Affinage

CEBPB

CCAAT/enhancer-binding protein beta · UniProt P17676

Round 2 corrected
Length
345 aa
Mass
36.1 kDa
Annotated
2026-04-28
130 papers in source corpus 35 papers cited in narrative 35 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

CEBPB is a bZIP transcription factor that functions as a master regulator of myeloid differentiation, adipogenesis, acute-phase inflammatory gene expression, and immune cell programming by binding CCAAT and enhancer core sequences as homo- or heterodimers and recruiting SWI/SNF chromatin-remodeling complexes and the co-activator p300 to target promoters (PMID:2112087, PMID:10619021, PMID:9343424). A single CEBPB mRNA produces the transcriptional activator LAP and the dominant-negative repressor LIP through alternative translational initiation governed by an upstream open reading frame that integrates PKR/eIF-2α and mTOR/eIF-4E signaling, and the LAP/LIP ratio shifts during differentiation and in cancer (PMID:1934061, PMID:10921906). CEBPB transcriptional output is tuned by MAPK phosphorylation at Thr-235, PKC phosphorylation at Ser-105, CaMKII phosphorylation at Ser-276, and GSK-3β-dependent phosphorylation within an internal regulatory domain, and is modulated by protein–protein interactions with CHOP (dominant-negative inhibition), NF-κB p50, Smad3, RB, PRDM16, and Mediator sub-complexes whose composition switches from repressive (CDK8-containing) to activating (CRSP70-containing) upon Ras signaling (PMID:8384717, PMID:1314426, PMID:1547942, PMID:14759369, PMID:19641492). Loss-of-function studies establish CEBPB as essential for macrophage bactericidal activity and G-CSF production, myeloid-derived suppressor cell generation, brown fat determination with PRDM16, and exercise-induced cardiac remodeling (PMID:7530603, PMID:20605485, PMID:19641492, PMID:21183071).

Mechanistic history

Synthesis pass · year-by-year structured walk · 18 steps
  1. 1990 High

    Identification of CEBPB as a C/EBP-family bZIP factor that binds CCAAT/enhancer motifs and activates IL-6 transcription established its dual role as a sequence-specific DNA-binding protein and mediator of inflammatory gene expression.

    Evidence cDNA cloning with DNA-binding reconstitution and promoter transactivation in transfected cells

    PMID:2112087

    Open questions at the time
    • No in vivo loss-of-function data
    • Dimerization partners not yet characterized
    • No post-translational regulatory mechanism known
  2. 1991 High

    Discovery that LAP and LIP are translated from the same mRNA via alternative AUG usage, with LIP acting as a dominant-negative repressor, revealed an intrinsic translational switch controlling CEBPB transcriptional output during differentiation.

    Evidence In vitro translation, immunoprecipitation, and transient transfection in hepatoma and liver cells

    PMID:1934061

    Open questions at the time
    • Upstream signals controlling AUG choice unknown
    • Relative isoform contributions in specific tissues not determined
  3. 1991 High

    Characterization of C/EBP family homo- and heterodimerization via leucine zippers, combined with the positioning of CEBPB early in the adipogenic transcriptional cascade upstream of C/EBPα and PPARγ, defined CEBPB as an obligate dimer and a differentiation-initiating transcription factor.

    Evidence Bacterially expressed protein binding assays for pairwise dimers; temporal expression profiling during adipocyte differentiation

    PMID:1840554 PMID:1884998

    Open questions at the time
    • Whether heterodimerization alters DNA-site selectivity in vivo unresolved
    • Direct binding to C/EBPα or PPARγ promoters not yet shown by ChIP
  4. 1992 High

    Identification of CHOP as a dominant-negative binding partner that blocks CEBPB DNA binding, and NF-κB p50 as a cooperative partner, defined the first positive and negative protein–protein regulatory axes of CEBPB.

    Evidence In vitro DNA-binding inhibition by CHOP-CEBPB heterodimers; direct p50-CEBPB interaction with domain mapping

    PMID:1518839 PMID:1547942

    Open questions at the time
    • In vivo stoichiometry of CHOP-CEBPB versus p50-CEBPB complexes unknown
    • Genomic targets of the p50-CEBPB complex not identified
  5. 1992 High

    Demonstration that CaMKII phosphorylates CEBPB at Ser-276 to confer calcium-regulated transcriptional activation established the first kinase-specific post-translational regulatory mechanism for this factor.

