrix penetration and embryonic lethality by E18.5. |
Conditional NFATC1 knockout in EPDCs, RANKL treatment of PE-derived cell cultures, in vivo CTSK expression analysis, calcineurin inhibitor experiments |
Development |
High |
21447555
|
| 2009 |
NFATc1 is required for lymphatic endothelial development; in NFATc1-null mice, lymphatic endothelial cells fail to properly coalesce into lymph sacs; calcineurin inhibition with cyclosporin A reduces podoplanin and FGFR-3 expression in lymphatics; NFATc1 siRNA reduces VEGFR-3 and podoplanin expression and NFATc1 activates lymphatic-specific gene promoters. |
NFATc1 knockout mouse analysis, cyclosporin A treatment in utero, siRNA knockdown, reporter assays, immunofluorescence co-localization |
Mechanisms of development |
High |
19233265
|
| 2013 |
Cartilage-specific ablation of NFATc1 in NFATc2-deficient mice leads to early onset aggressive osteoarthritis with loss of proteoglycans, collagen/aggrecan degradation, osteophyte formation, and joint instability, indicating NFATc1 and NFATc2 cooperate to repress spontaneous OA in chondrocytes. |
Cartilage-specific NFATc1 conditional knockout in NFATc2-/- mice, histomorphometry, micro-CT, analysis of human OA cartilage samples |
Proceedings of the National Academy of Sciences |
High |
24248346
|
| 2016 |
IKKε phosphorylates NFATc1 during T cell activation, promoting its cytoplasmic retention and inhibiting T cell antitumor and antiviral immune responses; loss of IKKε elevates T cell immunity, while constitutively nuclear NFATc1 restores sorafenib resistance in IKKε-activated contexts. |
Kinase assay, T cell activation assays, IKKε knockout mice, tumor and viral infection models |
Cell reports |
Medium |
27346349
|
| 2017 |
NFATc1 controls cytotoxic T lymphocyte effector functions including cytoskeleton organization, recruitment of cytosolic organelles to immunological synapses, and glycolytic metabolic switching; NFATc1-deficient CD8+ T cells show impaired cytotoxicity and glycolysis that can be restored by IL-2. Genome-wide ChIP-seq confirms NFATc1 binding to genes controlling CTL activity including Tbx21 and Gzmb. |
Nfatc1 conditional KO in T cells, genome-wide ChIP-seq, transcriptome analysis, metabolic assays, in vivo infection/tumor models |
Nature communications |
High |
28894104
|
| 2017 |
DYRK1A phosphorylates NFATc1/αA at S261, S278, S403, and S409, which interferes with NFATc1 ubiquitination and proteasomal degradation, thereby stabilizing the protein and increasing its transcriptional activity—contrary to its suppressive role on NFATc2. |
In vitro kinase assay with site-specific mutagenesis, ubiquitination assay, protein stability assay, transcriptional reporter assay |
PloS one |
Medium |
28235034
|
| 2021 |
SUMOylation of NFATc1 represses IL-2 production in T cells in vivo; transgenic mice in which NFATc1 SUMOylation is prevented show elevated IL-2, expanded regulatory T cells, and ameliorated autoimmune encephalomyelitis and graft-versus-host disease. Mechanistically, increased IL-2 counteracts IL-17/IFN-γ through STAT5 and Blimp-1 induction. |
SUMO-site mutant transgenic mouse generation, in vivo EAE and GVHD models, cytokine and transcription factor analysis |
The Journal of experimental medicine |
High |
32986812
|
| 2019 |
STAT3 drives NFATc1 transcription by directly binding to the NFATc1 promoter in osteoclast precursors; conditional deletion of Stat3 in osteoclasts reduces NFATc1 expression and impairs osteoclast differentiation, and enforced NFATc1 expression rescues the Stat3-deficient differentiation defect. |
