Affinage

NAB2

NGFI-A-binding protein 2 · UniProt Q15742

Length
525 aa
Mass
56.6 kDa
Annotated
2026-06-10
100 papers in source corpus 24 papers cited in narrative 25 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 6/6 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

NAB2 (MADER) is a transcriptional coregulator that governs the output of EGR-family transcription factors, functioning canonically as a corepressor that limits EGR-driven mitogenic and fibrotic gene programs (PMID:8668170, PMID:11327726). It binds the R1 domain of NGFI-A (Egr-1) and Krox20 through its first conserved domain (NCD1) and represses their transcriptional activation (PMID:8668170), with repression depending in part on direct interaction with CHD4, a subunit of the NuRD nucleosome-remodeling and deacetylase complex, which NAB2 recruits to target promoters such as Rad and COL1A2 to reduce histone H4 acetylation (PMID:16574654, PMID:19888474). NAB2 is itself a delayed early-response gene induced by EGR1/2/3 through Egr/Sp1 cis-elements and represses its own EGR-induced promoter, establishing a conserved negative feedback loop (PMID:16260776, PMID:20506119); it is induced downstream of serum, NGF, TGF-β, mechanical arterial injury, and FGF23, in each case curbing EGR-1–dependent responses including neuronal differentiation, collagen synthesis, myofibroblast differentiation, tissue factor expression, and angiogenesis (PMID:9722618, PMID:10514413, PMID:12427750, PMID:19888474, PMID:17174939). In a context-dependent reversal, NAB2 acts as an EGR-1 coactivator at the IL-2 promoter in T cells and participates in TRAIL and BCAR1/p130Cas regulation in immune and cancer cells (PMID:17142725, PMID:22128144, PMID:22431919). Its activity is gated by nuclear import through a KKXK (K343–K346) nuclear localization signal (PMID:30411343). In solitary fibrous tumors, a recurrent NAB2-STAT6 gene fusion joins the EGR-binding domain of NAB2 to the STAT6 transactivation domain, converting the repressor into a constitutive coactivator that redirects NAB1, NAB2, and EGR1 to the nucleus and drives an EGR1-target enhancer program—including a neuroendocrine signature and IGF2 induction—to promote tumor cell proliferation (PMID:23313952, PMID:40875449, PMID:32216968).

Mechanistic history

Synthesis pass · year-by-year structured walk · 23 steps
  1. 1996 High

    Established the founding mechanism by identifying NAB2 as a direct corepressor of EGR factors and mapping the interaction to defined protein domains, defining how EGR transcriptional output is restrained.

    Evidence Interaction mapping and reporter assays showing NCD1 binding to the R1 domain of NGFI-A and Krox20 with repression; Northern blot showing serum/NGF induction

    PMID:8668170

    Open questions at the time
    • Did not define the corepression machinery recruited downstream of binding
    • Negative feedback inferred from induction kinetics, not directly demonstrated at this stage
  2. 1997 Medium

    Showed that alternative splicing controls NAB2 function, since an exon-3-deleted isoform loses repression, and located NAB2 adjacent to STAT6 on 12q13 — a genomic juxtaposition later proving oncogenically relevant.

    Evidence Genomic sequencing, RT-PCR, and reporter assays of splice isoforms

    PMID:9126479

    Open questions at the time
    • Functional importance of the 12q13 NAB2/STAT6 proximity not yet appreciated
    • Mechanism by which exon-3 loss abolishes repression not resolved
  3. 1998 High

    Demonstrated a cellular phenotype for NAB2 corepression by showing it blocks NGF-induced neuronal differentiation and growth arrest specifically through delayed response genes, placing NAB2 downstream of immediate-early signaling.

    Evidence Stable, transient, and adenoviral overexpression in PC12 cells with growth and gene-induction readouts

    PMID:9722618

    Open questions at the time
    • Did not identify the chromatin machinery mediating delayed-gene repression
    • Endogenous loss-of-function not tested
  4. 1999 Medium

    Extended NAB2's corepressor role to the vasculature, showing injury- and PMA-induced NAB2 inhibits Egr-1-dependent transcription in smooth muscle, linking it to vascular injury responses.

    Evidence Western/Northern blot, in vivo arterial injury model, reporter assays in VSMC

    PMID:10514413

    Open questions at the time
    • Causal contribution to neointima formation not established by loss-of-function
    • Target gene set incompletely defined
  5. 2001 Medium

    Mapped NAB2's anti-mitogenic/anti-fibrotic reach by showing it blocks Egr-1 induction of tissue factor and multiple growth factors, and that a dominant-negative mutant defines functional domains required for repression.

    Evidence Reporter assays, dominant-negative mutagenesis, ELISA, in vitro angiogenesis assay

    PMID:11327726

    Open questions at the time
    • Direct promoter occupancy not shown for most targets
    • Single-lab observation
  6. 2002 High

    Showed NAB2 functionally suppresses angiogenesis by blocking VEGF-induced tissue factor and proangiogenic gene programs, broadening its physiological role to vessel formation.

    Evidence Adenoviral overexpression, RT-PCR, reporter assays, in vitro and in vivo Matrigel angiogenesis assays

    PMID:12427750

    Open questions at the time
    • Endogenous NAB2 requirement in angiogenesis not tested by depletion
    • Chromatin mechanism not addressed
  7. 2005 High

    Closed the regulatory circuit by showing Egr-1 directly activates the NAB2 promoter via Egr/Sp1 sites while NAB2 represses its own promoter, formally establishing the negative feedback loop.