    Evidence In vivo phosphorylation in pituitary cells; Ser276 mutagenesis with transcriptional reporter readout

    PMID:1314426

    Open questions at the time
    • Structural consequence of Ser-276 phosphorylation on leucine zipper not known
    • Physiological calcium signals that activate this pathway in vivo unclear
  6. 1993 High

    Mapping of Ras/MAPK phosphorylation at Thr-235 and PKC phosphorylation at Ser-105, each required for transcriptional activation, revealed CEBPB as a convergence point for multiple mitogenic and differentiation signaling cascades.

    Evidence In vitro kinase assays; site-directed mutagenesis; Ras co-expression and transient transfection reporter assays

    PMID:8336793 PMID:8384717

    Open questions at the time
    • Combinatorial effects of simultaneous multi-site phosphorylation not determined
    • Phosphatases that reverse these marks unidentified
  7. 1994 High

    Evidence that CEBPB is intrinsically repressed and activated by signal-dependent derepression — rather than simple enhancement — shifted the conceptual model from activator to repressed activator, explaining how diverse kinases converge on a single output.

    Evidence Domain deletion of repressor region; kinase epistasis with v-erbB, Ras, and raf; chromatin-embedded reporter assays

    PMID:7958933

    Open questions at the time
    • Molecular identity of the internal repressor fold not structurally resolved
    • Whether derepression alters DNA-binding or cofactor recruitment not distinguished
  8. 1995 High

    CEBPB knockout mice revealed essential non-redundant roles in macrophage bactericidal function (Listeria escape from phagosomes) and G-CSF induction, and RB was identified as a direct coactivator, connecting CEBPB to cell-cycle control during myeloid differentiation.

    Evidence Gene-targeted knockout mice with electron microscopy and cytokine assays; co-IP and in vitro binding of RB-CEBPB with functional transactivation

    PMID:7530603 PMID:8552662

    Open questions at the time
    • Phagosomal escape mechanism downstream of CEBPB targets not identified
    • Whether RB-CEBPB interaction is phosphorylation-dependent in vivo unclear
  9. 1997 High

    Identification of p300 as a coactivator and CREB as an upstream transcriptional activator of the CEBPB promoter completed a core regulatory circuit: PKA/CREB → CEBPB transcription → p300 recruitment → chromatin remodeling.

    Evidence Co-IP of p300-CEBPB; E1A epistasis; CREB gel-shift and supershift on CEBPB promoter; nuclear run-off during liver regeneration

    PMID:9199295 PMID:9343424

    Open questions at the time
    • Genome-wide p300-CEBPB co-occupancy not mapped
    • Whether CREB dependence is tissue-specific not addressed
  10. 1999 High

    Demonstration that CEBPB's N-terminal domain recruits the SWI/SNF chromatin-remodeling complex, and that this domain is portable, established CEBPB as a pioneer-like factor capable of opening chromatin at myeloid gene loci.

    Evidence Co-IP of CEBPB with SWI/SNF subunits; domain-grafting chimera onto Myb with chromatin-template transcription assay

    PMID:10619021

    Open questions at the time
    • Pioneer factor activity not formally tested by ATAC-seq or nucleosome reconstitution
    • Whether SWI/SNF recruitment is isoform-specific (LAP vs LIP) not resolved
  11. 2000 High

    Elucidation of the uORF-dependent translational control mechanism integrating PKR/eIF-2α and mTOR/eIF-4E inputs into the LAP/LIP ratio unified the earlier isoform observations with signaling pathway identity and explained how deregulated isoform ratios can drive transformation.

    Evidence PKR and mTOR pathway modulation; uORF mutagenesis; differentiation and transformation assays in 3T3-L1 cells

    PMID:10921906

    Open questions at the time
    • Ribosome profiling on endogenous CEBPB mRNA not performed
    • Cell-type-specific usage of the uORF not characterized
  12. 2004 High

    Discovery that Ras signaling switches CEBPB from a repressive CDK8-Mediator complex to an activating CRSP70-Mediator complex via the CRSP130/Sur2 subunit provided a structural basis for the derepression model and linked CEBPB directly to the general transcription machinery.