Osteoclast-specific Stat3 conditional knockout (Ctsk-Cre), promoter binding by ChIP, NFATc1 rescue experiments, STAT3 inhibitor (AG490) |
The Journal of biological chemistry |
High |
31462535
|
| 2014 |
NFATc1 directly binds the Itpr2 promoter and regulates InsP3R2 (type 2 IP3 receptor) gene expression in cardiomyocytes; calcineurin-NFATc1 signaling upregulates InsP3R2 in cardiac hypertrophy, forming a positive feedback loop because InsP3R2-mediated Ca2+ release activates calcineurin-NFATc. |
Promoter-reporter assay, chromatin immunoprecipitation, calcineurin transgenic mice, calcineurin inhibitor studies |
The Journal of biological chemistry |
High |
24415751
|
| 2009 |
FOXP3 competes with NFAT1 for binding to the endogenous NFAT2 (NFATc1) promoter, suppressing NFAT2 transcription in regulatory T cells; ectopic NFAT2 expression in FOXP3+ Treg cells partially restores IL-2 production, indicating FOXP3-mediated NFAT2 repression contributes to the anergic phenotype. |
Chromatin immunoprecipitation, inducible FOXP3 expression, retroviral NFAT2 overexpression, promoter reporter assays |
Journal of immunology |
High |
19564342
|
| 2014 |
NF-κB1/p50 and c-Rel control the induction of NFATc1/αA in BCR-stimulated B cells via two composite κB/NFAT-binding sites in the inducible Nfatc1 P1 promoter. |
B cell-specific NF-κB knockouts, promoter-reporter assays with binding site analysis, BCR stimulation experiments |
European journal of immunology |
Medium |
25179582
|
| 2024 |
Transient activation of the serine synthesis pathway (SSP) is required for osteoclastogenesis; SSP-derived α-ketoglutarate is necessary for histone demethylases that remove repressive histone methylation marks at the Nfatc1 gene locus, thereby inducing NFATc1 expression and osteoclast maturation. Deletion of the rate-limiting SSP enzyme phosphoglycerate dehydrogenase in osteoclast progenitors impairs differentiation. |
Osteoclast progenitor-specific PHGDH deletion, chromatin/histone methylation analysis, metabolite supplementation, OVX mouse model |
Nature metabolism |
High |
38200114
|
| 2023 |
NFATc1 transcriptionally upregulates SLC7A11 (xCT) during RANKL-induced osteoclastogenesis, increasing cystine import in osteoclast precursors; during TXNRD1 inhibition this causes cystine accumulation and disulfidptosis, selectively killing osteoclast precursors over BMDMs. |
NFATc1 ChIP/transcriptional assay for SLC7A11 promoter, TXNRD1 inhibitor treatment, rescue with SLC7A11 inhibitors, OVX mouse model |
Redox biology |
Medium |
37148740
|
| 2012 |
Cot (Tpl-2) serine/threonine kinase directly phosphorylates NFATc1 (and all other NFATc family members) and increases NFATc1 protein stability, promoting Ca2+ oscillation/calcineurin-independent osteoclastogenesis through osteoblast-osteoclast cell-cell contact. |
In vitro kinase assay, co-culture system, Cot overexpression/knockdown, NFATc1 stability assay |
Molecular and cellular biology |
High |
22615493
|
| 2005 |
CCR1 is a direct transcriptional target of NFATc1/NFAT2 during RANKL-induced osteoclastogenesis; the CCR1 upstream regulatory region shows RANKL-dependent, cyclosporin A-suppressible promoter activity; CCR1 signaling downstream of NFAT2 enhances migration of differentiating osteoclasts. |
Microarray analysis, quantitative RT-PCR, luciferase promoter reporter assay, CCR1 siRNA, Boyden chamber migration assay |
Journal of bone and mineral research |
Medium |
16355273
|
| 2007 |
