Affinage

MAFK

Transcription factor MafK · UniProt O60675

Length
156 aa
Mass
17.5 kDa
Annotated
2026-06-10
42 papers in source corpus 26 papers cited in narrative 27 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MAFK is a small MAF family bZIP transcription factor that operates as an obligate dimerization module: a nuclear protein retaining a conserved bZIP domain but lacking the acidic transactivation domain of large Mafs, so its transcriptional output is dictated by its dimer partner (PMID:8361754). As a homodimer it binds NF-E2/MARE/ARE sites and represses MARE-dependent transcription, including at the IL-2 and IL-4 promoters and at antioxidant-response genes such as NQO1 and GST Ya (PMID:7706310, PMID:11013233, PMID:11737266). Conferring DNA-binding to CNC partners, MAFK heterodimerizes with p45/NF-E2 and Nrf2 to enable transcriptional activation — driving erythroid differentiation and globin induction (PMID:7638211, PMID:9009092), activating the GST-P enhancer during hepatocarcinogenesis (PMID:14960151), and, at the β-globin locus, mediating NF-E2 occupancy, active histone marks, RNA Pol II loading, and LCR-to-promoter chromatin looping (PMID:18308612). Its partnership with the BTB-bZIP Bach1/Bach2 proteins instead yields context-dependent repressive complexes at MARE sites, with heme-driven exchange between Bach and Nrf2 partners switching target genes between repressed and activated states (PMID:8887638, PMID:24652768). MAFK couples extracellular signals to this transcriptional logic: it is a NGF-responsive immediate-early gene controlled by atypical PKC that drives neurite outgrowth (PMID:12388604), and TGF-β induces MAFK to displace Nrf2 from the HO-1 ARE and repress cytoprotective HO-1 expression (PMID:23737527). Genetically, MAFK acts redundantly with MAFG — compound Mafg/Mafk mutant mice display anemia, thrombocytopenia, neurological defects, and progressive lens/cataract phenotypes — establishing essential roles in erythropoiesis, megakaryopoiesis, neuronal function, and lens fiber differentiation (PMID:10716933, PMID:25896808, PMID:36092713). In cancer, TGF-β-induced MAFK promotes epithelial-mesenchymal transition and malignant progression by directly activating GPNMB and AREG, with its SUMOylation consensus sequence required for EMT, stemness, and drug-resistance functions (PMID:28400538, PMID:41316921, PMID:42180617). Tissue-restricted expression of MAFK is itself controlled by dual mesodermal/neuronal promoters and a GATA-dependent hematopoietic/cardiac enhancer (PMID:9140066, PMID:10856242).

Mechanistic history

Synthesis pass · year-by-year structured walk · 22 steps
  1. 1993 Medium

    Established that MafK is a nuclear bZIP protein lacking a transactivation domain, framing it as a partner-dependent factor rather than an autonomous activator.

    Evidence cDNA cloning, sequence comparison, and immunofluorescence of retrovirally overexpressed protein

    PMID:8361754

    Open questions at the time
    • Did not identify physiological dimer partners
    • No direct DNA target defined
  2. 1995 High

    Showed MafK binds NF-E2 sites as a repressive homodimer but confers site-specific DNA binding to p45, which supplies the activation function — defining the homodimer-repressor/heterodimer-activator paradigm.

    Evidence EMSA and transient transfection reporter assays with p45 co-expression

    PMID:7706310

    Open questions at the time
    • In vitro binding only for the homodimer repression step
    • Endogenous target genes not yet defined
  3. 1995 High

    Demonstrated MafK is sufficient and required to drive terminal erythroid differentiation, linking the factor to a defined cellular program.

    Evidence Conditional/antisense overexpression in murine erythroleukemia cells with hemoglobin and EMSA readouts

    PMID:7638211 PMID:9009092

    Open questions at the time
    • Did not resolve which heterodimeric partner mediates the differentiation effect at endogenous loci
  4. 1996 High

    Identified Bach1/Bach2 as MafK partners, extending the dimer repertoire and showing that partner identity and cell type determine activation versus repression.