    Evidence Co-IP of distinct Mediator sub-complexes; siRNA knockdown of CRSP130/Sur2; oncogenic Ras epistasis

    PMID:14759369

    Open questions at the time
    • Cryo-EM or structural data for CEBPB-Mediator interface lacking
    • Whether Mediator switching occurs genome-wide or at select loci unknown
  13. 2009 High

    Identification of the PRDM16-CEBPB(LAP) complex as sufficient to reprogram fibroblasts into functional brown adipocytes, confirmed by transplantation, established CEBPB as a lineage-determining factor in thermogenic fat.

    Evidence Co-IP/mass spectrometry; retroviral co-expression in naive fibroblasts; ectopic brown fat generation in mice with PET-FDG imaging

    PMID:19641492

    Open questions at the time
    • PRDM16-CEBPB target gene set not comprehensively defined
    • Whether beige/brite adipocyte conversion also requires PRDM16-CEBPB unclear
  14. 2010 High

    Conditional myeloid-specific knockout showed CEBPB is the essential molecular switch for MDSC generation and immunosuppressive function, connecting its role in myelopoiesis to tumor immune evasion; separately, CEBPB with STAT3 was shown to specify the mesenchymal glioma program.

    Evidence Myeloid-restricted CEBPB deletion; T cell suppression and allograft assays; CEBPB/STAT3 co-expression in neural stem cells and knockdown in glioma

    PMID:20032975 PMID:20605485

    Open questions at the time
    • Direct CEBPB target genes in MDSCs not comprehensively mapped
    • Whether CEBPB-STAT3 synergy involves direct physical interaction not tested
  15. 2010 High

    Reduction of cardiac CEBPB was found to phenocopy exercise-induced hypertrophy and proliferation via CITED4, revealing an unexpected repressive role in the heart and suggesting CEBPB tonically restrains cardiomyocyte growth.

    Evidence siRNA knockdown; cardiac-specific transgenic reduction; pressure-overload model; CITED4 epistasis

    PMID:21183071

    Open questions at the time
    • Direct CEBPB binding sites on CITED4 promoter not shown
    • Mechanism of CEBPB-mediated cardiomyocyte proliferation control unclear
  16. 2011 High

    Ancestral protein resurrection revealed that amino-acid substitutions in the placental-mammal stem lineage rewired GSK-3β-dependent phosphorylation from a repressive to an activating signal, demonstrating evolutionary tuning of CEBPB's regulatory logic.

    Evidence Resurrected ancestral CEBPB proteins; site-directed mutagenesis; GSK-3β kinase assays; transcriptional reporters

    PMID:22080951

    Open questions at the time
    • Physiological consequence of the evolutionary switch for specific target genes unknown
    • Whether other C/EBP family members underwent parallel rewiring not explored
  17. 2018 Medium

    Aerobic glycolysis in triple-negative breast cancer was shown to sustain CEBPB-LAP levels by suppressing AMPK-ULK1 autophagy, linking tumor metabolism to MDSC-mediated immunosuppression through the LAP/G-CSF/GM-CSF axis.

    Evidence AMPK/ULK1 pathway modulation; isoform-specific knockdown/overexpression; 4T1 and Py8119 tumor models with MDSC quantification

    PMID:29805099

    Open questions at the time
    • Whether CEBPB-LAP is a direct autophagy substrate or indirectly affected not resolved
    • Generalizability beyond triple-negative breast cancer not tested
  18. 2023 Medium

    SQSTM1/p62-mediated selective autophagy was identified as a degradation pathway for CEBPB in macrophages; autophagy deficiency causes CEBPB accumulation, driving SOCS1/3 transcription and blocking JAK1-STAT6-dependent M2 polarization, connecting CEBPB turnover to allergic inflammation.

