Affinage

MAZ

Myc-associated zinc finger protein · UniProt P56270

Length
477 aa
Mass
48.6 kDa
Annotated
2026-06-10
92 papers in source corpus 45 papers cited in narrative 45 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

MAZ is a C2H2 zinc finger transcription factor that recognizes GC-rich GA-box elements (consensus GGGAGGG/G5AG5) and non-canonical G-quadruplex structures to control transcription initiation, termination, and downstream RNA processing across developmental and oncogenic gene programs (PMID:1502157, PMID:7988563, PMID:23471001). First isolated through its binding to the c-MYC ME1a1 GA-box and to insulin/IAPP GAGA boxes, MAZ acts as a sequence-specific transactivator whose DNA-binding requires consecutive zinc fingers (the third and fourth fingers) and overlaps the binding specificity of Sp1 at shared GC-rich elements (PMID:1502157, PMID:1454839, PMID:11395515). MAZ is bifunctional: it activates many promoters but also represses transcription through an N-terminal proline/alanine-rich domain and a second internal repressive domain, and it recruits a repressive HDAC1/RBBP7/CUL4B complex to deacetylate target promoters such as CSK (PMID:10383467, PMID:11259406, PMID:40618395). At G5AG5 sites between closely spaced genes MAZ bends DNA and drives RNA polymerase II transcriptional termination, and at intragenic MAZ elements it pauses elongating RNAPII to alter alternative splicing outcomes (PMID:7988563, PMID:15126509). Beyond direct promoter control, MAZ organizes genome architecture by physically interacting with the cohesin subunit RAD21 to arrest cohesin sliding and act as a CTCF cofactor at topologically associating domain and Hox cluster boundaries, where loss of MAZ motifs derepresses posterior Hox genes (PMID:33558242, PMID:35145304). MAZ also binds and remodels G-quadruplexes in the KRAS, HRAS, and CCND1 promoters, and at G4-containing promoters it forms phase-separated nuclear condensates—via G4 recognition by zinc finger 2 and condensation driven by zinc fingers 3–5—that concentrate coactivators including BRD4, MED1, CDK9 and active RNAPII (PMID:23471001, PMID:25013182, PMID:38316778). MAZ activity is tuned post-translationally: casein kinase II phosphorylation at Ser480 is required for binding the c-MYC nuclease-hypersensitive element, while Akt phosphorylation at Thr385 releases MAZ from the p53 promoter to relieve repression (PMID:10448092, PMID:26902421). Functionally, MAZ governs cell-cycle entry and proliferation, erythroid differentiation through an erythroid gene program and the MAZ–MYB–fetal hemoglobin axis, and is required for development, as homozygous Maz deletion in mice causes perinatal lethality with congenital anomalies of the kidney and urinary tract (PMID:29432158, PMID:34351390, PMID:41331317).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 1992 High

    Establishing what MAZ is required defining its DNA target and its dual role at both promoter-proximal and termination sequences, which set the agenda for all later mechanistic work.

    Evidence Expression cloning by binding-site library screening and EMSA with fusion proteins, mapping binding to the c-MYC ME1a1 GA-box, P2 attenuator, and C2 termination region; parallel cloning as Pur-1 showing transactivation of insulin/IAPP promoters

    PMID:1454839 PMID:1502157

    Open questions at the time
    • No structural basis for sequence recognition at this stage
    • Dual initiation/termination role inferred from binding correlation, not directly dissected
  2. 1994 High

    Connecting MAZ binding to a mechanistic output, MAZ-induced DNA bending at G5AG5 sites was shown to drive RNAPII transcriptional termination between closely spaced genes.

    Evidence In vitro binding, consensus-site mutagenesis, and in vivo termination assays at the C2/Factor B and g11 loci

    PMID:7988563

    Open questions at the time
    • Molecular link between DNA bending and termination machinery not defined
    • No identification of polymerase-associated cofactors
  3. 1996 Medium

    Resolving how MAZ relates to other GC-box factors, it was shown to bind GC-rich promoter motifs that overlap Sp1 sites and to act both as an initiator-element factor and as a single-stranded NHE binder.