    Evidence Yeast two-hybrid screen, EMSA, and reporter assays in fibroblast and erythroid cells

    PMID:8887638

    Open questions at the time
    • Did not define the signal that selects Bach versus CNC partners
    • No endogenous target loci mapped
  5. 1996 High

    Resolved that MafK expression is governed by distinct mesodermal and neuronal promoters and that neuronal MafK uses a non-p45 partner, indicating tissue-specific regulatory logic.

    Evidence Northern blot developmental profiling, promoter mapping, and transgenic reporter assays

    PMID:9140066 PMID:9893024

    Open questions at the time
    • Neuronal dimer partner not identified
    • Upstream regulators of each promoter unknown
  6. 2000 High

    Connected MafK to antioxidant-response transcription, showing homodimers repress ARE genes (NQO1, GST Ya) while Nrf2-MafK heterodimers bind the ARE.

    Evidence EMSA/supershift and transfection assays in HepG2 cells, including a negative result for Maf-Nrf1

    PMID:11013233

    Open questions at the time
    • Did not test endogenous ARE occupancy by ChIP
    • Activation by Nrf2-MafK shown only as binding
  7. 2000 High

    Genetically established that small Mafs are redundantly essential in vivo, with Mafg/Mafk double-null mice showing anemia, thrombocytopenia, and neurological defects.

    Evidence Compound germline knockout mouse genetics with hematological and histological phenotyping

    PMID:10716933

    Open questions at the time
    • Cannot separate MafK-specific from MafG-specific functions
    • Molecular targets driving phenotypes not defined
  8. 2000 High

    Defined how MafK expression is targeted to hematopoietic and cardiac tissue through a GATA-dependent enhancer, linking lineage transcription factors to MafK levels.

    Evidence Transgenic reporter assays, enhancer mutagenesis, and GATA-factor EMSA

    PMID:10856242

    Open questions at the time
    • Did not address regulation in other MafK-expressing tissues
  9. 2002 High

    Placed MafK downstream of NGF/atypical PKC signaling as an immediate-early effector of neurite outgrowth, coupling extracellular cues to MafK induction.

    Evidence SAGE, pharmacological pathway dissection, siRNA, and dominant-negative neurite assays in PC12 and telencephalic neurons

    PMID:12388604

    Open questions at the time
    • Transcriptional targets in neurons not identified
    • Dimer partner mediating neurite effect unknown
  10. 2004 High

    Provided in vivo chromatin evidence that Nrf2-MafK activates GST-P during hepatocarcinogenesis, occupying GPE1 selectively in pre-neoplastic and tumor cells.

    Evidence EMSA, DNase I footprinting, reporter assays, and ChIP in hepatocytes and hepatoma cells

    PMID:14960151

    Open questions at the time
    • Did not establish what restricts GPE1 occupancy to transformed cells
  11. 2008 High

    Mechanistically linked MafK to chromatin architecture, showing it is required for NF-E2 occupancy, active histone marks, Pol II loading, and LCR-promoter looping at the β-globin locus.

    Evidence siRNA knockdown with ChIP and 3C in MEL cells

    PMID:18308612

    Open questions at the time
    • Did not define the looping factors recruited via MafK
    • Generalizability to other loci untested at the time
  12. 2008 Medium

    Showed MafK can be co-opted into corepressor recruitment, with NF-κB p65 promoting HDAC3 association at the ARE partly through MafK.

    Evidence Co-IP, ChIP, and reporter assays with overexpression/knockdown

    PMID:18241676

    Open questions at the time
    • MafK-HDAC3 interaction shown by Co-IP without reciprocal/structural validation
    • Direct versus indirect recruitment not resolved
  13. 2013 High

    Defined a signal-driven partner-switch mechanism in which TGF-β induces MafK to displace Nrf2 at the HO-1 ARE and repress a cytoprotective gene.

    Evidence siRNA, overexpression, and ChIP at the HO-1 ARE with Smad co-occupancy

    PMID:23737527

    Open questions at the time
    • Did not establish whether MafK acts as homodimer or Bach heterodimer at HO-1
  14. 2013 High

    Identified JDP2 as a positive cofactor that binds the ARE and the Nrf2-MafK complex to enhance ARE binding and activation, modulating cellular ROS.

