| 1989 |
EGR2/Krox-20 expression is induced by serum via a serum response element (SRE/CArG box) in its promoter that binds the same nuclear protein as the c-fos SRE, linking EGR2 to the immediate-early serum response gene network. Alternative splicing of the 5'-most intron produces proteins with different N-termini. |
Promoter deletion analysis, mutagenesis, gel-shift assays, Northern blot, genomic mapping |
Molecular and cellular biology |
High |
2496302
|
| 1990 |
The EGR2 promoter contains two CArG elements (CArG-1 and CArG-2); serum and PMA responsiveness maps specifically to CArG-1, and both protein kinase C-dependent and -independent pathways converge on this element to drive EGR2 transcription. |
Deletion analysis, mutagenesis, transient CAT reporter assays, S1 nuclease/primer extension |
Nucleic acids research |
High |
2111009
|
| 1993 |
Krox20 protein directly binds three Krox20-binding sites in the HoxB2 r3/r5 enhancer (demonstrated in vitro) and is required in vivo for rhombomere-restricted HoxB2 expression; ectopic Krox20 can transactivate a HoxB2 r3/r5 enhancer reporter in transgenic mice, establishing Krox20 as a direct transcriptional activator of HoxB2 during hindbrain segmentation. |
In vitro binding/competition assays with bacterially expressed Krox20, transgenic reporter mice, ectopic expression |
Cell |
High |
8093858
|
| 1993 |
Targeted deletion of Krox20 (including the zinc-finger DNA-binding domain) in mice results in perinatal lethality with loss of rhombomeres 3 and 5, establishing an essential in vivo role for Krox20 in hindbrain segmentation. |
Gene targeting/knockout in mice, histological and neuroanatomical analysis |
Genes & development |
High |
8224839
|
| 1995 |
NAB1, identified by yeast two-hybrid, binds the R1 inhibitory domain of NGFI-A/Egr1 and represses transcriptional activation by both NGFI-A and Krox20/EGR2, but not Egr3 or NGFI-C, providing a mechanism for differential regulation within the EGR family. |
Yeast two-hybrid, transcriptional repression assays |
Proceedings of the National Academy of Sciences of the United States of America |
Medium |
7624335
|
| 1996 |
NAB2, a second corepressor highly related to NAB1, interacts with the R1 domain of NGFI-A and represses transcriptional activity of both NGFI-A and Krox20/EGR2; NAB2 expression is induced by the same stimuli that activate NGFI-A, creating a feedback repression loop. |
Protein interaction assays, transcriptional reporter assays, expression analysis |
Molecular and cellular biology |
Medium |
8668170
|
| 1996 |
Krox-20 directly activates Hoxa-2 expression in rhombomeres 3 and 5: Krox20 protein binds two sites in the Hoxa-2 r3/r5 enhancer in vitro; mutation of these sites abolishes r3/r5 activity in transgenic mice; ectopic Krox20 in r4 transactivates the Hoxa-2/lacZ reporter, demonstrating direct transcriptional control of multiple group-2 Hox paralogs. |
In vitro binding/competition assays, transgenic analysis with lacZ reporters, mutational analysis, ectopic expression |
Development (Cambridge, England) |
High |
8625806
|
| 1999 |
In Krox-20-null Schwann cells, SCIP expression is converted from transient to sustained, and both Schwann cell proliferation and apoptosis are markedly increased at postnatal stages, demonstrating that Krox20 controls SCIP expression, cell cycle exit, and susceptibility to apoptosis during Schwann cell development. |
Krox-20 knockout mouse analysis, immunohistochemistry, cell proliferation and apoptosis assays |
Development (Cambridge, England) |
High |
10068633
|
| 2001 |