    Evidence Promoter cloning, EMSA, reporter assays, siRNA knockdown

    PMID:16260776

    Open questions at the time
    • Quantitative dynamics of the feedback loop not modeled
    • Did not address coactivator contexts
  8. 2006 High

    Identified the chromatin-modifying mechanism of NAB2 repression by showing it recruits CHD4 of the NuRD complex and co-occupies an endogenous target promoter, explaining how EGR-bound NAB2 silences transcription.

    Evidence Co-IP, GST pulldown, ChIP at the Rad promoter, mutagenesis, reporter assays in Schwann cells

    PMID:16574654

    Open questions at the time
    • Whether NuRD recruitment is universal across all NAB2 targets not established
    • How splicing toggles the CHD4 interaction mechanistically unresolved
  9. 2006 High

    Revealed NAB2's context-dependent reversal to coactivation, showing it is recruited to the IL-2 promoter Egr-1 site and is required for IL-2 transcription in T cells, breaking the strict-corepressor view.

    Evidence Overexpression, siRNA, ELISA, ChIP, reporter assays in T cells

    PMID:17142725

    Open questions at the time
    • Molecular switch determining repression versus activation not defined
    • Cofactors driving coactivation not identified
  10. 2006 Medium

    Showed FGF23 signaling induces nuclear NAB2 isoforms that suppress Egr-1, generalizing the feedback motif to renal FGF23 signaling.

    Evidence RT-PCR, immunolocalization, reporter assays in kidney cells

    PMID:17174939

    Open questions at the time
    • Physiological consequence in vivo not tested
    • Single-lab expression-level observation
  11. 2008 Medium

    Placed NAB2 within an EGR regulatory hierarchy in T cells, showing Egr-1/NAB2 promote and Egr-2/Egr-3 suppress T cell responsiveness, defining opposing arms of an immune fate decision.

    Evidence Egr-2/Egr-3 knockout and Egr-3 transgenic mice, in vivo pneumonitis model, T cell functional assays

    PMID:18203138

    Open questions at the time
    • Direct NAB2 loss-of-function in this circuit not isolated
    • Mechanism of Egr-2/3 suppression of NAB2 not detailed
  12. 2009 High

    Established NAB2 as an anti-fibrotic brake in vivo, showing TGF-β-induced NAB2 recruits NuRD to the COL1A2 promoter to limit collagen and myofibroblast differentiation, with Nab2-null mice accumulating dermal collagen.

    Evidence Overexpression, siRNA, ChIP, histone acetylation assay, Nab2 knockout mouse

    PMID:19888474

    Open questions at the time
    • Whether fibrosis phenotype generalizes beyond skin not addressed
    • Relative contribution of NAB1 not parsed
  13. 2010 Medium

    Generalized the feedback architecture by showing all three EGR factors activate NAB2 and NAB2 represses each, confirming a conserved EGR-NAB2 autoregulatory loop across cell types.

    Evidence Overexpression, siRNA, reporter assays in neuroectodermal and epithelial cells

    PMID:20506119

    Open questions at the time
    • Direct promoter binding for EGR2/EGR3 not shown here
    • Single-lab reporter-based evidence
  14. 2011 High

    Linked NAB2 coactivator function to immune memory, showing IL-2-induced NAB2 represses TRAIL to enable helped CD8+ T cell secondary responses, with dominant-negative NAB2 rescued by TRAIL blockade.

    Evidence Retroviral overexpression, dominant-negative, TRAIL blockade, FACS, in vivo T cell assays

    PMID:22128144

    Open questions at the time
    • Direct TRAIL promoter occupancy by NAB2 not shown
    • Repressor versus activator role at TRAIL ambiguous across cell types
  15. 2012 Medium

    Identified a positive feedback role in cancer, showing EGR1 and NAB2 jointly upregulate p130Cas/BCAR1 in breast cancer with reciprocal reinforcement, again departing from pure corepression.

    Evidence Overexpression, siRNA, ChIP, RT-PCR, Western blot

    PMID:22431919

    Open questions at the time
    • Mechanism converting NAB2 to coactivator at BCAR1 not defined
    • Single-lab cell-line study
  16. 2013 High

    Established NAB2 as an oncogenic driver by identifying recurrent NAB2-STAT6 fusions in essentially all solitary fibrous tumors, with the fusion converting the repressor into an EGR-target activator that drives proliferation.

    Evidence Whole-exome and transcriptome sequencing across 51 SFTs, RT-PCR, overexpression with proliferation and expression readouts

    PMID:23313952

    Open questions at the time
    • Genome-wide enhancer targets of the fusion not mapped at this stage
    • Mechanism of repressor-to-activator conversion not yet detailed
  17. 2013 High

    Provided a diagnostic and mechanistic signature of the fusion by showing NAB2-STAT6 drives aberrant nuclear relocalization of normally cytoplasmic STAT6, detectable by PLA and IHC.

    Evidence Proximity ligation assay, immunohistochemistry, exome sequencing across meningeal SFT/HPC versus meningiomas

    PMID:23575898

    Open questions at the time
    • Functional consequence of relocalization on transcription not directly assayed here
    • Did not address downstream gene program
  18. 2013 Medium

    Showed NAB2/EGR-1 reciprocally regulate TRAIL in NK cells, with NAB2 promoting and EGR-1 braking TRAIL induction, refining the context-dependence of the NAB2-EGR axis.