    Evidence ChIP-qPCR, EMSA, reporter assays, and Jdp2-knockout MEFs

    PMID:24232097

    Open questions at the time
    • Structural basis of the JDP2-MafK-Nrf2 ternary complex not defined
  15. 2014 High

    Generalized the Bach/Nrf2 partner-switch to exocrine zymogen genes and showed heme triggers the Bach1b-for-Nrf2a exchange at MafK-occupied MARE sites.

    Evidence Reporter assays, zebrafish overexpression/morpholino, and ChIP

    PMID:24652768

    Open questions at the time
    • Did not determine whether MafK remains constitutively bound during partner exchange in mammals
  16. 2015 High

    Extended small-Maf function to the lens, showing Mafg/Mafk dosage controls oxidative-stress and sterol-synthesis genes whose dysregulation causes cataract.

    Evidence Compound Mafg-/-:Mafk+/- mouse genetics with microarray profiling

    PMID:25896808

    Open questions at the time
    • Direct MafK target genes in lens not validated by ChIP
  17. 2017 High

    Established an oncogenic role: TGF-β-induced MAFK drives EMT and metastasis by directly activating GPNMB.

    Evidence Bidirectional overexpression/knockdown in TNBC cells and mouse xenograft/orthotopic models with RNA-seq target identification

    PMID:28400538

    Open questions at the time
    • Dimer partner driving GPNMB activation not defined
    • Whether MAFK acts as activator independent of CNC partners unclear
  18. 2020 High

    Showed MafK enforces cell-type-specific silencing of IRF8 via chromatin remodeling, with genome-wide binding mapped and a causal intronic site identified.

    Evidence shRNA screen, ChIP-Seq, CRISPR deletion of binding sites, and ATAC-Seq

    PMID:32534063

    Open questions at the time
    • Repressive partner/corepressor at the IRF8 locus not identified
  19. 2022 High

    Refined the lens role to early embryonic fiber-cell differentiation, with double-null lenses showing cytoskeletal and cell-cycle gene misexpression.

    Evidence Mafg-/-:Mafk-/- mouse genetics, immunostaining, and RNA-seq of E16.5 lenses

    PMID:36092713

    Open questions at the time
    • Direct versus indirect regulation of cytoskeletal/ECM genes not resolved
  20. 2022 Medium

    Linked MafK overexpression to epithelial apoptosis and increased Salmonella susceptibility, implicating it in mucosal cell death.

    Evidence MafK transgenic mouse infection model with caspase-3 readouts and in vitro apoptosis assays

    PMID:35260530

    Open questions at the time
    • Direct transcriptional targets mediating apoptosis not identified
    • Single-lab overexpression model
  21. 2025 Medium

    Identified MAFK SUMOylation as a functional requirement for its EMT, stemness, and ABCG2-dependent drug-resistance activities.

    Evidence Non-SUMOylatable mutant overexpression with EMT, sphere-formation, and doxorubicin-resistance assays

    PMID:41316921

    Open questions at the time
    • SUMO E3 ligase and modification site not biochemically validated
    • Abstract-level detail, single lab
  22. 2026 Medium

    Showed MAFK directly activates AREG to enable escape from doxorubicin-induced senescence in NSCLC, extending its oncogenic target repertoire.

    Evidence ChIP at the AREG promoter with senescence, colony-formation, and flow-cytometry assays

    PMID:42180617

    Open questions at the time
    • Dimer partner at AREG promoter undefined
    • Single-lab study

Open questions

Synthesis pass · forward-looking unresolved questions
  • It remains unresolved how MAFK switches between repressive (homodimer/Bach) and activating (CNC) modes at a given locus in a signal- and tissue-specific manner, and whether its reported activating oncogenic roles (GPNMB, AREG, EMT) reflect a canonical heterodimer or a distinct mechanism.
  • No structural model of MAFK dimer/DNA complexes in the corpus
  • Mechanism selecting partner identity per locus undefined
  • Activating partner for oncogenic targets not identified