    Evidence Macrophage-specific Atg5 conditional knockout; MC903-induced atopic dermatitis model; p62-CEBPB co-IP; SOCS1/3 reporter assays

    PMID:37963021

    Open questions at the time
    • Whether p62 recognizes a specific degron on CEBPB not defined
    • Ubiquitin linkage type directing CEBPB to autophagy not characterized
    • Relevance to non-macrophage cell types not tested

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the genome-wide pioneer factor activity of CEBPB at chromatin, the structural basis of the Mediator complex switch, the complete set of direct transcriptional targets in MDSCs and brown fat, and how multiple phosphorylation marks are integrated combinatorially to specify context-dependent transcriptional output.
  • No genome-wide nucleosome-resolution pioneer factor assay reported
  • No structural model of CEBPB-Mediator or CEBPB-SWI/SNF interfaces
  • Combinatorial phosphorylation code not systematically decoded

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 9 GO:0003677 DNA binding 4
Localization
GO:0005634 nucleus 7
Pathway
R-HSA-74160 Gene expression (Transcription) 8 R-HSA-162582 Signal Transduction 6 R-HSA-1266738 Developmental Biology 3 R-HSA-168256 Immune System 3 R-HSA-9612973 Autophagy 2 R-HSA-4839726 Chromatin organization 1
Partners
DDIT3EP300MED23NFKB1PRDM16RB1SMAD3STAT3
Complex memberships
Mediator (CRSP70-containing and CDK8-containing forms)PRDM16-CEBPBSWI/SNF