    Evidence Overexpression, knockdown, FACS, TRAIL expression assays in NK cells

    PMID:23416169

    Open questions at the time
    • Direct promoter occupancy not shown
    • Opposite directionality of TRAIL regulation versus CD8+ T cells unexplained
  19. 2017 Medium

    Identified WT1 as an upstream activator that both induces NAB2 and recruits it to the IRF8 promoter, expanding NAB2's coregulator partnerships beyond EGR factors.

    Evidence ChIP, reporter assays, overexpression, siRNA in leukemic cells

    PMID:29152069

    Open questions at the time
    • Whether NAB2 represses or activates WT1 targets context-dependent
    • NuRD involvement in WT1-NAB2 complexes not tested
  20. 2018 Medium

    Defined the molecular basis of NAB2 nuclear access by mapping its NLS to the KKXK (K343–K346) motif, which is necessary and sufficient for nuclear localization — a control point later exploited by the STAT6 fusion.

    Evidence Site-directed mutagenesis, fluorescence localization, fusion-protein sufficiency test

    PMID:30411343

    Open questions at the time
    • Import receptors recognizing KKXK not identified
    • Regulation of NLS usage under signaling not addressed
  21. 2020 Medium

    Defined a proliferative effector axis of the fusion by showing NAB2-STAT6 upregulates EGR-1 and IGF2 and drives cell-cycle entry, with IGF2 inhibition reducing proliferation.

    Evidence Transfection, Western blot, RT-PCR, proliferation assay, pharmacological IGF2 inhibition in NIH-3T3 cells

    PMID:32216968

    Open questions at the time
    • IGF2 dependence shown in fibroblast model, not primary SFT
    • Full enhancer program not mapped
  22. 2023 Medium

    Validated the fusion transcript as a therapeutic target by showing ASO and CRISPR/CasRx knockdown reduce fusion expression, proliferation, and xenograft growth.

    Evidence Engineered cell models, ASO, AAV2-CRISPR/CasRx, proliferation and xenograft assays

    PMID:37370737

    Open questions at the time
    • Modest proliferation reduction relative to transcript knockdown
    • In vivo therapeutic efficacy not established
  23. 2025 High

    Provided the integrated mechanistic model of oncogenesis, showing NAB2-STAT6 acts as an EGR1-enhancer coactivator that redirects NAB1/NAB2/EGR1 to the nucleus via the STAT6 moiety and activates a neuroendocrine gene program.

    Evidence Inducible cell model, ChIP-seq/ATAC-seq, primary SFT samples, subcellular fractionation, co-IP

    PMID:40875449

    Open questions at the time
    • How STAT6 transactivation domain overrides NuRD-based repression at the chromatin level not fully resolved
    • Therapeutic targeting of the activated program not addressed

Open questions

Synthesis pass · forward-looking unresolved questions
  • The molecular switch that determines whether wild-type NAB2 represses (via NuRD/CHD4) or coactivates EGR-targeted genes in a given cellular context remains undefined.
  • No structural or biochemical basis for context-dependent corepressor/coactivator switching
  • Signaling inputs and post-translational marks that toggle NAB2 function not mapped

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 5 GO:0140097 catalytic activity, acting on DNA 2
Localization
GO:0005634 nucleus 4 GO:0005829 cytosol 2
Pathway
R-HSA-1643685 Disease 3 R-HSA-168256 Immune System 3 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-4839726 Chromatin organization 2
Partners
CHD3CHD4EGR1EGR2EGR3NAB1STAT6WT1
Complex memberships
NuRD complex