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 7 GO:0003677 DNA binding 6 GO:0060090 molecular adaptor activity 3
Localization
GO:0000228 nuclear chromosome 2 GO:0005634 nucleus 1
Pathway
R-HSA-74160 Gene expression (Transcription) 4 R-HSA-8953897 Cellular responses to stimuli 3 R-HSA-1643685 Disease 2 R-HSA-4839726 Chromatin organization 2
Partners
BACH1BACH2HDAC3JDP2NFE2NFE2L2RELA
Complex memberships
Bach1/Bach2-MafK heterodimerNrf2-MafK heterodimerp45/NF-E2-MafK heterodimer

Evidence

Reading pass · 27 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1993 MafK (mafK) encodes a nuclear bZIP protein that lacks the amino-terminal acidic transactivation domain present in c-Maf, yet retains a conserved bZIP domain. When overexpressed via retroviral vector, MafK protein localizes predominantly to the nucleus. cDNA cloning, retroviral overexpression, immunofluorescence/immunostaining with specific antibody, soft-agar colony formation assay Oncogene Medium 8361754
1995 MafK binds to consensus NF-E2 sites as a homodimer in vitro and represses transcription of NF-E2 site-dependent reporter genes; when co-expressed with p45 (NF-E2 large subunit), MafK confers site-specific DNA-binding activity to p45 and p45 in turn mediates transcriptional activation via its amino-terminal proline-rich domain. In vitro DNA-binding assay (EMSA), transient transfection reporter assays, cDNA isolation and structural analysis The Journal of biological chemistry High 7706310
1995 Conditional overexpression of MafK in murine erythroleukemia cells induced hemoglobin accumulation (terminal erythroid differentiation) and increased DNA-binding activities containing MafK, demonstrating MafK is sufficient to promote the erythroid differentiation program. Stable transfection with metallothionein-driven MafK, hemoglobin assay, EMSA for DNA-binding activity Proceedings of the National Academy of Sciences of the United States of America High 7638211
1996 Bach1 and Bach2, novel BTB-bZIP transcription factors, heterodimerize with MafK (identified by yeast two-hybrid screen) and bind NF-E2 sites in vitro. Bach1/MafK and Bach2/MafK heterodimers function as transcriptional repressors in fibroblasts; Bach1/MafK acts as an activator while Bach2/MafK acts as a repressor in erythroid cells. Yeast two-hybrid screen, in vitro DNA-binding assay (EMSA), transfection reporter assays in fibroblast and erythroid cells Molecular and cellular biology High 8887638
1996 MafK expression in mesoderm is driven by a distal promoter (IM), while neuronal expression is directed by a distinct proximal promoter (IN) located ~6 kb 3' to the mesodermal promoter; in neurons, MafK associates with a partner molecule distinct from p45. Northern blot analysis during murine development, promoter mapping, transgenic mouse reporter assays Genes to cells : devoted to molecular & cellular mechanisms High 9140066
1997 MafK (NF-E2p18) is required for DMSO-induced erythroid differentiation in Friend erythroleukemia cells: overexpression of MafK induced globin transcripts and increased NF-E2 DNA-binding activity, while antisense inhibition of MafK blocked DMSO-induced differentiation and reduced NF-E2 DNA-binding activity. Stable transfection of sense/antisense constructs, Northern blot for globin transcripts, EMSA for NF-E2 DNA-binding, transient transfection reporter assays Leukemia High 9009092
1998 The core region (nt -67 to -9) of the mafK neuronal IN promoter is sufficient to direct neuron-specific transcription in the ventral spinal cord both in cell transfection assays and in transgenic mice in vivo. Transient transfection reporter assays, transgenic mouse reporter assays Genes to cells : devoted to molecular & cellular mechanisms Medium 9893024
1998 Human MAFK gene is located at chromosome 7p22, consists of a conserved bZIP-containing structure, and its gene organization is highly conserved with murine mafK. Restriction enzyme mapping, Southern blot hybridization, nucleotide sequencing, FISH Cytogenetics and cell genetics Medium 9763667
2000 MafG and MafK homodimers bind the NQO1 antioxidant response element (ARE) and repress ARE-mediated expression and antioxidant induction of NQO1 and GST Ya genes; MafK-Nrf2 heterodimers also bind the ARE. Maf-Nrf1 heterodimers failed to bind the NQO1 ARE. Transient transfection overexpression assays in HepG2 cells, EMSA/supershift assays with NQO1 ARE and nuclear proteins The Journal of biological chemistry High 11013233