Evidence

Reading pass · 35 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1990 CEBPB (NF-IL6) was cloned and identified as a member of the C/EBP family with a leucine zipper structure; the recombinant protein binds CCAAT homology and viral enhancer core sequences and activates the human IL-6 promoter in a sequence-specific manner; NF-IL6 mRNA is induced by LPS, IL-1, or IL-6. cDNA library screening with DNA-binding sequence as ligand; bacterial fusion protein DNA-binding assay; promoter transactivation in transfected cells; Northern blot The EMBO journal High 2112087
1991 LAP (CEBPB) and LIP are translated from the same mRNA using two in-frame AUGs; LAP is a transcriptional activator and LIP is a repressor that lacks the activation domain; LIP attenuates LAP-driven transcription at substoichiometric amounts; the LAP/LIP ratio increases ~5-fold during terminal liver differentiation. In vitro translation, transient transfection, immunoprecipitation, Western blot Cell High 1934061
1991 C/EBP beta (CRP2/NF-IL6/LAP) was characterized as one of a family of C/EBP-related proteins that form homo- and heterodimers via leucine zippers; all pairwise dimer combinations are possible and each member activates transcription from C/EBP-binding site promoters. Reduced-stringency genomic library screening; bacterially expressed protein DNA-binding assays; gel assay for covalent dimers; co-transfection transcription assays Genes & development High 1884998
1991 C/EBP beta and C/EBP delta are expressed early during adipocyte differentiation (before C/EBP alpha) and are directly induced by adipogenic hormones, suggesting they initiate a transcriptional cascade that controls terminal adipocyte differentiation. Western blot, Northern blot, transient transfection in hepatoma cells Genes & development High 1840554
1992 CHOP-10 dimerizes with CEBPB (LAP) via the leucine zipper, forming heterodimers unable to bind DNA, thereby acting as a dominant-negative inhibitor of CEBPB-driven transcription; co-immunoprecipitation from transfected cells confirmed direct in vivo interaction. Bacteriophage expression library screen with 32P-labeled LAP zipper probe; co-immunoprecipitation; in vitro DNA-binding inhibition assay; transient transfection reporter assay Genes & development High 1547942
1992 Calcium-calmodulin-dependent protein kinase phosphorylates CEBPB at Ser-276 within the leucine zipper in pituitary cells; this phosphorylation confers calcium-regulated transcriptional stimulation of CEBPB target promoters. In vivo phosphorylation assay in pituitary cells with calcium mobilization; site-directed mutagenesis (Ser276); transcriptional reporter assay Science High 1314426
1992 NF-kB p50 directly interacts with NF-IL6 (CEBPB); the Rel homology domain of p50 and the leucine zipper of NF-IL6 are required for interaction, enabling co-regulation of immune and acute-phase response genes. 32P-labeled NF-kB-p50 fusion protein Western blot probing and bacteriophage expression library screen; direct protein-protein binding assays Proceedings of the National Academy of Sciences of the United States of America High 1518839
1993 Protein kinase C pathway stimulation increases phosphorylation of Ser-105 within the activation domain of NF-IL6/LAP (CEBPB) and enhances its transcriptional efficacy. In vivo phosphorylation assay; site-directed mutagenesis; transient transfection reporter assay Nature High 8336793
1993 Ras-dependent MAP kinases phosphorylate CEBPB (NF-IL6) at Thr-235 located N-terminal to the DNA-binding domain; mutation of Thr-235 abolishes ras-dependent activation of NF-IL6 transactivation. In vitro kinase assay with purified MAP kinase; site-directed mutagenesis (Thr235); co-expression with oncogenic p21ras; transient transfection reporter assay Proceedings of the National Academy of Sciences of the United States of America High 8384717
1994 CEBPB (NF-M/C/EBP beta chicken homolog) is an intrinsically repressed transcription factor; repression is abolished by signal transduction kinases including v-erbB, polyoma middle T, Ras, and mil/raf, or by point mutation of a critical MAPK phosphorylation site, demonstrating activation through derepression rather than enhancement of the transactivation domain. Deletion analysis of repressor domains; kinase co-expression; point mutagenesis of phosphorylation site; chromatin-embedded reporter gene assays Genes & development High 7958933
1994 LIP (the short inhibitory isoform of CEBPB, translated from the same mRNA) arrests hepatoma cell proliferation before the G1/S boundary only when it retains the DNA-binding and leucine zipper domains; full-length LAP (but not C/EBP alpha) also arrests the cell cycle, requiring intact dimerization and activation domains. Cell cycle analysis by flow cytometry; deletion mutagenesis; transient overexpression in hepatoma cells The EMBO journal High 7906646
1995 Retinoblastoma protein (RB) directly interacts with CEBPB (NF-IL6) through the SV40 T antigen-binding domain of RB; NF-IL6 uses two distinct regions to bind the hypophosphorylated form of RB; wild-type but not mutant RB enhances NF-IL6 DNA-binding activity in vitro and promoter transactivation in cells. Co-immunoprecipitation from differentiating U937 cells; in vitro binding assays; electrophoretic mobility shift assay; transient transfection reporter assay Proceedings of the National Academy of Sciences of the United States of America High 8552662
1995 CEBPB is essential for macrophage bactericidal and tumoricidal activities in vivo; NF-IL6−/− mice show escape of Listeria from phagosomes and severely impaired tumor cytotoxicity despite normal TNF/IFN-gamma induction and normal NO formation; NF-IL6 is also essential for G-CSF induction in macrophages and fibroblasts. Gene targeting (knockout mice); electron microscopy of macrophage phagosomes; functional macrophage cytotoxicity assays; cytokine and NO measurement Cell High 7530603