Evidence

Reading pass · 25 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1996 NAB2 (MADER) acts as a transcriptional corepressor that directly interacts with the R1 domain of NGFI-A (Egr-1) and Krox20 via its first conserved domain (NCD1), repressing transcriptional activation by both factors. Protein interaction mapping, transcriptional reporter assays, molecular cloning Molecular and cellular biology High 8668170
1996 NAB2 (MADER) is a delayed early response gene whose expression is induced by serum stimulation of fibroblasts and NGF stimulation of PC12 cells — the same stimuli that induce Egr-1 — consistent with a negative feedback role. Northern blot, expression kinetics analysis Molecular and cellular biology Medium 8668170
1997 The Nab2 and Stat6 genes share a common transcription termination region on chromosome 12q13; an alternatively spliced form of Nab2 lacking exon 3 produces a protein that cannot repress NGFI-A or Krox20 transcription. Genomic sequencing, RT-PCR, transcriptional reporter assays Genomics Medium 9126479
1998 NAB2 overexpression in PC12 cells blocks NGF-induced neuronal differentiation, prevents growth arrest, and suppresses induction of delayed NGF response genes (TGF-β1, MMP-3) and p21(WAF1), without altering early MAP kinase activation or immediate-early gene induction. Stable transfection, transient transfection, adenoviral infection, immunoblot, growth assays The Journal of cell biology High 9722618
1999 NAB2 is rapidly and transiently induced in vascular smooth muscle cells (VSMC) by PMA and in vivo mechanical arterial injury, at the protein and mRNA level, trailing Egr-1 induction, and NAB2 expression inhibits Egr-1-dependent gene expression in VSMC. Western blot, Northern blot, in vivo arterial injury model, transcriptional reporter assays The American journal of pathology Medium 10514413
2001 NAB2 blocks Egr-1-mediated activation of the tissue factor promoter and Egr-1-stimulated production of PDGF-AB, HGF, TGF-β1, and VEGF; a dominant-negative NAB2 mutant fails to abrogate Egr-1-driven promoter activity or tubule formation in an angiogenesis assay. Reporter gene assay, dominant-negative mutagenesis, ELISA, in vitro angiogenesis assay Biochemical and biophysical research communications Medium 11327726
2002 NAB2 completely blocks VEGF-induced tissue factor reporter gene activity, inhibits upregulation of tissue factor, VEGF receptor-1, and urokinase plasminogen activator mRNAs, and significantly reduces tubule/sprout formation and vessel-like structure invasion in angiogenesis assays when overexpressed via adenovirus in endothelial cells. Adenoviral overexpression, RT-PCR, reporter gene assay, in vitro and in vivo (Matrigel) angiogenesis assays The Journal of biological chemistry High 12427750
2005 Egr-1 directly activates the NAB2 promoter through a cluster of Egr/Sp1 binding sites (−329 to −260 bp), and NAB2 in turn represses its own promoter activity, establishing a negative feedback loop. Sp1 constitutively binds the promoter region while stimulation induces Egr-1 binding. Depletion of Egr-1 by siRNA reduces NAB2 expression and inducibility. Promoter cloning, EMSA, reporter gene assay, siRNA knockdown The Journal of biological chemistry High 16260776
2006 NAB2 represses transcription through at least two domains, one of which requires interaction with CHD4 (chromodomain helicase DNA-binding protein 4), a subunit of the NuRD nucleosome remodeling and deacetylase complex. Both NAB1 and NAB2 can bind CHD3 or CHD4. Repression of the endogenous Rad gene by NAB2 involves CHD4, and NAB2 and CHD4 colocalize on the Rad promoter in myelinating Schwann cells. Alternative splicing of NAB2 mRNA regulates the CHD4 interaction. Co-immunoprecipitation, GST pulldown, ChIP, mutagenesis, reporter gene assay The Journal of biological chemistry High 16574654
2006 NAB2 is induced by TCR engagement and costimulation, and acts as a coactivator of Egr-1 to enhance IL-2 transcription; NAB2 is recruited to the Egr-1 binding site of the IL-2 promoter as shown by ChIP, and siRNA to NAB2 markedly inhibits IL-2 expression. Overexpression, siRNA knockdown, ELISA, ChIP, reporter gene assay Journal of immunology High 17142725
2008 TCR-induced Egr-1 and NAB2 enhance T cell function, while Egr-2 and Egr-3 suppress Egr-1 and NAB2 expression. Egr-3 is upstream of Egr-2 in this pathway. T cells from Egr-2/Egr-3 null mice are hyperresponsive; Egr-3 transgenic T cells are hyporesponsive, demonstrating opposing roles for NAB2/Egr-1 versus Egr-2/Egr-3 in T cell fate. Genetic knockout, transgenic overexpression, in vivo pneumonitis model, T cell functional assays European journal of immunology Medium 18203138
2009 TGF-β induces NAB2 expression in normal fibroblasts; ectopic NAB2 expression blocks Egr-1-dependent transcriptional responses, abrogates TGF-β-induced collagen synthesis and myofibroblast differentiation, and involves recruitment of the NuRD complex to the COL1A2 promoter with reduced histone H4 acetylation. Nab2 knockout mice display increased dermal collagen accumulation. Ectopic overexpression, siRNA knockdown, reporter gene assay, ChIP, histone acetylation assay, Nab2 knockout mouse PloS one High 19888474