Krox20 is essential for specification of rhombomere identity: in Krox20-null embryos, r3 cells acquire r2/r4 identity and r5 cells acquire r6 identity; chimeric analysis shows r3/r5 mutant cells adopt even-numbered rhombomere mingling properties, demonstrating Krox20 couples segment formation, cell segregation, and regional identity specification. |
Genetic fate mapping, molecular marker analysis, embryonic chimeras |
Development (Cambridge, England) |
High |
11748134
|
| 2002 |
Krox20 expression in Schwann cells is controlled by two axon-dependent cis-acting elements—an immature Schwann cell element (ISE) and a myelinating Schwann cell element (MSE, ~35 kb downstream)—acting in succession during development; the MSE requires the POU-domain factor Oct6 and contains multiple Oct6 binding sites, indicating Oct6 directly activates Krox20 transcription. |
Transgenic reporter analysis, in vivo nerve regeneration experiments, genetic epistasis with Oct6 mutants |
Development (Cambridge, England) |
High |
11782409
|
| 2002 |
Krox20 synergizes with kreisler to activate Hoxb3 transcription via direct binding to the Hoxb3 r5 enhancer; Krox20 is required for enhancer activity specifically in r5 (the overlap domain of Krox20 and kreisler), demonstrating combinatorial transcriptional control. |
Genetic analysis (Krox20 mutant mice), mutational analysis of enhancer, ectopic expression, in vitro binding |
The EMBO journal |
High |
11823429
|
| 2003 |
HCF-1 functions as a transcriptional coactivator for Krox20; Krox20 contains a functional HCF-binding motif in its N-terminal activation domain; mutation of this motif reduces both transactivation and association with the HCF-1 β-propeller domain; HCF-1's C-terminal activation domain contributes to Krox20-mediated activation, possibly through recruitment of p300. |
Coimmunoprecipitation, transcriptional reporter assays, mutagenesis |
The Journal of biological chemistry |
Medium |
14532282
|
| 2003 |
EGR2 directly transactivates BNIP3L and BAK expression as demonstrated by cDNA microarray and functional studies, inducing apoptosis through mitochondrial membrane permeability changes, cytochrome c release, and caspase-3, -8, and -9 activation downstream of the PTEN-EGR2 pathway. |
Adenovirus-mediated gene transfer, cDNA microarray, caspase activity assays, cytochrome c release assays |
Oncogene |
Medium |
12687019
|
| 2003 |
Krox20 neural crest expression requires a cis-acting enhancer (NCE) 26 kb upstream containing two conserved Krox20-binding sites that mediate direct autoregulation, plus an HMG-box binding element responsive to Sox10; Sox10 synergizes with Krox20 to activate the NCE in vitro, and Sox10 inactivation prevents maintenance of Krox20 expression in migrating neural crest. |
Transgenic analysis with reporter constructs, mutagenesis of binding sites, in vitro transcription assays, Sox10 knockout analysis |
Development (Cambridge, England) |
High |
12538520
|
| 2004 |
Krox-20 cell-autonomously inactivates the JNK-c-Jun pathway in Schwann cells, thereby coordinately suppressing both neuregulin-1-induced proliferation and TGFβ/serum deprivation-induced death; Krox-20 also upregulates the JNK scaffold protein JIP-1, suggesting a mechanism for JNK regulation. |
Enforced Krox-20 expression in Schwann cells and fibroblasts, proliferation and apoptosis assays, JNK pathway activation assays |
The Journal of cell biology |
High |
14757751
|
| 2005 |
EGR2/Egr2 directly binds a conserved element in the first intron of Myelin Protein Zero (Mpz) containing Egr2 binding sites; this element is transactivated by Egr2 and repressed by NAB corepressors; Egr2 binds this intron element in vivo (ChIP); Egr2 and Sox10 synergistically activate the element, while forskolin and IGF-1 induce Mpz in an Egr2-dependent manner. |
Chromatin immunoprecipitation (ChIP), transactivation reporter assays, mutagenesis, pharmacological inducers |