1995 Estrogen receptor directly interacts with NF-kB and CEBPB, repressing the IL-6 promoter without an ER binding site; the DNA-binding domain and region D of ER interact with the Rel homology domain of NF-kB and the bZIP region of CEBPB. In vitro binding assay with domain-mapping mutants; transient transfection reporter assay in osteoblasts Molecular and cellular biology High 7651415
1997 CREB binds directly to two sites in the CEBPB (LAP/C/EBP beta) promoter; these sites maintain basal promoter activity and mediate PKA-pathway inducibility; CREB phosphorylation in vivo correlates with CEBPB mRNA transcription during liver regeneration. Deletion analysis; gel-shift, cross-linking, supershift, and competition assays with recombinant CREB; transfection with CREB site mutant constructs; nuclear run-off transcription; Western blot during hepatectomy Molecular and cellular biology High 9199295
1997 p300 directly interacts with CEBPB through its E1A-binding region, acting as a coactivator; CEBPB-dependent transactivation is inhibited by adenovirus E1A in a p300-binding-dependent manner, reversed by ectopic p300; p300 also mediates synergy between CEBPB and Myb. Co-immunoprecipitation; domain-mapping with deletion mutants; E1A co-expression inhibition assay; transient transfection reporter assay Molecular and cellular biology High 9343424
1999 The full-length (LAP) isoform of CEBPB recruits the SWI/SNF chromatin-remodeling complex via its N-terminal domain to activate myeloid target genes embedded in chromatin; grafting this domain onto Myb reconstitutes SWI/SNF recruitment and chromatin-dependent gene activation. Co-immunoprecipitation of CEBPB with SWI/SNF subunits; domain-grafting chimera experiment; chromatin-template transcription assay Molecular cell High 10619021
2000 CEBPB isoform expression is controlled at the translational level: PKR signaling through eIF-2alpha and mTOR signaling through eIF-4E regulate the ratio of full-length (LAP) to truncated (LIP) isoforms; an evolutionarily conserved upstream open reading frame in the CEBPB mRNA integrates translation factor signals; deregulated isoform ratios disrupt differentiation and induce transformation. Translation inhibitor experiments; PKR and mTOR pathway modulation; mutational analysis of upstream ORF; differentiation and transformation assays in 3T3-L1 cells Genes & development High 10921906
2003 TGF-beta inhibits adipocyte differentiation by signaling through Smad3, which physically interacts with CEBPB and represses its transcriptional activity without reducing DNA binding; Smad3/4 inhibit CEBPB transactivation function at C/EBP binding sites on the PPARgamma2 and leptin promoters. Co-immunoprecipitation of Smad3/4 with CEBPB; transient transfection reporter assays; adipogenesis rescue experiments in NIH3T3 cells The Journal of biological chemistry High 12524424
2004 Oncogenic Ras activation causes a conformational change in CEBPB and exchanges the repressive CDK8-containing Mediator complex for the transcriptionally active CRSP70-containing Mediator complex, both interacting through the CRSP130/Sur2 subunit; knockdown of CRSP130/Sur2 prevents Mediator binding and abolishes CEBPB transactivation. Co-immunoprecipitation of CEBPB with distinct Mediator complexes; siRNA knockdown of CRSP130/Sur2; oncogenic Ras co-expression; activating CEBPB mutations Molecular cell High 14759369
2009 PRDM16 forms a transcriptional complex with the LAP isoform of CEBPB; forced co-expression of PRDM16 and CEBPB-LAP is sufficient to induce a complete brown fat program in naive fibroblasts including human skin fibroblasts; transplantation of these cells generates ectopic functional brown fat tissue. Co-immunoprecipitation; mass spectrometry; retroviral overexpression in fibroblasts; transplantation into mice; PET-FDG imaging Nature High 19641492
2009 ER stress induces CEBPB expression in mesangial cells preferentially via PERK and IRE1 branches of the unfolded protein response; overexpressed CEBPB suppresses TNF-alpha-induced NF-kB activation independent of its transactivation potential; siRNA knockdown of CEBPB reverses ER stress-induced NF-kB suppression. siRNA knockdown; overexpression; dominant-negative UPR branch mutants; NF-kB reporter assay; mouse ER stress preconditioning model Journal of the American Society of Nephrology Medium 19875812
2010 CEBPB is required for tumor-induced MDSC generation; BM-MDSCs generated by GM-CSF+IL-6 depend entirely on CEBPB for immunosuppressive activity; C/EBPbeta-deficient myeloid cells cannot suppress CD8+ T cell priming or allow allograft acceptance; adoptive transfer experiments confirm C/EBPbeta as the critical molecular switch. Conditional knockout (myeloid-restricted CEBPB deletion); bone marrow MDSC generation assays; T cell suppression assays; allograft transplantation; adoptive transfer Immunity High 20605485
2010 C/EBPbeta and STAT3 co-expression is necessary and sufficient to reprogram neural stem cells into an aberrant mesenchymal glioma lineage; elimination of both factors in glioma cells collapses the mesenchymal transcriptional signature and reduces tumor aggressiveness. Ectopic co-expression in neural stem cells; siRNA knockdown of C/EBPbeta and STAT3 in glioma cells; transcriptional network reverse engineering; in vivo tumor assays Nature High 20032975