2010 EGR1, EGR2, and EGR3 all activate NAB2 transcription in cells of neuroectodermal and epithelial origin via similar cis-regulatory elements; NAB2 in turn represses each EGR-induced promoter activity, establishing a conserved negative feedback loop. Depletion of EGR2 or EGR3 by siRNA reduces endogenous NAB2 levels. Overexpression, siRNA knockdown, reporter gene assay Journal of cellular biochemistry Medium 20506119
2011 NAB2 is selectively induced in helped CD8+ T cells (by IL-2 signaling) and prevents TRAIL induction after restimulation; enforced NAB2 expression prevents TRAIL induction in helpless CD8+ T cells, while dominant-negative NAB2 impairs secondary proliferative response (reversible by TRAIL blockade), identifying NAB2 as a mediator of Th-dependent CD8+ T cell memory through TRAIL regulation. Retroviral overexpression, dominant-negative expression, TRAIL blockade, FACS, in vivo T cell response assays Blood High 22128144
2012 EGR1 and NAB2 act in concert to positively regulate p130(Cas)/BCAR1 expression in breast cancer cells; ChIP shows EGR1 binding to the BCAR1 5' region; p130(Cas) depletion reduces EGR1 and NAB2 expression in tamoxifen-sensitive cells, forming a positive feedback loop. Overexpression, siRNA knockdown, ChIP, RT-PCR, Western blot Neoplasia Medium 22431919
2013 Recurrent NAB2-STAT6 gene fusions are present in all solitary fibrous tumors tested (51/51 SFTs). The predicted fusion protein harbors the EGR-binding domain of NAB2 fused to the activation domain of STAT6. Overexpression of NAB2-STAT6 induces cell proliferation and activates EGR-responsive genes, converting a transcriptional repressor into a transcriptional activator. Whole-exome sequencing, transcriptome sequencing, RT-PCR, overexpression in cultured cells, gene expression analysis Nature genetics High 23313952
2013 The NAB2-STAT6 fusion protein causes nuclear relocalization of STAT6 protein (which is normally cytoplasmic), detectable by immunohistochemistry and proximity ligation assay; tissues lacking the fusion show nuclear NAB2 and cytoplasmic STAT6. Proximity ligation assay (Duolink), immunohistochemistry, exome sequencing Acta neuropathologica High 23575898
2013 NAB2 is induced in NK cells by IL-2 and IL-15 and promotes TRAIL induction, while EGR-1 (induced by the same stimuli) acts as a brake on TRAIL expression in NK cells, establishing reciprocal NAB2/EGR-1 regulation of TRAIL. Overexpression, knockdown, FACS, TRAIL expression assays Immunology letters Medium 23416169
2017 WT1 (Wilms' tumor gene 1 protein) directly binds and transactivates the proximal NAB2 promoter; WT1 overexpression increases NAB2 levels while WT1 suppression decreases NAB2 expression in leukemic cells. WT1 recruits NAB2 to the IRF8 promoter, modulating WT1 transcriptional activity. ChIP, reporter gene assay, overexpression, siRNA knockdown, gene expression correlation Oncotarget Medium 29152069
2018 The NAB2 nuclear localization signal (NLS) maps to the KKXK (K343–K346) motif; mutation of KKXK to AAXA causes cytoplasmic localization of NAB2, while upstream K(X2)R mutations have no effect. Fusion of the KKXK motif to cytoplasmic eIF2Bε is sufficient for nuclear localization. Site-directed mutagenesis, fluorescence microscopy (localization assay), fusion protein construct FEBS letters Medium 30411343
2020 NAB2-STAT6 fusion protein upregulates EGR-1 and the EGR-1 target gene IGF2, increases p-Rb (Ser795) and cyclin D1 levels, enhances cell proliferation, and promotes oncogenic progression in NIH-3T3 cells; IGF2 inhibitor treatment reduces proliferation in NAB2-STAT6-expressing cells. Transfection, Western blot, RT-PCR, cell proliferation assay, pharmacological inhibition Biochemical and biophysical research communications Medium 32216968
2025 NAB2-STAT6 operates as a transcriptional coactivator for EGR1-targeted enhancers and promoters. In physiological conditions, NAB2 is primarily cytoplasmic with only a small nuclear fraction. NAB2-STAT6 redirects NAB1, NAB2, and EGR1 to the nucleus. The STAT6 moiety is the major driver of nuclear localization and enhances co-activating function. NAB2-STAT6 activates a neuroendocrine gene signature in primary SFT samples. Inducible cell model, ChIP-seq/ATAC-seq (enhancer/promoter mapping), primary tumor samples, subcellular fractionation, co-immunoprecipitation eLife High 40875449
2024 NAB2-STAT6 fusion activates a neuroendocrine gene signature in SFTs; STAT6 moiety drives nuclear localization and co-activating function of the fusion protein (preprint version of peer-reviewed eLife paper above). Inducible cell model, primary tumor samples, genomic profiling bioRxivpreprint Medium 38659891
2006 FGF23 induces expression of two isoforms of NAB2 in kidney cells; both isoforms localize to the nucleus and suppress the transcriptional activity of Egr-1, suggesting a negative feedback loop in FGF23 signaling. RT-PCR, immunolocalization, reporter gene assay Biochemical and biophysical research communications Medium 17174939
2023 ASO treatment targeting NAB2-STAT6 fusion transcript caused 58% reduction in fusion transcript expression and 22% reduction in cell proliferation in vitro; AAV2-mediated CRISPR/CasRx led to 59% reduction in fusion transcript and 55% reduction in xenograft growth ex vivo, validating the fusion transcript as a therapeutic target. CRISPR/SpCas9 engineered cell models, antisense oligonucleotide treatment, AAV2-mediated CRISPR/CasRx, cell proliferation assay, xenograft model Cancers Medium 37370737