The Journal of biological chemistry |
High |
16373334
|
| 2005 |
Egr2/Krox20 and SREBP transcription factors synergistically activate promoters of several cholesterol/lipid biosynthetic genes during myelination; Egr2 does not regulate SREBP pathway component levels but directly co-activates SREBP target gene promoters as part of the myelination program. |
Reporter assays, expression analysis during sciatic nerve development |
Journal of neurochemistry |
Medium |
15836632
|
| 2005 |
Krox20 stimulates adipogenesis by transactivating the C/EBPβ promoter and increasing C/EBPβ expression in 3T3-L1 preadipocytes; RNAi knockdown of C/EBPβ diminishes the proadipogenic effect of Krox20; coexpression of Krox20 with C/EBPβ in naïve NIH3T3 cells induces a fully differentiated adipocyte phenotype. |
Overexpression, RNAi knockdown, reporter assays, adipogenesis assays in cell lines |
Cell metabolism |
High |
16054051
|
| 2005 |
Overexpression of Egr-2 and Egr-3 in T cells increases E3 ubiquitin ligase Cbl-b expression and inhibits T cell activation; Egr3-/- T cells have lower Cbl-b expression and are resistant to in vivo peptide-induced tolerance, identifying Egr2 and Egr3 as negative regulators of T cell activation that act through Cbl-b. |
Overexpression, knockout mice, in vivo tolerance assays, gene expression analysis |
Nature immunology |
High |
15834410
|
| 2006 |
Krox20 expression in Schwann cells during the promyelin-myelin transition is directly activated by POU proteins Oct6 and Brn2 acting on the myelinating Schwann cell enhancer (MSE); synergism between POU proteins and Sox10 on this enhancer suggests Krox20 expression requires this combination of upstream factors, placing Krox20 downstream of Oct6/Brn2/Sox10 in the myelination transcription factor cascade. |
Cell culture transactivation assays, transgenesis, mutagenesis of binding sites |
EMBO reports |
High |
16311519
|
| 2006 |
Specific inactivation of Krox20 in adult Schwann cells results in severe demyelination with Schwann cell dedifferentiation and increased proliferation, demonstrating that Krox20 is required not only for onset of myelination but also for maintenance of the myelinating state in adult peripheral nerve. |
Conditional Krox20 knockout in adult mice, histological and ultrastructural analysis |
The Journal of neuroscience |
High |
16988048
|
| 2006 |
In vivo ChIP assays in myelinating rat sciatic nerve demonstrate direct Egr2 binding to the Schwann cell enhancer of the myelin basic protein (MBP) gene, to a conserved site in the myelin-associated glycoprotein (MAG) gene, and to an intronic site in the Desert Hedgehog (Dhh) gene, establishing direct regulation of these targets. |
Chromatin immunoprecipitation (ChIP) in vivo in myelinating nerve |
Journal of neurochemistry |
High |
16923174
|
| 2006 |
Three long-range (>200 kb) enhancer elements (A, B, C) control Krox20 transcription in the hindbrain; elements B and C function as initiators in r5 and r3-r5 respectively independent of Krox20 protein; element A contains Krox20-binding sites required for activity, establishing a direct positive autoregulatory loop; element B contains a vHNF1 binding site required for its activity, identifying vHNF1 as a direct initiator. |
Transgenic analysis with reporter constructs, enhancer knockout mice, mutagenesis of binding sites |
Development (Cambridge, England) |
High |
16495311
|
| 2007 |
Neuropathy-associated dominant EGR2 mutants disrupt EGR2/SOX10 synergy at the Mpz intron element: the mutants do not perturb EGR2 binding but attenuate SOX10 binding at both the Mpz intron and MAG gene elements (shown by ChIP), demonstrating that dominant EGR2 mutations cause peripheral neuropathy by antagonizing SOX10 binding at cooperative regulatory sites. |