NFATc (NFATc4 expressed in tendons) binds TSE1 in nuclear extracts from tendon fibroblasts and transactivates the COL1a1 promoter through this element; inhibition of NFATc nuclear translocation strongly inhibits COL1a1 gene expression, suggesting NFATc and scleraxis cooperate to activate type I collagen expression specifically in tendon fibroblasts. |
Gel shift assay (EMSA), transfection/reporter assays, pharmacological NFATc nuclear translocation inhibition |
The Journal of biological chemistry |
Medium |
17430895
|
| 2007 |
NFATc1 is required for TGF-β-mediated transcriptional induction of fibronectin in mesangial cells; constitutively active calcineurin increases fibronectin transcription, and dominant-negative NFATc or NFATc1 inhibition blocks TGF-β-mediated fibronectin promoter activation. |
Calcineurin inhibitors, constitutively active calcineurin overexpression, dominant-negative NFATc expression, promoter reporter assay |
Biochemical and biophysical research communications |
Medium |
17719012
|
| 2013 |
High glucose activates NFATc1 (NFAT2) in podocytes via increased intracellular Ca2+ leading to calcineurin activation, and NFATc1 mediates podocyte apoptosis through transcriptional upregulation of Bax; calcineurin/NFAT2 inhibition blocks both nuclear accumulation and apoptosis. |
Immunofluorescence, western blot, flow cytometry, Ca2+ imaging with Fluo-3/AM, calcineurin inhibitors, NFAT2-specific inhibitor (11R-VIVIT) |
Experimental cell research |
Medium |
23340267
|
| 2012 |
The calcineurin/NFATc1 signaling pathway promotes HCC cell proliferation; calcineurin-regulated NFATc1 nuclear import/export is demonstrated in HepG2 cells, and NFATc1 knockdown causes G1 cell cycle arrest and reduces c-Myc and COX-2 expression, suggesting NFATc1 drives proliferation through these oncogenes. |
NFATc1 siRNA knockdown, immunofluorescence, western blot, flow cytometry cell cycle analysis, ionomycin/cyclosporin A treatment |
Digestive diseases and sciences |
Medium |
22722879
|
| 2015 |
NFATc1 drives EMT reprogramming and maintains pancreatic cancer cells in a stem cell-like state through Sox2-dependent transcription of EMT and stemness factors; NFATc1-Sox2 complex-mediated dedifferentiation is opposed by p53-miR200c signaling, and inactivation of the p53 pathway is required for NFATc1-driven tumor dedifferentiation. |
NFATc1 gain/loss of function, Sox2 co-expression analysis, genetically engineered mouse models, transcriptional reporter assays, human PDAC analysis |
The EMBO journal |
Medium |
25586376
|
| 2023 |
The deubiquitinase UCHL1 deubiquitinates and stabilizes TAZ at K46 by removing K48-linked polyubiquitination; stabilized TAZ inhibits NFATc1 dephosphorylation and nuclear transport by competing with calcineurin A for binding to NFATc1, thereby negatively regulating osteoclastogenesis. |
Osteoclast-specific UCHL1 conditional KO, proteomic analysis, ubiquitination assay, Co-IP (TAZ-calcineurin-NFATc1 competition), OVX mouse model |
International journal of biological sciences |
Medium |
37215988
|
| 2020 |
Zebrafish Nfatc1 is required for valve interstitial cell (VIC) formation in cardiac valve development by promoting proliferation and endocardial/neural crest cell recruitment; Nfatc1 promotes expression of twist1b (a regulator of endothelial-to-mesenchymal transition) as a downstream effector; loss of Nfatc1 results in valvular dysfunction with persistent retrograde blood flow. |
Zebrafish nfatc1 mutants, live imaging, high-speed microscopy, echocardiography, transcriptional target analysis |
Circulation research |
Medium |
32070236