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2013 Identification of recurrent NAB2-STAT6 gene fusions in solitary fibrous tumor by integrative sequencing. Nature genetics 616 23313952
1996 NAB2, a corepressor of NGFI-A (Egr-1) and Krox20, is induced by proliferative and differentiative stimuli. Molecular and cellular biology 329 8668170
2013 Meningeal hemangiopericytoma and solitary fibrous tumors carry the NAB2-STAT6 fusion and can be diagnosed by nuclear expression of STAT6 protein. Acta neuropathologica 287 23575898
2014 Solitary fibrous tumors/hemangiopericytomas with different variants of the NAB2-STAT6 gene fusion are characterized by specific histomorphology and distinct clinicopathological features. The American journal of pathology 189 24513261
1993 NAB2: a yeast nuclear polyadenylated RNA-binding protein essential for cell viability. Molecular and cellular biology 157 8474438
2015 NAB2-STAT6 fusion types account for clinicopathological variations in solitary fibrous tumors. Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc 129 26226844
2014 Distinct clinicopathological features of NAB2-STAT6 fusion gene variants in solitary fibrous tumor with emphasis on the acquisition of highly malignant potential. Human pathology 117 25582503
2014 Nuclear relocation of STAT6 reliably predicts NAB2-STAT6 fusion for the diagnosis of solitary fibrous tumour. Histopathology 104 24702701
2008 Opposing regulation of T cell function by Egr-1/NAB2 and Egr-2/Egr-3. European journal of immunology 98 18203138
2006 NAB2 represses transcription by interacting with the CHD4 subunit of the nucleosome remodeling and deacetylase (NuRD) complex. The Journal of biological chemistry 97 16574654
2009 Purification of nuclear poly(A)-binding protein Nab2 reveals association with the yeast transcriptome and a messenger ribonucleoprotein core structure. The Journal of biological chemistry 95 19840948
2005 Egr-1 induces the expression of its corepressor nab2 by activation of the nab2 promoter thereby establishing a negative feedback loop. The Journal of biological chemistry 90 16260776
2002 NAB2, a corepressor of EGR-1, inhibits vascular endothelial growth factor-mediated gene induction and angiogenic responses of endothelial cells. The Journal of biological chemistry 88 12427750
2010 EGR1, EGR2, and EGR3 activate the expression of their coregulator NAB2 establishing a negative feedback loop in cells of neuroectodermal and epithelial origin. Journal of cellular biochemistry 66 20506119
2008 Functional significance of the interaction between the mRNA-binding protein, Nab2, and the nuclear pore-associated protein, Mlp1, in mRNA export. The Journal of biological chemistry 66 18682389
2018 The impact of histopathology and NAB2-STAT6 fusion subtype in classification and grading of meningeal solitary fibrous tumor/hemangiopericytoma. Acta neuropathologica 64 30584643
2015 The clinicopathological significance of NAB2-STAT6 gene fusions in 52 cases of intrathoracic solitary fibrous tumors. Cancer medicine 62 26686340
1998 Identification and functional characterization of a novel nuclear localization signal present in the yeast Nab2 poly(A)+ RNA binding protein. Molecular and cellular biology 62 9488461
2016 NAB2-STAT6 Gene Fusion in Meningeal Hemangiopericytoma and Solitary Fibrous Tumor. Journal of neuropathology and experimental neurology 57 26883114
2001 Frequent and early loss of the EGR1 corepressor NAB2 in human prostate carcinoma. Human pathology 55 11567222
2016 The Evolutionarily-conserved Polyadenosine RNA Binding Protein, Nab2, Cooperates with Splicing Machinery to Regulate the Fate of pre-mRNA. Molecular and cellular biology 54 27528618
1998 The transcriptional corepressor NAB2 inhibits NGF-induced differentiation of PC12 cells. The Journal of cell biology 50 9722618
2021 Clinical and molecular implications of NAB2-STAT6 fusion variants in solitary fibrous tumour. Pathology 49 33745702
2016 Analysis of NAB2-STAT6 Gene Fusion in 17 Cases of Meningeal Solitary Fibrous Tumor/Hemangiopericytoma: Review of the Literature. The American journal of surgical pathology 48 26927892
1999 Vascular smooth muscle cells express the transcriptional corepressor NAB2 in response to injury. The American journal of pathology 45 10514413
2005 The nuclear exosome contributes to autogenous control of NAB2 mRNA levels. Molecular and cellular biology 44 15713618
2001 The transcriptional corepressor NAB2 blocks Egr-1-mediated growth factor activation and angiogenesis. Biochemical and biophysical research communications 44 11327726
2007 Structure of the N-terminal Mlp1-binding domain of the Saccharomyces cerevisiae mRNA-binding protein, Nab2. Journal of molecular biology 40 18190927
2010 Recognition of polyadenosine RNA by the zinc finger domain of nuclear poly(A) RNA-binding protein 2 (Nab2) is required for correct mRNA 3'-end formation. The Journal of biological chemistry 39 20554526
2016 NAB2-STAT6 gene fusion and STAT6 immunoexpression in extrathoracic solitary fibrous tumors: the association between fusion variants and locations. Pathology international 38 27039712
2012 The long and the short of it: the role of the zinc finger polyadenosine RNA binding protein, Nab2, in control of poly(A) tail length. Biochimica et biophysica acta 35 22484098
2006 Cutting Edge: TCR-induced NAB2 enhances T cell function by coactivating IL-2 transcription. Journal of immunology (Baltimore, Md. : 1950) 35 17142725
2016 Clinicopathological differences between variants of the NAB2-STAT6 fusion gene in solitary fibrous tumors of the meninges and extra-central nervous system. Brain tumor pathology 34 27271270