    Evidence cDNA cloning, DNase I footprinting of the serotonin 1a receptor promoter, in vitro initiator assays, and EMSA of single-stranded c-MYC NHE binding by a MAZ-like zinc finger

    PMID:8626793 PMID:8940139

    Open questions at the time
    • THZif-1 identity as canonical MAZ not fully established
    • Competition vs cooperation with Sp1 on native chromatin unresolved
  4. 1999 Medium

    Recognizing MAZ as bifunctional, studies mapped a repressive domain and demonstrated context-dependent repression of the c-MYC promoter.

    Evidence GAL4 fusion assays and promoter deletion/mutation in COS cells localizing repression to the N-terminal Pro/Ala-rich region

    PMID:10383467

    Open questions at the time
    • Corepressor identity unknown at this stage
    • Switch between activation and repression not mechanistically explained
  5. 1999 High

    Establishing post-translational control, casein kinase II phosphorylation at Ser480 was shown to be required for MAZ binding to the c-MYC NHE and for transactivation.

    Evidence Site-specific mutagenesis (S480A), in vitro/in vivo phosphorylation, EMSA, and luciferase reporter assays in HeLa cells

    PMID:10448092

    Open questions at the time
    • In vivo kinase responsible under physiological signaling not confirmed
    • Effect on genome-wide binding not assessed
  6. 2000 Medium

    Linking MAZ to growth control, gain-of-function showed it can act as a growth suppressor by slowing G1 transit and lowering c-myc and cyclin levels.

    Evidence Retroviral overexpression in NIH3T3 with colony formation, growth curves, flow cytometry, and cyclin immunoblots

    PMID:11012087

    Open questions at the time
    • Direct vs indirect transcriptional targets driving the phenotype not separated
    • Context dependence (activator vs suppressor) unexplained
  7. 2004 High

    Extending MAZ beyond initiation/termination, intragenic MAZ elements were shown to pause elongating RNAPII and thereby alter alternative splicing.

    Evidence FGFR2 minigene cotransfection, RT-PCR elongation assays, promoter swaps, and in vitro transcribed RNA transfection

    PMID:15126509

    Open questions at the time
    • Direct demonstration of MAZ protein occupancy during pausing limited
    • Generality across splicing events not established
  8. 2013 Medium

    Defining a structural mode of recognition, MAZ was shown to bind G-quadruplexes in the KRAS and HRAS promoters and to unfold/remodel them to control transcription.

    Evidence EMSA with GST-MAZ on G4 DNA, G4-unfolding assays with complementary strands, mutational separation of binding from quadruplex motifs, reporters, and G4-decoy xenograft experiments

    PMID:23471001 PMID:25013182

    Open questions at the time
    • Which zinc fingers mediate G4 recognition not pinpointed in these studies
    • In vivo G4 occupancy genome-wide not mapped
  9. 2016 Medium

    A second phosphorylation switch was identified: Akt phosphorylation at Thr385 releases MAZ from the p53 promoter, converting repression into derepression in response to oncogene activation.

    Evidence In vitro Akt phosphorylation, Thr385 mutagenesis, ChIP at the p53 promoter, and luciferase reporters

    PMID:26902421

    Open questions at the time
    • Structural consequence of Thr385 phosphorylation on DNA binding undefined
    • Single lab, no reciprocal validation
  10. 2021 High

    MAZ was elevated from a promoter-level factor to a genome-architecture organizer by showing it binds cohesin (RAD21), arrests cohesin sliding, and shapes TAD boundaries with CTCF.

    Evidence Reciprocal Co-IP (MAZ-RAD21), insulator and RNAPII pause assays, ChIP-seq of MAZ/CTCF co-occupancy, and Hi-C on MAZ depletion

    PMID:33558242

    Open questions at the time
    • Domain of MAZ mediating RAD21 contact not mapped
    • Interplay between condensate formation and cohesin arrest not addressed
  11. 2022 High

    An unbiased screen plus in vivo genetics established MAZ as a bona fide CTCF cofactor at chromatin boundaries with developmental consequences.

    Evidence Genome-wide CRISPR KO screen, Co-IP with RAD21, MAZ/CTCF ChIP-seq, and MAZ motif deletion mice at the HoxA cluster producing homeotic transformations

    PMID:35145304

    Open questions at the time
    • Quantitative contribution of MAZ vs CTCF at individual boundaries not resolved
    • Mechanism distinguishing MAZ-only from CTCF/MAZ boundaries unclear
  12. 2024 High

    The G4 and condensate functions were unified by domain mapping: zinc finger 2 reads G4s while zinc fingers 3-5 drive phase separation, organizing coactivator-rich nuclear puncta at G4 promoters.