2000 Compound mafG/mafK double-null mice survive embryogenesis but die postnatally, and exhibit synthetic phenotypes including severe anemia with abnormal erythrocyte morphology/membrane protein composition, exacerbated thrombocytopenia with proplatelet formation defects, and severe neurological disorders, establishing redundant but essential roles of small Maf proteins in erythropoiesis, megakaryopoiesis, and neuronal function. Germline targeted null mutations, compound mutant mouse genetic analysis, hematological and histological phenotyping The EMBO journal High 10716933
2000 A tissue-specific enhancer 3' to the mafK gene (HCEK) directs mafK transcription in both hematopoietic and cardiac muscle cells; two specific GATA consensus motifs within HCEK are required for activity in both tissues, and GATA-1, GATA-4, and GATA-6 each bind these sites with high specificity. Transgenic mouse reporter assays, deletion/mutation analysis of enhancer, EMSA for GATA factor binding The EMBO journal High 10856242
2001 Transgenic overexpression of MafK specifically in T cells suppresses T cell proliferation and cytokine secretion (IL-2, IL-4); overexpressed MafK forms homodimers that bind to MARE-like sequences in the IL-2 and IL-4 promoters, repressing MARE-dependent transcription. T cell-specific transgenic mouse model, EMSA for MafK-promoter binding, RT-PCR for cytokine mRNA, immunological phenotyping Genes to cells : devoted to molecular & cellular mechanisms High 11737266
2002 MafK is an NGF-responsive immediate early gene in PC12 cells regulated by an atypical PKC isoform (but not MEK, PLCγ, or PI3K); interference with MafK expression (siRNA) or activity (dominant negative) suppresses NGF-promoted neurite outgrowth in PC12 cells and immature telencephalic neurons, identifying MafK as a regulator of neuronal differentiation. Serial analysis of gene expression (SAGE), Northern blot/Western blot for expression, pharmacological inhibitor studies, siRNA knockdown, dominant-negative overexpression, neurite outgrowth assay The Journal of neuroscience : the official journal of the Society for Neuroscience High 12388604
2004 The Nrf2/MafK heterodimer specifically binds the GST-P enhancer element GPE1 and activates GST-P gene transcription during hepatocarcinogenesis; chromatin immunoprecipitation showed both Nrf2 and MafK occupy GPE1 in pre-neoplastic hepatocytes and hepatoma cells but not normal hepatocytes. EMSA, DNase I footprinting with wild-type and mutant GPE1, reporter transfection assays, Northern blot, ChIP assays The Biochemical journal High 14960151
2007 MafK/NF-E2 p18 knockdown reduces NF-E2 occupancy at the beta-globin locus, decreases H3 acetylation, H3-K4 methylation, and RNA Pol II deposition at the beta-globin gene cluster, and reduces the spatial proximity (looping frequency) between the LCR hypersensitive site HS2 and downstream active beta-globin gene promoters, establishing MafK's role in mediating LCR-gene looping for transcriptional activation. siRNA knockdown in MEL cells, ChIP assays for NF-E2, histone marks and RNA Pol II, Chromosome Conformation Capture (3C) assay The international journal of biochemistry & cell biology High 18308612
2008 NF-κB p65 represses Nrf2-ARE pathway through two mechanisms involving MafK: (1) p65 competitively deprives CBP from Nrf2 via the CH1-KIX domain interaction (dependent on PKA-mediated S276 phosphorylation of p65); (2) p65 facilitates recruitment of HDAC3 corepressor to ARE by promoting HDAC3 interaction with either CBP or MafK, leading to local histone hypoacetylation. Co-immunoprecipitation, reporter assays, chromatin immunoprecipitation, overexpression and knockdown experiments Biochimica et biophysica acta Medium 18241676
2013 TGF-β induces MafK and Bach1 expression; elevated MafK is sufficient to suppress electrophile-inducible HO-1 expression even with nuclear Nrf2 present; siRNA knockdown of MafK and Bach1 abolishes TGF-β-dependent HO-1 suppression; ChIP assays show TGF-β pretreatment increases MafK binding to the HO-1 ARE (E2 site) together with Smads, displacing Nrf2. siRNA knockdown, overexpression, ChIP assays for Nrf2/Bach1/MafK at HO-1 ARE, RT-PCR/Western blot The Journal of biological chemistry High 23737527
2013 JDP2 (Jun dimerization protein 2) directly binds the ARE core sequence and associates with both Nrf2 and MafK via bZIP domains, increasing the DNA-binding activity of the Nrf2-MafK complex to ARE and the transcription of ARE-dependent genes; Jdp2-knockout MEFs show impaired Nrf2-MafK-dependent ARE activation and increased intracellular ROS. ChIP-qPCR, EMSA, ARE-reporter assays, Jdp2 knockout MEFs, ROS measurements Cell death & disease High 24232097