Chromatin immunoprecipitation (ChIP), transcriptional reporter assays, mutagenesis |
Molecular and cellular biology |
High |
17325040
|
| 2008 |
Egr2 directly represses genes (including Id2, Id4, and Rad) during myelination in conjunction with NAB corepressors: in vivo ChIP in myelinating sciatic nerve shows developmental association of both Egr2 and NAB2 on these promoters; NAB2 represses transcription by recruiting CHD4, a subunit of the NuRD chromatin remodeling complex; repression of Id2 augments Mpz activation. |
Chromatin immunoprecipitation (ChIP) in vivo, gene expression screen, epistasis experiments |
The Journal of biological chemistry |
High |
18456662
|
| 2008 |
Krox20-null mutation of the Nab interaction domain (I268F) in mice causes severe hypomyelination mimicking congenital hypomyelinating neuropathy in humans; the Krox20-Nab interaction is required for regulation of most Krox20 target genes, but the molecular function of this interaction is target-dependent. |
Knock-in mouse model, immunohistochemical, ultrastructural, and expression analyses |
The Journal of neuroscience |
High |
18524893
|
| 2008 |
Egr2 is required for sustained Bcl-2 upregulation during late stages of positive selection in the thymus; enforced Bcl-2 expression rescues T cell development in Egr2-/- thymocytes, placing Egr2 upstream of Bcl-2 in the survival pathway during positive selection. |
Egr2 knockout mice, gene expression analysis, Bcl-2 rescue experiments |
Journal of immunology |
High |
19017967
|
| 2008 |
Rostral Krox20 enhancer element C contains functional binding sites for Meis and Hox/Pbx factors that synergize to activate the enhancer; mutation of these sites shows that Krox20 is under direct transcriptional control of both Meis (presumably Meis2) and Hox/Pbx in r3; Hoxb1 binds to element C in vivo. |
In vivo ChIP, transgenic analysis with mutated enhancer constructs |
Development (Cambridge, England) |
High |
18787068
|
| 2008 |
EGR2 and MeCP2 reciprocally regulate each other: ChIP shows EGR2 binding to the MECP2 promoter and MeCP2 binding to the EGR2 intron 1 enhancer; RNAi-mediated reduction of either EGR2 or MeCP2 reciprocally reduces the other's expression and protein levels. |
Chromatin immunoprecipitation, RNAi knockdown, quantitative expression analysis |
Human molecular genetics |
Medium |
19000991
|
| 2009 |
The HECT-type E3 ubiquitin ligase AIP2 interacts with EGR2 and promotes its ubiquitin-mediated proteasomal degradation; AIP2 suppresses EGR2-mediated FasL expression, thereby inhibiting activation-induced T-cell death; siRNA knockdown of AIP2 upregulates EGR2, inhibits EGR2 ubiquitination, and enhances T-cell apoptosis. |
Coimmunoprecipitation, ubiquitination assays, siRNA knockdown, apoptosis assays |
Molecular and cellular biology |
High |
19651900
|
| 2010 |
EGR1 and EGR2 directly bind the Col1a1 promoter tendon regulatory regions (shown by ChIP) and transactivate the mouse Col1a1 proximal promoter; FGF4 activates Egr gene expression and tendon collagen expression in chick limbs; Egr1 or Egr2 misexpression in chick induces de novo scleraxis, Col1a1, and other tendon collagen expression; Egr1/Egr2 mouse mutants show reduced Col1a1 transcripts and fewer collagen fibrils. |
Chromatin immunoprecipitation, reporter assays, gain-of-function in chick, knockout mouse analysis |
The Journal of biological chemistry |
High |
21173153
|
| 2010 |
EGR1 and EGR3 activate NAB2 transcription in melanoma and carcinoma cells through similar cis-regulatory elements, and EGR2 also induces NAB2 expression (less potently); NAB2 in turn represses each EGR's activity on the NAB2 promoter, establishing a negative feedback loop; siRNA reduction of EGR2 reduces endogenous NAB2 levels. |