    Evidence ZF2 and ZF3-5 mutagenesis, condensate imaging, coactivator ChIP (BRD4/MED1/CDK9/RNAPII), G4 co-localization, and HCC xenografts

    PMID:38316778

    Open questions at the time
    • Composition and stoichiometry of condensates not fully characterized
    • Relationship of condensates to TAD/cohesin function not tested
  13. 2025 Medium

    MAZ's repressive arm was given molecular identity by purifying its corepressor complex and an erythroid program by defining the MAZ-MYB-fetal hemoglobin axis.

    Evidence Immunoaffinity/MS interactome identifying HDAC1/RBBP7/CUL4B with ChIP at CSK; MAZ knockdown and MYB rescue in HUDEP-2 and patient-derived β-thalassemia erythroid cells with HbF quantification

    PMID:40618395 PMID:41331317

    Open questions at the time
    • Stoichiometry/assembly of the HDAC1/RBBP7/CUL4B complex unresolved
    • Recruitment determinants of the corepressor by MAZ not mapped

Open questions

Synthesis pass · forward-looking unresolved questions
  • How MAZ's distinct activities—sequence-specific activation/repression, G4 remodeling, phase separation, RNAPII pausing, and cohesin-dependent boundary formation—are coordinated at a single locus and selectively deployed across cell types remains unresolved.
  • No integrated model linking condensate formation to cohesin arrest
  • Determinants of activator vs repressor mode at individual promoters undefined
  • No high-resolution structure of MAZ bound to GA-box or G4 DNA

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003677 DNA binding 5 GO:0140110 transcription regulator activity 5
Localization
GO:0005634 nucleus 3 GO:0005654 nucleoplasm 1
Pathway
R-HSA-74160 Gene expression (Transcription) 5 R-HSA-1266738 Developmental Biology 3 R-HSA-4839726 Chromatin organization 3 R-HSA-1640170 Cell Cycle 2 R-HSA-8953854 Metabolism of RNA 2
Partners
CTCFCUL4BEWSR1HDAC1RAD21RBBP7SP1ZIP7
Complex memberships
HDAC1/RBBP7/CUL4B corepressor complex