2014 In zebrafish, the Bach1b-MafK heterodimer represses exocrine zymogen promoters via MARE motifs, while the Nrf2a-MafK heterodimer activates them; heme stimulates exchange of Bach1b for Nrf2a at MafK-occupied MARE sites; ChIP shows MafK binds MARE sites in 5' regulatory regions of zymogen genes. In vitro luciferase reporter assays, overexpression and morpholino knockdown in zebrafish, ChIP assays Disease models & mechanisms High 24652768
2015 Compound Mafg-/-:Mafk+/- mice develop progressive lens defects leading to cataract by age 4 months with severely disorganized fiber cells; microarray profiling identifies 97 differentially regulated genes including oxidative stress and sterol synthesis pathway genes, establishing Mafg and Mafk as regulators of non-crystallin cataract-associated genes in lens fiber cells. Compound null-allele mouse genetics, high-resolution phenotypic characterization, microarray expression profiling, integrative bioinformatics analysis Human genetics High 25896808
2017 MAFK is induced by TGF-β signaling in TNBC cells and promotes epithelial-mesenchymal transition (EMT) and malignant progression; MAFK directly induces expression of the GPNMB gene; knockdown of MAFK suppresses tumor growth and metastasis, while overexpression of MAFK in NMuMG cells induces EMT, tumor formation, and invasion in mice. Overexpression and knockdown in cell lines and mouse xenograft/orthotopic models, RNA-seq/gene expression analysis to identify GPNMB as direct target, in vivo tumor implantation assays Science signaling High 28400538
2020 MafK mediates chromatin remodeling to silence IRF8 expression in non-immune cells in a cell-type-specific manner; ChIP-Seq identified three MafK binding regions within the IRF8 locus (-25 kb, -20 kb, and 6th intron); CRISPR-Cas9 deletion of the MafK-intron6 binding region caused accessible chromatin conformation at the IRF8 locus and significantly increased basal and IFN-γ-induced IRF8 expression. shRNA library screen, ChIP-Seq, lentiviral reporter constructs, CRISPR-Cas9 deletion of binding sites, ATAC-Seq/chromatin accessibility assays Journal of molecular biology High 32534063
2022 Mafg-/-:Mafk-/- double knockout embryonic lenses (E16.5) show abnormally multilayered epithelium, abnormal F-actin distribution at the fulcrum region, and misexpression of cytoskeleton/cell cycle/extracellular matrix genes (including Cdk1, Cdkn1c, Camsap1, Col3a1, Epha5, Pxdn), establishing early embryonic roles for Mafg and Mafk in lens fiber cell differentiation. Double knockout mouse genetics, E-cadherin/nuclear/F-actin immunostaining, RNA-sequencing of E16.5 lenses, RT-qPCR validation Frontiers in cell and developmental biology High 36092713
2022 MafK overexpression in transgenic mice increases susceptibility to Salmonella mucosal infection by promoting epithelial cell apoptosis through rapid caspase-3 cleavage, facilitating Salmonella dissemination and inflammation. MafK transgenic mouse oral Salmonella infection model, histological analysis, in vitro cell apoptosis assays, caspase-3 activation measurement Aging Medium 35260530
2025 The SUMOylation consensus sequence (ψKxE) of MAFK is functionally important: a non-SUMOylatable MAFK mutant shows impaired ability to induce EMT, cellular migration/invasion, tumor and sphere formation, stem-like properties, and drug resistance against doxorubicin; these effects depend on ABCG2 expression. Non-SUMOylation mimic mutant overexpression, EMT/migration/invasion assays, tumor/sphere formation assays, drug resistance assays, ABCG2 expression analysis Cancer science Medium 41316921
2026 MAFK directly binds the AREG promoter region and transcriptionally activates AREG; elevated MAFK-AREG signaling enables NSCLC cells to escape doxorubicin-induced senescence and promotes proliferation. ChIP assay for MAFK binding at AREG promoter, Western blot/RT-qPCR, senescence-associated β-galactosidase assay, colony formation, flow cytometry Oncology letters Medium 42180617
2024 MAFK knockdown in macrophages in vivo (using lipidoid nanoparticles in MI mice) significantly improved cardiac function and suppressed fibrosis, and computational analysis identified MAFK as a contact-forming transcription factor at transposable elements; MAFK knockdown decreased chromatin contacts and loops at and between TE sequences. In vivo macrophage-specific knockdown via lipidoid nanoparticles in MI mouse model, cardiac functional readout; computational pipeline (te_hic) for chromatin contact analysis; knockdown validation of chromatin loop reduction bioRxivpreprint Low