2010 C/EBPbeta represses cardiomyocyte growth and proliferation in the adult heart; reduction of C/EBPbeta in vitro and in vivo phenocopies endurance exercise (hypertrophy and proliferation); this effect is mediated at least in part by increased CITED4; mice with reduced cardiac C/EBPbeta display resistance to cardiac failure upon pressure overload. RT-PCR screen; siRNA knockdown; cardiac-specific transgenic reduction; pressure-overload model; cardiomyocyte proliferation and hypertrophy assays Cell High 21183071
2011 IMiD compounds (lenalidomide/pomalidomide) down-regulate CEBPB protein in multiple myeloma cells through translational control via eIF4E without altering mRNA levels or protein stability; overexpression of CEBPB rescues MM cells from IMiD-induced proliferation inhibition; inhibition of the eIF4E-CEBPB axis by IMiDs impairs downstream IRF4 transcription. Western blot; mRNA stability and protein stability assays; eIF4E modulation; CEBPB overexpression rescue; 4E-BP1 phosphorylation inhibition; patient bone marrow longitudinal samples Blood Medium 21389327
2011 Amino-acid substitutions in an internal regulatory domain of CEBPB in the stem-lineage of placental mammals reorganized key phosphorylation sites, adding a new site and removing two ancestral sites, reversing the response to GSK-3beta-mediated phosphorylation from repression to activation; identified by functional analysis of resurrected ancestral CEBPB proteins. Ancestral protein resurrection; site-directed mutagenesis; kinase (GSK-3beta) phosphorylation assay; transcriptional reporter assay comparing ancestral and derived proteins Nature High 22080951
2014 CEBPB acts upstream of C/EBPalpha and PPARgamma in the adipogenic transcriptional cascade, directly transactivating their expression; CEBPB function during adipogenesis is regulated by multiple post-translational modifications critical for proper activation of the adipogenic program, including phosphorylation controlling mitotic clonal expansion. Chromatin immunoprecipitation; promoter reporter assays; post-translational modification mapping studies in 3T3-L1 cells (review synthesizing experimental data) The Journal of biological chemistry High 25451943
2015 MDR (multi-drug-resistant) cancer cells lack the LIP isoform of CEBPB due to ubiquitin-mediated lysosomal and proteasomal degradation; overexpression of LIP reverses the MDR phenotype in vitro and in tumor-bearing mice by activating the CHOP-caspase-3 death axis and upregulating calreticulin to trigger immunogenic cell death. LIP overexpression in MDR cells; ubiquitination assay; proteasome and lysosome inhibitor rescue; orthotopic xenograft mouse model; calreticulin and CD8+ T cell assays Journal of the National Cancer Institute Medium 25766403
2018 Aerobic glycolysis in triple-negative breast cancer promotes expression of the CEBPB-LAP isoform via suppression of the AMPK-ULK1 and autophagy pathways; CEBPB-LAP in turn controls G-CSF and GM-CSF expression to support MDSC development and tumor immunosuppression; glycolysis restriction reduces LAP levels and MDSCs. AMPK/ULK1 pathway modulation; autophagy induction/inhibition; CEBPB-LAP isoform-specific knockdown and overexpression; MDSC quantification; tumor models (4T1 and Py8119) Cell metabolism Medium 29805099
2021 A delta-secretase-generated truncated APP fragment (C586-695) directly binds CEBPB, enhances its nuclear translocation, and augments CEBPB transcriptional activity on the APP, MAPT (tau), delta-secretase, and inflammatory cytokine promoters, escalating Alzheimer's disease pathology; blockade of delta-secretase cleavage reduces CEBPB stimulation and alleviates amyloid pathology. Co-immunoprecipitation; nuclear fractionation; luciferase reporter assays; viral overexpression mouse model; APP cleavage site mutagenesis; antibody clearance in 5xFAD mice Brain Medium 33880508
2023 CircDYM binds directly to CEBPB in the cytoplasm and prevents its nuclear translocation; LPS-induced CEBPB nuclear entry downregulates ZC3H4 expression, which promotes autophagy and apoptosis in microglia; circDYM-CEBPB interaction thus attenuates microglial apoptosis in a depression model. RNA immunoprecipitation (RIP) of circDYM-CEBPB; subcellular fractionation; CEBPB nuclear translocation assay; ZC3H4 reporter and knockdown experiments; LPS mouse model International journal of biological macromolecules Medium 37944732
2023 Autophagy degrades CEBPB via SQSTM1/p62-mediated selective autophagy; autophagy deficiency in macrophages causes CEBPB accumulation, which drives transcription of SOCS1/3 suppressor genes, inhibits JAK1-STAT6 pathway activation, and blocks M2 macrophage polarization, thereby reducing atopic dermatitis inflammation. Macrophage-specific Atg5 conditional knockout mice; MC903-induced AD model; CEBPB overexpression/knockdown; SOCS1/3 reporter assays; STAT6 phosphorylation assays; p62-CEBPB co-IP Cell reports Medium 37963021
2006 CEBPB is a critical transcriptional target required for ALK (NPM-ALK)-mediated cellular transformation and survival of ALK-positive ALCL cells; RNAi functional screening demonstrated that CEBPB knockdown alone collapses transformation/survival, placing CEBPB downstream of constitutive ALK signaling. Inducible ALK RNAi; ALK kinase inhibitors; gene expression profiling; RNAi functional screen for transcriptional targets The Journal of clinical investigation Medium 17111047
2006 BCR/ABL oncogene represses CEBPB expression via translational regulation dependent on the CUG-repeat RNA-binding protein CUGBP1 and the CUG-rich intercistronic region of CEBPB mRNA; imatinib treatment re-induces CEBPB; constitutive or conditional CEBPB expression induces differentiation and inhibits proliferation of BCR/ABL cells via GADD45A induction, requiring intact DNA-binding. CUGBP1 expression/knockdown; CEBPB mRNA intercistronic region analysis; DNA-binding-deficient mutant; conditional CEBPB activation; in vitro and in vivo proliferation/differentiation assays Blood Medium 16418324