2004 Epstein-Barr virus is integrated between REL and BCL-11A in American Burkitt lymphoma cell line (NAB-2). Laboratory investigation; a journal of technical methods and pathology 34 15241441
2012 Structural basis for polyadenosine-RNA binding by Nab2 Zn fingers and its function in mRNA nuclear export. Structure (London, England : 1993) 32 22560733
2004 Nuclear export of the yeast mRNA-binding protein Nab2 is linked to a direct interaction with Gfd1 and to Gle1 function. The Journal of biological chemistry 32 15208322
2016 The NAB2-STAT6 gene fusion in solitary fibrous tumor can be reliably detected by anchored multiplexed PCR for targeted next-generation sequencing. Cancer genetics 29 27292373
2017 Structural basis for the dimerization of Nab2 generated by RNA binding provides insight into its contribution to both poly(A) tail length determination and transcript compaction in Saccharomyces cerevisiae. Nucleic acids research 28 28180315
2017 Recurrent NAB2-STAT6 gene fusions and oestrogen receptor-α expression in pulmonary adenofibromas. Histopathology 27 28072477
1996 Mader: a novel nuclear protein over expressed in human melanomas. Oncogene 27 8649813
2020 Widespread Transcriptional Readthrough Caused by Nab2 Depletion Leads to Chimeric Transcripts with Retained Introns. Cell reports 26 33113357
2013 Poly(A) tail-mediated gene regulation by opposing roles of Nab2 and Pab2 nuclear poly(A)-binding proteins in pre-mRNA decay. Molecular and cellular biology 25 24081329
2016 Solitary fibrous tumour of the genitourinary tract: a clinicopathological study of 11 cases and their association with the NAB2-STAT6 fusion gene. Journal of clinical pathology 24 27802414
2015 The poly(A)-binding protein Nab2 functions in RNA polymerase III transcription. Genes & development 24 26220998
2011 Nab2 functions in the metabolism of RNA driven by polymerases II and III. Molecular biology of the cell 24 21680710
2009 Regulation of NAB2 mRNA 3'-end formation requires the core exosome and the Trf4p component of the TRAMP complex. RNA (New York, N.Y.) 23 19369424
2009 The transcriptional cofactor nab2 is induced by tgf-Beta and suppresses fibroblast activation: physiological roles and impaired expression in scleroderma. PloS one 23 19888474
2019 Structure-function relationships in the Nab2 polyadenosine-RNA binding Zn finger protein family. Protein science : a publication of the Protein Society 22 30578643
2012 Regulation of p130(Cas)/BCAR1 expression in tamoxifen-sensitive and tamoxifen-resistant breast cancer cells by EGR1 and NAB2. Neoplasia (New York, N.Y.) 22 22431919
2020 NAB2-STAT6 fusion protein mediates cell proliferation and oncogenic progression via EGR-1 regulation. Biochemical and biophysical research communications 21 32216968
2011 Nab2 regulates secondary CD8+ T-cell responses through control of TRAIL expression. Blood 21 22128144
2013 Crystal structure of human Karyopherin β2 bound to the PY-NLS of Saccharomyces cerevisiae Nab2. Journal of structural and functional genomics 20 23535894
2007 An interaction between two RNA binding proteins, Nab2 and Pub1, links mRNA processing/export and mRNA stability. Molecular and cellular biology 20 17636033
2013 Structural basis for the molecular recognition of polyadenosine RNA by Nab2 Zn fingers. Nucleic acids research 18 24071581
1997 The Nab2 and Stat6 genes share a common transcription termination region. Genomics 18 9126479
2019 Recurrent Sinonasal CD34-Negative Malignant Solitary Fibrous Tumor Diagnosed on STAT6 Immunohistochemistry and NAB2-STAT6 Fusion. Head and neck pathology 16 30623305
2012 New kid on the ID block: neural functions of the Nab2/ZC3H14 class of Cys₃His tandem zinc-finger polyadenosine RNA binding proteins. RNA biology 16 22614829
2023 Glucose stress causes mRNA retention in nuclear Nab2 condensates. Cell reports 15 38113140
2020 Altered rRNA processing disrupts nuclear RNA homeostasis via competition for the poly(A)-binding protein Nab2. Nucleic acids research 14 33137177
2016 'Papillary' solitary fibrous tumor/hemangiopericytoma with nuclear STAT6 expression and NAB2-STAT6 fusion. Brain tumor pathology 13 26746203
2006 FGF23 induces expression of two isoforms of NAB2, which are corepressors of Egr-1. Biochemical and biophysical research communications 13 17174939
2015 NAB2-STAT6 fusion gene analysis in two cases of meningeal solitary fibrous tumor/hemangiopericytoma with late distant metastases. Brain tumor pathology 12 25893823
2015 A GRIA2 and PAX8-positive renal solitary fibrous tumor with NAB2-STAT6 gene fusion. Diagnostic pathology 12 26337721
2013 NAB2 and EGR-1 exert opposite roles in regulating TRAIL expression in human Natural Killer cells. Immunology letters 12 23416169
2022 The disease-associated proteins Drosophila Nab2 and Ataxin-2 interact with shared RNAs and coregulate neuronal morphology. Genetics 11 34791182
2022 Teratocarcinosarcoma-Like and Adamantinoma-Like Head and Neck Neoplasms Harboring NAB2::STAT6: Unusual Variants of Solitary Fibrous Tumor or Novel Tumor Entities? Head and neck pathology 11 35303277
2015 FDG PET/CT and MR imaging of CD34-negative soft-tissue solitary fibrous tumor with NAB2-STAT6 fusion gene. Anticancer research 11 25667482
2014 Commentary on "integrative genomic analyses reveal an androgen-driven somatic alteration landscape in early-onset prostate cancer." Weischenfeldt J, Simon R, Feuerbach L, Schlangen K, Weichenhan D, Minner S, Wuttig D, Warnatz HJ, Stehr H, Rausch T, Jäger N, Gu L, Bogatyrova O, Stütz AM, Claus R, Eils J, Eils R, Gerhäuser C, Huang PH, Hutter B, Kabbe R, Lawerenz C, Radomski S, Bartholomae CC, Fälth M, Gade S, Schmidt M, Amschler N, Haß T, Galal R, Gjoni J, Kuner R, Baer C, Masser S, von Kalle C, Zichner T, Benes V, Raeder B, Mader M, Amstislavskiy V, Avci M, Lehrach H, Parkhomchuk D, Sultan M, Burkhardt L, Graefen M, Huland H, Kluth M, Krohn A, Sirma H, Stumm L, Steurer S, Grupp K, Sültmann H, Sauter G, Plass C, Brors B, Yaspo ML, Korbel JO, Schlomm T, Genome Biology Unit, European Molecular Biology Laboratory (EMBL), Heidelberg, Germany.: Cancer Cell 2013;23(2):159-70. Urologic oncology 11 24445294