Source papers

Stage 0 corpus · 42 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2008 NF-kappaB/p65 antagonizes Nrf2-ARE pathway by depriving CBP from Nrf2 and facilitating recruitment of HDAC3 to MafK. Biochimica et biophysica acta 586 18241676
1996 Bach proteins belong to a novel family of BTB-basic leucine zipper transcription factors that interact with MafK and regulate transcription through the NF-E2 site. Molecular and cellular biology 571 8887638
2016 Small Maf proteins (MafF, MafG, MafK): History, structure and function. Gene 199 27058431
2000 Small maf (MafG and MafK) proteins negatively regulate antioxidant response element-mediated expression and antioxidant induction of the NAD(P)H:Quinone oxidoreductase1 gene. The Journal of biological chemistry 183 11013233
1993 Two new members of the maf oncogene family, mafK and mafF, encode nuclear b-Zip proteins lacking putative trans-activator domain. Oncogene 162 8361754
2012 The small MAF transcription factors MAFF, MAFG and MAFK: current knowledge and perspectives. Biochimica et biophysica acta 127 22721719
2004 Transcription factor Nrf2/MafK regulates rat placental glutathione S-transferase gene during hepatocarcinogenesis. The Biochemical journal 115 14960151
1995 Activity and expression of murine small Maf family protein MafK. The Journal of biological chemistry 106 7706310
2000 Perinatal synthetic lethality and hematopoietic defects in compound mafG::mafK mutant mice. The EMBO journal 78 10716933
2017 The transcription factor MAFK induces EMT and malignant progression of triple-negative breast cancer cells through its target GPNMB. Science signaling 71 28400538
1995 Conditional expression of the ubiquitous transcription factor MafK induces erythroleukemia cell differentiation. Proceedings of the National Academy of Sciences of the United States of America 63 7638211
2013 Jun dimerization protein 2 is a critical component of the Nrf2/MafK complex regulating the response to ROS homeostasis. Cell death & disease 60 24232097
2013 Transforming growth factor-β induces transcription factors MafK and Bach1 to suppress expression of the heme oxygenase-1 gene. The Journal of biological chemistry 53 23737527
2015 Compound mouse mutants of bZIP transcription factors Mafg and Mafk reveal a regulatory network of non-crystallin genes associated with cataract. Human genetics 46 25896808
2014 Oleanolic acid regulates NF-κB signaling by suppressing MafK expression in RAW 264.7 cells. BMB reports 40 25059280
2002 The basic region and leucine zipper transcription factor MafK is a new nerve growth factor-responsive immediate early gene that regulates neurite outgrowth. The Journal of neuroscience : the official journal of the Society for Neuroscience 38 12388604
1996 Mesodermal- vs. neuronal-specific expression of MafK is elicited by different promoters. Genes to cells : devoted to molecular & cellular mechanisms 37 9140066
2002 Differential induction of mafF, mafG and mafK expression by electrophile-response-element activators. The Biochemical journal 33 11772409
1997 NF-E2p18/mafK is required in DMSO-induced differentiation of Friend erythroleukemia cells by enhancing NF-E2 activity. Leukemia 26 9009092
2021 Optimization of Jiuzao protein hydrolysis conditions and antioxidant activity in vivo of Jiuzao tetrapeptide Asp-Arg-Glu-Leu by elevating the Nrf2/Keap1-p38/PI3K-MafK signaling pathway. Food & function 25 33876788
2014 Heme acts through the Bach1b/Nrf2a-MafK pathway to regulate exocrine peptidase precursor genes in porphyric zebrafish. Disease models & mechanisms 20 24652768