Source papers

Stage 0 corpus · 130 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2012 Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease. Nature 3725 23128233
2004 Roles of CHOP/GADD153 in endoplasmic reticulum stress. Cell death and differentiation 2429 14685163
1991 Regulated expression of three C/EBP isoforms during adipose conversion of 3T3-L1 cells. Genes & development 1512 1840554
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
1990 A nuclear factor for IL-6 expression (NF-IL6) is a member of a C/EBP family. The EMBO journal 1463 2112087
2010 Network organization of the human autophagy system. Nature 1286 20562859
2009 A census of human transcription factors: function, expression and evolution. Nature reviews. Genetics 1191 19274049
1992 CHOP, a novel developmentally regulated nuclear protein that dimerizes with transcription factors C/EBP and LAP and functions as a dominant-negative inhibitor of gene transcription. Genes & development 1062 1547942
2009 The transcriptional network for mesenchymal transformation of brain tumours. Nature 1019 20032975
1991 A liver-enriched transcriptional activator protein, LAP, and a transcriptional inhibitory protein, LIP, are translated from the same mRNA. Cell 947 1934061
2017 Impact of cytosine methylation on DNA binding specificities of human transcription factors. Science (New York, N.Y.) 934 28473536
2005 TRB3, a novel ER stress-inducible gene, is induced via ATF4-CHOP pathway and is involved in cell death. The EMBO journal 848 15775988
2010 Tumor-induced tolerance and immune suppression depend on the C/EBPbeta transcription factor. Immunity 738 20605485
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
2017 Multi-omics analysis identifies ATF4 as a key regulator of the mitochondrial stress response in mammals. The Journal of cell biology 672 28566324
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
2009 Initiation of myoblast to brown fat switch by a PRDM16-C/EBP-beta transcriptional complex. Nature 600 19641492
1995 Repression of the interleukin-6 promoter by estrogen receptor is mediated by NF-kappa B and C/EBP beta. Molecular and cellular biology 563 7651415
1990 LAP, a novel member of the C/EBP gene family, encodes a liver-enriched transcriptional activator protein. Genes & development 563 2253878
1993 Phosphorylation at threonine-235 by a ras-dependent mitogen-activated protein kinase cascade is essential for transcription factor NF-IL6. Proceedings of the National Academy of Sciences of the United States of America 546 8384717
1991 A family of C/EBP-related proteins capable of forming covalently linked leucine zipper dimers in vitro. Genes & development 541 1884998
1992 IL-6 and NF-IL6 in acute-phase response and viral infection. Immunological reviews 472 1380488
1995 Targeted disruption of the NF-IL6 gene discloses its essential role in bacteria killing and tumor cytotoxicity by macrophages. Cell 469 7530603
2004 The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). Genome research 438 15489334
2000 Translational control of C/EBPalpha and C/EBPbeta isoform expression. Genes & development 402 10921906
2018 Aerobic Glycolysis Controls Myeloid-Derived Suppressor Cells and Tumor Immunity via a Specific CEBPB Isoform in Triple-Negative Breast Cancer. Cell metabolism 369 29805099
2005 Krüppel-like transcription factor KLF5 is a key regulator of adipocyte differentiation. Cell metabolism 361 16054042
1996 CCAAT enhancer-binding protein (C/EBP) and AML1 (CBF alpha2) synergistically activate the macrophage colony-stimulating factor receptor promoter. Molecular and cellular biology 360 8622667
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