Promoter reporter assays, siRNA knockdown, expression analysis |
Journal of cellular biochemistry |
Medium |
20506119
|
| 2010 |
Krox20/EGR2 haploinsufficiency accelerates growth and differentiation in preosteoclast cultures derived from splenocytes; Krox20 silencing increases cFms (M-CSFR) expression and response to M-CSF, leading to cell-autonomous stimulation of cell-cycle progression in preosteoclasts, resulting in increased bone resorption and low bone mass in vivo. |
Conditional KO/haploinsufficiency mice, preosteoclast cultures, siRNA, cell proliferation assays, microcomputed tomography |
Blood |
Medium |
20716776
|
| 2011 |
TGF-β induces EGR2 expression in fibroblasts via a Smad3-dependent mechanism; EGR2 overexpression is sufficient to stimulate collagen gene expression and myofibroblast differentiation; EGR2 depletion attenuates TGF-β profibrotic responses, establishing EGR2 as a necessary and sufficient mediator of TGF-β-induced fibrosis. |
Smad3-dependent reporter assays, overexpression, siRNA depletion, gene expression profiling |
The American journal of pathology |
Medium |
21514423
|
| 2012 |
Egr2 binds the promoter of Zbtb16 (encoding PLZF) and the promoter of Il2rb (IL-2Rβ) in NKT precursors, directly activating their transcription (shown by ChIP-seq); higher and more prolonged Egr2 expression in NKT precursors specifies both early and late stages of NKT lineage differentiation. |
Chromatin immunoprecipitation followed by deep sequencing (ChIP-seq), conditional knockout analysis |
Nature immunology |
High |
22306690
|
| 2012 |
Egr2 and Egr3 double-deficient B and T cells exhibit hyperactive STAT1 and STAT3 and severely impaired AP-1 activation; Egr2 and/or Egr3 directly induce expression of SOCS1 and SOCS3 (inhibitors of STAT1/3), and block the function of Batf (an AP-1 inhibitor), establishing these factors as regulators of cytokine signaling balance. |
Conditional double-knockout mice, reporter assays, gene expression analysis |
Immunity |
High |
23021953
|
| 2012 |
Genome-wide ChIP-seq of EGR2 and SOX10 in myelinating peripheral nerve identifies extensive co-binding at myelin gene regulatory regions; EGR2 represses a set of early developmental genes that SOX10 activates independently of EGR2, demonstrating coordinate and antagonistic gene regulation during myelination. |
ChIP-seq in vivo in myelinating nerve, integration with loss-of-function expression arrays |
Nucleic acids research |
High |
22492709
|
| 2012 |
Conditional Egr2 deletion in peripheral T cells abolishes induced expression of DGK-α and other anergy genes, and restores Ras/MAPK signaling, IL-2 production, and proliferation upon attempted anergy induction; Egr2 is necessary for anergy induction in vivo using superantigen- and tumor-induced models, establishing Egr2 as an essential transcriptional regulator of the T cell anergy program. |
Conditional Egr2 knockout mice, in vivo anergy induction models, gene expression analysis, signaling assays |
The Journal of experimental medicine |
High |
23129747
|
| 2013 |
Egr2 directly binds and controls expression of genes regulating proliferation (Myc and Myb) and differentiation repressors (Bcl6, Id3), while repressing transcription factors required for effector function (Zeb2, RORa, RORc, Bhlhe40); Egr2 and 3 expression is regulated reciprocally by antigen and IFNγ; sustained Egr2 expression enhances expansion but impairs effector differentiation. |
ChIP, conditional knockout mice, overexpression, gene expression analysis |
The Journal of experimental medicine |
High |
28487311
|
| 2013 |