2000 One enhancer mediates mafK transcriptional activation in both hematopoietic and cardiac muscle cells. The EMBO journal 20 10856242
2001 Transgenic over-expression of MafK suppresses T cell proliferation and function in vivo. Genes to cells : devoted to molecular & cellular mechanisms 16 11737266
2022 Deficiency of the bZIP transcription factors Mafg and Mafk causes misexpression of genes in distinct pathways and results in lens embryonic developmental defects. Frontiers in cell and developmental biology 14 36092713
2019 Association between genetic polymorphisms of NRF2, KEAP1, MAFF, MAFK and anti-tuberculosis drug-induced liver injury: a nested case-control study. Scientific reports 14 31586142
2009 MafA-deficient and beta cell-specific MafK-overexpressing hybrid transgenic mice develop human-like severe diabetic nephropathy. Biochemical and biophysical research communications 13 19715672
2007 MafK/NF-E2 p18 is required for beta-globin genes activation by mediating the proximity of LCR and active beta-globin genes in MEL cell line. The international journal of biochemistry & cell biology 12 18308612
2015 Wnt1-induced MAFK expression promotes osteosarcoma cell proliferation. Genetics and molecular research : GMR 11 26214410
2010 Akt regulates the expression of MafK, synaptotagmin I, and syntenin-1, which play roles in neuronal function. Journal of biomedical science 11 20233453
2006 MafK overexpression in pancreatic beta-cells caused impairment of glucose-stimulated insulin secretion. Biochemical and biophysical research communications 10 16780794
1998 A core region of the mafK gene IN promoter directs neurone-specific transcription in vivo. Genes to cells : devoted to molecular & cellular mechanisms 10 9893024
2023 miR-503 targets MafK to inhibit subcutaneous preadipocyte adipogenesis causing a decrease of backfat thickness in Guanzhong Black pigs. Meat science 7 36657261
2016 β-Cell-Specific Mafk Overexpression Impairs Pancreatic Endocrine Cell Development. PloS one 6 26901059
2024 Transcription factor MAFK binds to circRPPH to regulate SIRT gene-mediated cellular pyroptosis and lung adenocarcinoma progression. International immunopharmacology 5 39602957
1998 Structure and chromosome mapping of the human small maf-genes MAFG and MAFK. Cytogenetics and cell genetics 4 9763667
2022 MafK accelerates Salmonella mucosal infection through caspase-3 activation. Aging 3 35260530
2017 Genetic polymorphisms of MAFK, encoding a small Maf protein, are associated with susceptibility to ulcerative colitis in Japan. World journal of gastroenterology 3 28839436
2020 MafK Mediates Chromatin Remodeling to Silence IRF8 Expression in Non-immune Cells in a Cell Type-SpecificManner. Journal of molecular biology 2 32534063
2012 A novel diabetes mellitus mouse model, MAFA-deficient and beta cell-specific MAFK-overexpressing hybrid transgenic mice, developed severe diabetic nephropathy and improved with TCV-116 (candesartan cilexetil) treatment. Experimental animals 2 22293672
2026 Breaking senescence restriction: MAFK-AREG axis promotes NSCLC cells to resist doxorubicin. Oncology letters 0 42180617
2025 Importance of SUMOylation Consensus Sequence of MAFK in Regulating EMT, Tumor Growth, Stemness, and Drug Resistance. Cancer science 0 41316921
2025 Salidroside Alleviates Lung Ischemia-Reperfusion Injury by Inhibiting Ferroptosis Through the MAFK/lncRNA PTOV1-AS2/miR-525-5p/ACE2 Axis. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 0 41329068

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