|
| 2019 |
NFAT2 (NFATc1) is a critical regulator of the anergic phenotype in CLL B cells; B cell-specific ablation of Nfat2 leads to loss of anergy and transformation to aggressive disease; NFAT2-dependent gene expression signature includes Cbl-b, Grail, Egr2, and Lck. |
B cell-specific Nfat2 conditional knockout mouse CLL models, gene expression analysis, human CLL biopsy analysis |
Nature communications |
High |
28970470
|
| 2014 |
NFATc1 activity is required for early B cell development; loss of NFATc1 in pro-B cells suppresses EBF1 expression, impairs immunoglobulin gene rearrangement and preBCR formation, arresting pro-B to pre-B cell transition and causing severe B cell lymphopenia. |
Multiple NFATc1-deficient mouse models, bone marrow analysis, flow cytometry, immunoglobulin rearrangement assays |
Cellular & molecular immunology |
High |
29907883
|
| 2022 |
NFATc1 drives NAFLD progression through chronic ER stress sensing and activation of the PERK-CHOP unfolded protein response pathway in hepatocytes; hepatocyte-specific NFATc1 depletion prevents disease acceleration in high-fat western diet-fed mice, and NFATc1-induced NASH progression can be blocked by TUDCA. |
Hepatocyte-specific NFATc1 transgenic/KO mice, western diet feeding, UPR pathway analysis, TUDCA treatment, human NAFLD patient samples |
Gut |
High |
35365570
|
| 2014 |
NFATc1 regulates dexamethasone-induced myocilin (MYOC) expression in human trabecular meshwork cells via calcineurin activation; dexamethasone causes calcium-independent NFATc1 nuclear translocation within 15 minutes, and both calcineurin inhibitors and NFATc1 siRNA block DEX-induced MYOC mRNA increase. |
Calcineurin inhibitors (cyclosporin A, INCA-6), NFATc1 siRNA, immunofluorescence nuclear translocation assay, qRT-PCR |
Experimental eye research |
Medium |
25450062
|
| 2013 |
NFATc1 regulates TRAIL expression in intestinal cells by activating the TRAIL promoter and negatively regulating Sp1 binding to the TRAIL promoter; knockdown of NFATc1 increases Sp1 binding and inhibition of Sp1 increases TRAIL expression, indicating an indirect regulatory mechanism. |
NFATc1 knockdown, Sp1 inhibition, promoter activity assay, chromatin analysis |
PloS one |
Medium |
21603612
|
| 2004 |
IL-2 and IL-15 oppositely regulate CX3CR1 expression through differential recruitment of NFAT2 versus NFAT1 to a κB-like NFAT site in the CX3CR1 promoter; IL-2 promotes NFAT2 binding while IL-15 promotes NFAT1 binding, as demonstrated by ChIP. |
Chromatin immunoprecipitation, NFAT1-/- mice, promoter mutation assays, luciferase reporter in PBMCs, NFAT inhibitor experiments |
The Journal of biological chemistry |
High |
15347678
|
| 2019 |
CR3 engagement by M. leprae PGL-I activates the Syk tyrosine kinase, which induces calcineurin-dependent nuclear translocation of NFATc in innate immune cells (macrophages, neutrophils, dendritic cells), selectively augmenting production of IL-2 (DCs), IL-10 (PMNs), and IL-1β (macrophages). |
CR3 engagement assays, Syk inhibition, calcineurin inhibition, NFATc nuclear translocation imaging, cytokine measurements, intranasal infection model |
Frontiers in immunology |
Medium |
31921172
|
| 2012 |
NFATc1-mediated calcineurin signaling activation in mesangial cells drives uPAR-ITGB3 pathway activation; calcineurin-NFATC inhibition by miR-30 family blocks this pathway. In cultured podocytes, calcineurin-NFATC signaling activates the uPAR-ITGB3 pathway, leading to Rho GTPase activation, synaptopodin downregulation, and cytoskeletal injury. |