Evidence

Reading pass · 45 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1992 MAZ (MYC-associated zinc finger protein) was cloned and shown to bind specifically to the ME1a1 GA-box sequence (GGGAGGG) in the c-MYC P2 promoter, to the P2 attenuator region in the first exon, and to a related sequence involved in transcriptional termination of the C2 gene, suggesting dual roles in transcription initiation and termination. Lambda gt11 library screening with concatamerized binding site probe, in vitro DNA binding with MAL-c fusion protein, EMSA Proceedings of the National Academy of Sciences of the United States of America High 1502157
1992 Pur-1 (MAZ) was cloned from a hamster insulinoma library and shown to bind GAGA boxes in the rat insulin I and II gene promoters and the human islet amyloid polypeptide gene promoter, and to function as a potent transcriptional transactivator in both pancreatic and nonpancreatic cells including HeLa cells. Lambda gt11 library screening, EMSA, transient transfection transactivation assays Proceedings of the National Academy of Sciences of the United States of America High 1454839
1994 MAZ binds to a G5AG5 consensus sequence between the closely spaced human complement genes C2 and Factor B, bends DNA, and its binding correlates with transcriptional termination activity in vivo; mutation of MAZ sites severely reduces termination activity. Inherently bent DNA was highly active as a terminator, suggesting MAZ-induced DNA bending is important for C2 and g11 termination. In vitro protein binding assays, MAZ consensus site identification, mutational analysis of termination sequences, in vivo termination assay The EMBO journal High 7988563
1996 MAZ (Pur-1/Zif87) protein was cloned from HeLa cells based on binding to a GC-rich motif (GGGG(C/A)GGGG) in the serotonin 1a receptor gene promoter. DNase I footprinting identified four MAZ binding sites, three of which overlap Sp1 binding sites. Overproduction of MAZ in transient transfection assays increased expression from the human serotonin 1a receptor 5'-flanking sequence more effectively than Sp1, and one GC-rich sequence functioned as a transcription initiator in vitro. cDNA cloning from HeLa library, DNase I footprinting, transient transfection, in vitro transcription initiator assay The Journal of biological chemistry High 8626793
1996 THZif-1 (a MAZ-like zinc finger protein) binds specifically to the single-stranded pyrimidine-rich DNA of the c-MYC nuclease-hypersensitive element (NHE) with a Kd ~0.077 μM, but does not bind the purine-rich strand or methylated double-stranded NHE. The second zinc finger motif is the primary DNA-binding domain for this activity. EMSA with GST-THZif-1 fusion protein and deletion mutants, Kd measurement The Journal of biological chemistry Medium 8940139
1997 MAZ binding activity at the ME1a1 site closely correlates with the kinetics of c-myc P2 promoter activity during retinoic acid-induced neuroectodermal differentiation of P19 cells, establishing MAZ as essential for the transient ME1a1-dependent expression of c-myc during this differentiation process. CAT reporter assay with c-myc promoter constructs, EMSA with ME1a1 probe in differentiating P19 cells Oncogene Medium 9294605
1997 MAZ and Sp1 both activate the adenovirus type 5 major late promoter by binding GC-rich sequences flanking the TATA box (MAZ binds at -18 and -36; Sp1 at -18). Evidence for physical interaction between MAZ and the adenovirus E1A protein was obtained by immunoprecipitation, and E1A enhances MAZ-mediated activation. DNase I footprinting, transient transfection, mutational analysis, immunoprecipitation with E1A Journal of virology Medium 9371624
1998 The human MAZ gene is located on chromosome 16p11.2, spans ~40 kb with five exons and four introns, and its promoter has features of a housekeeping gene (high GC, CpG-rich, no TATA/CAAT). Positive and negative autoregulatory elements were identified: MAZ positively autoregulates from -248 to -189 bp and negatively autoregulates from -383 to -248 bp. Genomic cloning, S1 nuclease protection assay, CAT reporter cotransfection with MAZ expression vector The Journal of biological chemistry Medium 9685418
1999 Casein kinase II (CKII) phosphorylates MAZ at serine 480 (identified by site-specific mutagenesis). This phosphorylation is required for maximum MAZ binding to the pyrimidine-rich NHE of the c-myc promoter. S480A mutation eliminates DNA-binding activity and abolishes MAZ-enhanced luciferase expression from a c-myc promoter reporter in HeLa cells. Site-specific mutagenesis, in vitro and in vivo phosphorylation assays, EMSA, luciferase reporter assay Biochemical and biophysical research communications High 10448092