Active Rac1 GTPase negatively regulates Schwann cell differentiation by upregulating c-jun and downregulating Krox20 through the MKK7-JNK pathway (not through Raf-ERK); ErbB2 signaling prevents MKK7 activation and c-jun induction; Rac inhibition blocks MKK7 activation and c-jun induction after axotomy. |
Primary Schwann cell cultures, Rac1 activation/inhibition, siRNA, kinase inhibitors, sciatic nerve axotomy model |
Glia |
Medium |
23505039
|
| 2014 |
EGR2 is a direct transcriptional regulator of Tbx21 and Notch1 (shown as direct target genes); EGR2 promotes peripheral naïve T-cell differentiation and is required for production of IFN-γ, IL-4, IL-9, and IL-17A, functioning as a positive regulator of naïve T-cell differentiation in contrast to its negative regulatory role in activated T cells. |
Conditional knockout mice, T-helper differentiation assays, direct target gene identification, viral infection model |
Proceedings of the National Academy of Sciences of the United States of America |
High |
25368162
|
| 2016 |
Egr2 and Egr3 expressed in T cells cooperatively control TGF-β3 secretion from CD4+CD25-LAG3+ regulatory T cells by maintaining expression of Ltbp3 (latent TGF-β binding protein 3); T cell-specific Egr2/Egr3 double-KO mice develop lupus-like disease with complete loss of TGF-β3 production from LAG3+ cells, adoptive transfer of WT LAG3+ cells rescues the phenotype. |
T cell-specific double-knockout mice, adoptive transfer, cytokine analysis, gene expression |
Proceedings of the National Academy of Sciences of the United States of America |
High |
27911796
|
| 2017 |
Egr2 and Egr3 physically interact with the T-box domain of T-bet, blocking T-bet DNA binding and inhibiting T-bet-mediated IFN-γ production; this interaction antagonizes Th1 differentiation. |
Co-immunoprecipitation, DNA binding assays, T cell differentiation assays, KO mice |
Journal of immunology |
High |
28455436
|
| 2017 |
The lysine acetyltransferase GCN5 directly acetylates EGR2, positively regulating EGR2 transcriptional activity; GCN5 deficiency blocks iNKT cell development in a cell-intrinsic manner and specifically inhibits EGR2 target gene transcription (Runx1, PLZF, IL-2Rβ, T-bet) in iNKT cells. |
Acetyltransferase assay, conditional KO mice, reporter assays, gene expression analysis |
Cell reports |
High |
28723564
|
| 2017 |
Egr2 binds and controls expression of Myc and Myb (proliferation genes) and differentiation repressors Bcl6 and Id3 while repressing Zeb2, RORa, RORc, and Bhlhe40; Egr2 and Egr3 operate as a checkpoint controlling the transition between clonal expansion and differentiation of effector T cells. |
ChIP, conditional DKO mice, OE, gene expression profiling |
The Journal of experimental medicine |
High |
28487311
|
| 2017 |
Endogenous KLF4 and Krox20 are dispensable for adipogenesis in culture and brown adipose tissue development in mice (as shown by conditional knockout), contrary to overexpression studies, while PPARγ remains essential. |
Conditional knockout mice, primary preadipocyte cultures |
Molecular and cellular biology |
Medium |
27777310
|
| 2020 |
CTCF establishes chromatin interaction loops between enhancer and promoter regulatory elements to promote EGR2 expression in Schwann cells; CTCF deletion blocks Schwann cell differentiation at the pro-myelinating stage while CTCF overexpression promotes myelination; CTCF also interacts with SUZ12 (PRC2 component) to repress genes negatively regulating Schwann cell maturation. |
CTCF conditional KO and OE, chromatin conformation capture, co-immunoprecipitation |
Nature communications |
High |
32807777
|
| 2020 |