Podocyte-specific miR-30 KO, calcineurin/NFATC inhibitors, Transwell co-culture system, podocyte-specific transgenic miR-30, cytoskeletal assays |
Cell death & disease |
Medium |
31127093
|
| 2017 |
KCa3.1 (a Ca2+-activated K+ channel) modulates Ca2+-induced NFATc1 activation during inflammatory osteoclastogenesis via the CaMKIV/CREB/c-Fos axis; KCa3.1 deficiency or TRAM-34 blockade reduces RANKL-induced Ca2+ transient amplitudes by ~50% and decreases NFATc1 expression and transcriptional activity. |
KCa3.1 knockout mice, TRAM-34 pharmacological inhibition, live cell Ca2+ imaging, western blot for pathway components, BMM culture osteoclastogenesis |
Journal of immunology |
Medium |
29246953
|
| 2023 |
The short NFATc1/αA isoform is essential for osteoclastogenesis and self-regulation; NFATc1/αA-specific knockout mice die in utero by E13.5, and in a novel hematopoietic stem cell differentiation culture system, loss of NFATc1/αA impairs osteoclast differentiation and expression of osteoclast markers and Nfatc1 regulators. |
Short-isoform-specific NFATc1/αA knockout mouse, novel HSC-to-osteoclast in vitro culture system, gene expression analysis |
Scientific reports |
Medium |
37914750
|
| 2020 |
Homer2 and Homer3 regulate NFATc1 function in osteoclastogenesis by interacting with NFATc1 and competing with its activation by calcineurin; RANKL treatment inhibits Homer-NFATc1 interaction, which is restored by calcineurin inhibition (cyclosporin A). Homer2/3 double knockout markedly decreases bone density. |
Homer2/3 double knockout mice, BMM osteoclastogenesis assay, Co-IP of Homer-NFATc1, calcineurin inhibitor experiments, micro-CT |
The Journal of endocrinology |
Medium |
31319381
|
| 2002 |
GATA5 and NF-ATc (NFATc1) synergistically activate endocardial transcription; inhibition of either GATA5 expression or NF-ATc activation blocks terminal endothelial-endocardial differentiation at a pre-endocardial stage in an in vitro model of cardiogenic differentiation. |
In vitro cardiogenic differentiation model, calcineurin/NF-ATc inhibition, GATA5 expression manipulation, transcriptional reporter assays |
Development |
Medium |
12163407
|
| 2013 |
NFATc1 (NFAT2) suppresses E-cadherin expression by transcriptionally upregulating Snail and Zeb1 in a TGF-β-independent manner, promoting cancer cell invasion; inducible constitutively active NFATc1 expression promotes invasion in A549 and MCF7 cells and in tumor xenografts in vivo. |
Inducible constitutively active NFATc1 expression, RNA interference, cell invasion assay, tumor xenograft, gene expression analysis |
Cancer research |
Medium |
23811942
|
| 2013 |
NFAT2 regulates HDAC1 transcriptional activity in glioblastoma stem cells; NFAT2-HDAC1 signaling maintains the mesenchymal phenotype, and loss of both NFAT2 and HDAC1 causes hyperacetylation of NF-κB, inhibiting NF-κB-dependent transcription. |
NFAT2 siRNA knockdown, HDAC1 rescue experiments, NFAT2 overexpression, NF-κB acetylation analysis, in vivo tumorigenicity |
Neuro-oncology |
Medium |
31400279
|
| 2019 |
RBP-J represses while NFATc1 activates miR182 expression in TNF-induced osteoclastogenesis through binding to specific open chromatin regions in the miR182 promoter; this RBP-J/NFATc1-miR182 regulatory network controls the balance between activating and repressive signals in inflammatory osteoclastogenesis. |
ChIP for NFATc1 and RBP-J binding to miR182 promoter, miR182 inhibition, open chromatin analysis, in vivo inflammatory arthritis model |
FASEB journal |
Medium |
31908034
|