1999 ZF87/MAZ overexpression in COS cells significantly represses transcription from the murine c-myc P2 promoter via the ME1a2 element at -86 relative to the P2 transcription start site. MAZ functions as a transcriptional repressor when fused to GAL4, and the repressive domain maps to the amino-terminal proline/alanine-rich region. Transient transfection/cotransfection in COS cells, GAL4 fusion assay, promoter deletion/mutation analysis The Journal of biological chemistry Medium 10383467
2000 MAZ/Pur-1 binds to ILPR G-quartet-forming sequences in the human insulin promoter, and both inter- and intramolecular G-quartet formation in the ILPR can influence transcriptional activity of the insulin gene, contributing to diabetes susceptibility associated with the IDDM2 locus. DNA structure analysis, transcriptional activity assays with mutant ILPR repeats designed to favor or disfavor G-quartet formation Proceedings of the National Academy of Sciences of the United States of America Medium 11070077
2000 FAC1 protein physically interacts with ZF87/MAZ, as shown by yeast two-hybrid and in vitro recombinant protein binding. The MAZ interaction domain maps to the FAC1 region containing a putative NLS/NES, while FAC1 recognizes a conformational interface including the Pro/Ala-rich domain and first zinc finger of MAZ. FAC1 co-expression reduces ZF87/MAZ-mediated transactivation of the SV40 promoter in a dose-dependent manner; a FAC1 mutant lacking the MAZ-interaction domain does not alter MAZ activity. Yeast two-hybrid, recombinant protein pulldown, deletion mutagenesis, cotransfection luciferase reporter assay Biochemistry Medium 10727212
2001 Sp1 and MAZ bind to the same GC-rich cis-elements in the MAZ gene promoter and independently repress MAZ expression. A novel repressive domain in MAZ maps to amino acids 127–292. Histone deacetylases are involved in MAZ autorepression, while DNA methyltransferase 1 is associated with Sp1-mediated repression of MAZ. EMSA, deletion/mutation analysis, cotransfection with reporter, HDAC inhibitor treatment, methyltransferase experiments The Journal of biological chemistry Medium 11259406
2001 The DNA-binding activity of Sp1 and MAZ depends on two consecutive zinc fingers: the second and third zinc fingers in Sp1, and the third and fourth zinc fingers in MAZ. Both proteins bind to overlapping GC-rich sequences (GGGCGG for Sp1, GGGAGGG for MAZ). EMSA with zinc finger deletion mutants, competition binding The Journal of biological chemistry Medium 11395515
2002 SP1 and MAZ bind to a 27-bp GC-rich region in the NR1 (NMDA receptor subunit 1) promoter. Mutations in SP1 and MAZ binding sites impair protein binding and decrease NR1 promoter activity during neuronal differentiation of P19 cells, despite binding activity of both factors remaining unchanged after differentiation. EMSA, mutagenesis of promoter binding sites, transient transfection reporter assay during P19 neuronal differentiation Brain research. Molecular brain research Medium 12425938
2003 MAZ is an autoantigen in Hodgkin's disease patients with paraneoplastic cerebellar degeneration. In neuronal cells, MAZ interacts with DCC (Deleted in Colorectal Cancer product), the receptor for the neuronal survival factor netrin-1, suggesting epitope spreading between the Tr antigen and the MAZ-DCC complex. Cerebellar expression library probing with patient sera, immunoblot, cell co-expression analysis Annals of neurology Low 12509857
2003 MAZ and Sp1 bind competitively to overlapping elements at -48 and -38 bp in the rat PNMT gene promoter. MAZ displaces/prevents Sp1 binding, with occupancy dependent on concentration and relative affinity. Phosphatase treatment of nuclear extracts prevents both MAZ- and Sp1-DNA binding complex formation. MAZ preferentially increases intron-retaining PNMT mRNA whereas Sp1 preferentially increases intronless mRNA. Gel mobility shift assay with in vitro translated proteins, PNMT promoter transient transfection assays, phosphatase treatment Molecular pharmacology Medium 14573768
2004 MAZ4 elements within the FGFR2 pre-mRNA locus function as RNA polymerase II pause sites. Insertion of MAZ4 5' to upstream silencing elements or between exon IIIb and downstream silencing elements decreases exon IIIb silencing, demonstrating that RNAPII pausing at MAZ elements can alter alternative splicing decisions. Changing the promoter alters both FGFR2 minigene splicing and the MAZ4 effect. Minigene cotransfection assay, RT-PCR elongation assay for RNAPII pausing, promoter-swap experiments, in vitro transcribed RNA transfection The Journal of biological chemistry High 15126509