EGR2 is a direct target of IL-4-activated STAT6 and acts as a molecular linchpin in alternative macrophage polarization; EGR2 binding results in chromatin opening and recruitment of chromatin remodelers and RNA polymerase II; EGR2 is required for 77% of the IL-4-induced gene signature including its own autoregulation and downstream PPARG induction; EGR2 interacts with the 5mC hydroxylase TET2 to initiate DNA demethylation at its binding sites. |
ChIP-seq, ATAC-seq, conditional KO, reporter assays, co-IP with TET2 |
Genes & development |
High |
33060136
|
| 2020 |
Egr2 recruits the Rnf40-containing E3 ubiquitin ligase (responsible for histone H2B monoubiquitination) to its target genes in myelinating Schwann cells; Rnf40/H2Bub1 is required for selective high expression of myelin and lipid biosynthesis genes and proper repression of immaturity genes during peripheral nerve myelination. |
Conditional Rnf40 KO mice, ChIP-seq, RNA-seq, co-immunoprecipitation/recruitment assays |
Nucleic acids research |
High |
32672815
|
| 2021 |
Chronic antigen exposure induces EGR2 selectively in progenitor exhausted CD8+ T cells; EGR2 enables terminal exhaustion and stabilizes the exhausted transcriptional state by direct EGR2-dependent control of exhaustion-associated genes and indirect maintenance of the exhausted epigenetic state. |
Conditional EGR2 deletion, chronic LCMV and tumor models, ATAC-seq, ChIP, transcriptomics |
Nature communications |
High |
33986293
|
| 2021 |
EGR2 is an epigenetic pioneer in differentiating human monocytes: EGR2 binding results in active DNA demethylation at both stable and transient binding sites; EGR2 physically interacts with TET2 (5mC hydroxylase); EGR2 is essential for monocyte differentiation and DNA methylation turnover. |
Genome-wide methylation profiling, ATAC-seq, ChIP-seq, co-immunoprecipitation, EGR2 KD |
Nature communications |
High |
33692344
|
| 2021 |
EGR2 directly binds and activates the ARF and p16 promoters to promote cellular senescence; EGR2 loss transiently reverses the senescent phenotype in human mammary epithelial cells and fibroblasts; EGR2 overexpression is sufficient to induce senescence, placing EGR2 as a direct transcriptional activator of the p16/pRB and ARF/p53/p21 pathways. |
ChIP, siRNA knockdown, overexpression, reporter assays, flow cytometry |
Aging cell |
Medium |
33547862
|
| 2021 |
Cell-intrinsic EGR2 is driven by TGF-β and GM-CSF in a PPAR-γ-dependent manner to control tissue-specific identity of alveolar macrophages; EGR2 is indispensable for repopulation of the alveolar niche after bleomycin-induced lung injury, and EGR2-dependent monocyte-derived alveolar macrophages are required for effective tissue repair. |
Conditional EGR2 KO mice, lung injury models, flow cytometry, gene expression |
Science immunology |
High |
34797692
|
| 2021 |
EGR2 transcription factor increases IGF2BP1/2/3 expression in renal cell carcinoma by directly binding IGF2BP promoters (validated by ChIP-qPCR and dual-luciferase reporter assays); IGF2BPs in turn regulate S1PR3 expression in an m6A-dependent manner by enhancing S1PR3 mRNA stability, promoting RCC tumorigenesis via the PI3K/AKT pathway. |
ChIP-qPCR, dual-luciferase reporter assays, RIP-qPCR, m6A assays, in vitro and in vivo functional assays |
Cell death & disease |
Medium |
34326314
|
| 2023 |
EGR2 knockout in CAR T cells blocks type I interferon-mediated inhibitory programming induced by chronic antigen stimulation, expands early memory CAR T cells, and improves antitumor efficacy; EGR2 ablation suppresses dysfunction by inhibiting type I interferon signaling, and the protective effect is overridden by exogenous interferon-β, establishing an EGR2-type I interferon axis in CAR T cell exhaustion. |
CRISPR/Cas9 EGR2 KO in primary CAR T cells, gene expression profiling, in vivo tumor models, interferon pathway assays |
Cancer discovery |
High |
37011008
|