2013 Inversion-mediated gene fusions involving NAB2-STAT6 in an unusual malignant meningioma. British journal of cancer 11 23860521
2023 Inducible CRISPR Epigenome Systems Mimic Cocaine Induced Bidirectional Regulation of Nab2 and Egr3. The Journal of neuroscience : the official journal of the Society for Neuroscience 10 36849419
2023 The Drosophila Nab2 RNA binding protein inhibits m6A methylation and male-specific splicing of Sex lethal transcript in female neuronal tissue. eLife 10 37458420
2021 Lipomatous Solitary Fibrous Tumors Harbor Rare NAB2-STAT6 Fusion Variants and Show Up-Regulation of the Gene PPARG, Encoding for a Regulator of Adipocyte Differentiation. The American journal of pathology 10 33887215
2012 The transcriptional regulator NAB2 reveals a two-step induction of TRAIL in activated plasmacytoid DCs. European journal of immunology 10 22806638
2023 Reduction of Tumor Growth with RNA-Targeting Treatment of the NAB2-STAT6 Fusion Transcript in Solitary Fibrous Tumor Models. Cancers 9 37370737
2020 Dbp5 associates with RNA-bound Mex67 and Nab2 and its localization at the nuclear pore complex is sufficient for mRNP export and cell viability. PLoS genetics 9 33002012
2013 Induction of DARPP-32 by brain-derived neurotrophic factor in striatal neurons in vitro is modified by histone deacetylase inhibitors and Nab2. PloS one 9 24204683
2020 Regulation of the early growth response-1 binding protein NAB2 in bovine granulosa cells and effect on connective tissue growth factor expression. Molecular and cellular endocrinology 8 33002529
2019 Papillary Solitary Fibrous Tumor/Hemangiopericytoma: An Uncommon Morphological Form With NAB2-STAT6 Gene Fusion. Journal of neuropathology and experimental neurology 8 31271432
2018 Solitary Fibrous Tumor of the Vulva: Report of 2 Cases, Including a De Novo Dedifferentiated Solitary Fibrous Tumor Diagnosed After Molecular Demonstration of NAB2-STAT6 Gene Fusion. International journal of gynecological pathology : official journal of the International Society of Gynecological Pathologists 8 28968297
2016 Case Report: Next generation sequencing identifies a NAB2-STAT6 fusion in Glioblastoma. Diagnostic pathology 8 26817999
2013 NAB2-STAT6 fusions are a hallmark of solitary fibrous tumors. Cancer discovery 8 23475888
2002 Search for mutations in the EGR2 corepressor proteins, NAB1 and NAB2, in human peripheral neuropathies. Neurogenetics 8 12030330
1998 Melanoma-associated adhesion molecule MUC18/MCAM (CD146) and transcriptional regulator mader in normal human CNS. Neuroimmunomodulation 8 9730695
2021 NAB2-STAT6 Gene Fusions to Evaluate Primary/Metastasis of Hemangiopericytoma/Solitary Fibrous Tumors. American journal of clinical pathology 7 34075396
2021 The RNA-binding protein Nab2 regulates the proteome of the developing Drosophila brain. The Journal of biological chemistry 7 34139237
2021 Determination of biological behavior of solitary fibrous tumors: correlation of expression of Ki-67, TPX2 and TERT mRNA subunit level and NAB2-STAT6 fusion compared to morphological aspects of SFTs. Neoplasma 7 34818026
2015 Importance of NAB2-STAT6 Fusion in the Diagnosis of Pancreatic Solitary Fibrous Tumor with Hamartoma-Like Features: A Case Report and Review of the Literature. Case reports in pathology 7 26425382
2022 The Nab2 RNA-binding protein patterns dendritic and axonal projections through a planar cell polarity-sensitive mechanism. G3 (Bethesda, Md.) 6 35471546
2022 Pancreatic hamartoma: detection of harbouring NAB2::STAT6 fusion gene. Histopathology 6 35758200
2022 Analysis of clinicopathological features and NAB2-STAT6 fusion variants of meningeal solitary fibrous tumor with ectopic salivary gland components in the cerebellopontine angle. Virchows Archiv : an international journal of pathology 6 36056239
2021 Roles and Cellular Localization of GBP2 and NAB2 During the Blood Stage of Malaria Parasites. Frontiers in cellular and infection microbiology 6 34604117
2017 NAB2 is a novel immune stimulator of MDA-5 that promotes a strong type I interferon response. Oncotarget 6 29464024
2024 NAB2::STAT6 fusions and genome-wide DNA methylation profiling: Predictors of patient outcomes in meningeal solitary fibrous tumors. Brain pathology (Zurich, Switzerland) 5 38523251
2021 Management of Polymicrobial Cierny-Mader Grade 3 and 4 Chronic Osteomyelitis of the Femur. Cureus 5 33628684
2020 A Genetic Screen Links the Disease-Associated Nab2 RNA-Binding Protein to the Planar Cell Polarity Pathway in Drosophila melanogaster. G3 (Bethesda, Md.) 4 32817074
2025 NAB2-STAT6 drives an EGR1-dependent neuroendocrine program in solitary fibrous tumors. eLife 3 40875449
2024 NAB2-STAT6 drives an EGR1-dependent neuroendocrine program in Solitary Fibrous Tumors. bioRxiv : the preprint server for biology 3 38659891
2024 The RNA-binding protein Nab2 regulates levels of the RhoGEF Trio to govern axon and dendrite morphology. Molecular biology of the cell 3 38985523
2018 Refining the nuclear localization signal within the Egr transcriptional coregulator NAB2. FEBS letters 3 30411343
2017 The transcriptional coregulator NAB2 is a target gene for the Wilms' tumor gene 1 protein (WT1) in leukemic cells. Oncotarget 3 29152069

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