2007 MAZ is overexpressed in MCF-7 breast cancer cells and binds the PPARgamma1 tumor-specific promoter (pA1) in vivo. Overexpression of MAZ in normal human mammary epithelial cells (HMEC) is sufficient to drive PPARgamma1 expression by recruiting the tumor-specific promoter pA1. Western blot (MAZ overexpression), chromatin immunoprecipitation (MAZ binding to pA1 promoter), transfection of MAZ into HMEC Breast cancer research and treatment Medium 17902047
2008 MAZ was identified by quantitative ICAT proteomics as a factor binding the conserved Muscle creatine kinase promoter element MPEX. MAZ transactivates the MCK promoter, binds the MPEX site in vitro, and is enriched at endogenous MCK, Skeletal alpha-actin, Desmin, and alpha-Myosin heavy chain promoters in skeletal and cardiac myocytes by ChIP. MAZ transcripts and DNA-binding activity are upregulated during skeletal myocyte differentiation. MAZ also occupies and transactivates the Six4 promoter in skeletal but not cardiac myocytes. ICAT quantitative proteomics, in vitro DNA binding, ChIP, transactivation reporter assays, RT-PCR of differentiation Molecular and cellular biology High 18710939
2012 MAZ is a transcriptional regulator of VEGF in glioblastoma-associated endothelial cells. miR-125b is down-regulated by VEGF in endothelial cells, resulting in increased MAZ expression; increased MAZ in turn promotes VEGF transcription, forming a feed-forward loop. MAZ-specific shRNAs attenuate primary human brain endothelial cell migration and tubule formation in vitro. shRNA knockdown, miR-125b inhibitor/mimic, migration and tubule formation assays, luciferase reporter FASEB journal Medium 22415301
2013 MAZ activates KRAS transcription by binding to G-quadruplex structures in the KRAS promoter nuclease-hypersensitive element (NHE). G4-decoy oligonucleotides mimicking KRAS quadruplexes suppress KRAS expression, reduce metabolic activity, inhibit colony formation, and activate apoptosis in Panc-1 cells; intratumoral injection in SCID mice reduced xenograft tumor growth by 64%. EMSA (MAZ binding to G4 DNA), luciferase reporter assay, G4-decoy oligonucleotide treatment, in vitro cell growth assays, in vivo xenograft Nucleic acids research Medium 23471001
2014 MAZ binds to G-quadruplex structures in the HRAS promoter (two neighboring G-elements) and unfolds them; in the presence of complementary strands, MAZ promotes rapid transformation of the HRAS G-quadruplexes into duplexes. The two neighboring G-quadruplexes synergistically repress HRAS transcription. Mutational dissection separated MAZ-binding sites from quadruplex-forming motifs. EMSA with GST-MAZ, G-quadruplex unfolding assay with complementary strands, mutational analysis of HRAS G-elements, reporter assays Nucleic acids research High 25013182
2014 HIF2α activates the Cav1 (caveolin-1) promoter in the colon in a HIF response element-independent manner, and MAZ is essential for this HIF2α-mediated activation. Hypoxic induction of CAV1 via this HIF2α/MAZ mechanism in the colon suppresses occludin expression, impairing intestinal barrier integrity. Mouse models with intestinal-specific HIF1α/HIF2α overexpression, reporter assays, MAZ functional requirement assessed Molecular and cellular biology Medium 24891620
2015 MAZ transcriptionally activates ZO-1, occludin, and claudin-5 promoters by binding to their GGGCGGG, CCCTCCC, and GGGAGGG elements, respectively, as confirmed by ChIP assay. Knockdown of MAZ impairs blood-tumor barrier integrity and increases permeability, downregulating ZO-1, occludin, and claudin-5. miR-34c targets and suppresses MAZ expression. ChIP assay (MAZ binding to tight junction gene promoters), dual-luciferase reporter, siRNA/shRNA knockdown, transendothelial electric resistance, HRP flux assay Journal of cellular physiology Medium 25201524
2016 Akt phosphorylates MAZ at Thr385 in response to oncogene activation. Phosphorylated MAZ is released from the p53 promoter, leading to transcriptional activation of p53. Un-phosphorylated MAZ acts as a transcriptional repressor of the p53 promoter. Phosphorylation assay (Akt + MAZ in vitro), mutagenesis of MAZ Thr385, ChIP (MAZ at p53 promoter), luciferase reporter assay Cancer letters Medium 26902421
2016 MAZ mediates cardiotrophin-1 (CT-1)-induced NOTCH1 signaling during gliogenesis by transcriptionally activating ADAM10 (a rate-limiting factor for NOTCH1 activation). MAZ knockdown inhibits CT-1-stimulated gliogenesis and can be rescued by overexpression of NICD (Notch intracellular domain). MAZ shRNA knockdown, gliogenesis assay, rescue with NICD overexpression, reporter assay for ADAM10 Scientific reports Medium 26867947
2017 MAZ (purified as Myb-sp) binds to and activates transcription via the E2F binding element in the MYB promoter, bypassing RB/p130-mediated repression. MAZ isoforms are major components of the Myb-sp activity. Forced RB or p130 expression represses the MYB-E2F element reporter, but co-expression of MAZ not only reverses repression but activates transcription. MAZ occupies the MYB promoter in vivo, and MAZ knockdown inhibits MYB expression during exit from quiescence. Biochemical purification of Myb-sp, EMSA, ChIP (MAZ at MYB promoter in vivo), luciferase reporter, RB/p130 cotransfection, siRNA knockdown Nucleic acids research High 28973440
2018 MAZ promotes bone metastasis of prostate cancer through transcriptional upregulation of KRas and HRas expression. ChIP and luciferase assays confirm MAZ binding to Ras gene promoters. RalGEF signaling downstream of KRas (not HRas) mediates the pro-bone metastasis effect of MAZ. MAZ overexpression/silencing bidirectionally regulates PCa invasion, migration in vitro and bone metastasis in vivo (cardiac ventricle inoculation model). ChIP, luciferase reporter, transwell assay, in vivo intracardiac bone metastasis model, western blot, pull-down assays Journal of experimental & clinical cancer research Medium 31488180
2018 Mechanistically, MAZ depletion in PDAC cells does not directly affect K-Ras mutant expression, but MAZ increases CRAF-ERK signaling activity via PAK and AKT/PKB cascades to promote PDAC cell invasiveness. Cyr61/CCN1 regulates MAZ expression upstream via Notch-1-sonic hedgehog signaling. Western blot (CRAF-ERK activity), siRNA knockdown of MAZ, invasion/migration/sphere formation assays, signaling pathway inhibitor experiments The Journal of biological chemistry Medium 29414775
2018 MAZ knockdown in HEK293 cells results in differential expression of WNT morphogens required for genitourinary development including Wnt11 and Wnt4, prevents efficient transition into S phase, affects transcription of cell-cycle regulators, and abrogates growth. Homozygous Maz deletion in CRISPR-Cas9 mice causes perinatal lethality with high penetrance of congenital anomalies of the kidney and urinary tract (CAKUTs); haploinsufficiency produces bladder development defects. siRNA knockdown in HEK293 cells, CRISPR-Cas9 mouse Maz deletion, gene expression profiling, cell cycle analysis Proceedings of the National Academy of Sciences of the United States of America High 29432158
2019 circ-CUX1 binds to EWSR1 to facilitate its interaction with MAZ, resulting in transactivation of MAZ and transcriptional alteration of genes associated with neuroblastoma tumor progression and aerobic glycolysis. RNA pulldown, co-immunoprecipitation (EWSR1-MAZ interaction), luciferase reporter (MAZ transactivation), lentiviral knockdown, inhibitory peptide blocking circ-CUX1-EWSR1 interaction EMBO molecular medicine Medium 31709724
2020 Maz disruption in mice causes developmental eye defects due to increased expression of Wnt pathway genes (Sfrp2, Wnt2b, Fzd4) in Maz-deficient eyes, yet the Wnt reporter TCF-Lef1 is significantly downregulated, indicating MAZ is necessary for activation of the canonical Wnt/β-catenin pathway and participates in ciliary margin patterning. CRISPR-Cas9 Maz knockout mouse, gene expression analysis, Wnt reporter (TCF-Lef1) assay, proliferation assays Disease models & mechanisms Medium 32571845
2021 MAZ physically interacts with the cohesin subunit RAD21 (independently of CTCF), can arrest cohesin sliding independently of CTCF, pauses the elongating form of RNA polymerase II (affecting alternative splicing), and insulates an enhancer from a promoter. CTCF/MAZ double sites sequester cohesin more effectively than CTCF-only sites. MAZ depletion disrupts local contacts within topologically associating domains (TADs) and TAD boundaries in Hi-C analysis. Co-immunoprecipitation (MAZ-RAD21), insulator assay, RNAPII pause assay, Hi-C (MAZ depletion), ChIP-seq (MAZ/CTCF co-occupancy), alternative splicing analysis Proceedings of the National Academy of Sciences of the United States of America High 33558242
2021 MAZ was identified by DNA affinity purification and mass spectrometry as a transcription factor binding the α-globin gene promoter in primary human erythroid cells. Genome-wide mapping shows MAZ occupies active promoters and GATA1-bound enhancers of key erythroid genes. MAZ knockdown reduces α-globin expression in K562 cells and impairs differentiation in primary human erythroid cells. DNA affinity purification + mass spectrometry, ChIP-seq, shRNA knockdown, erythroid differentiation assay Blood advances High 34351390
2022 A genome-wide CRISPR KO screen identified MAZ as a cofactor in CTCF-mediated insulation at HoxA cluster boundaries. MAZ colocalizes with CTCF at chromatin borders and interacts with cohesin subunit RAD21. MAZ motif deletions in mice lead to derepression of posterior Hox genes immediately after CTCF boundaries and homeotic transformations, phenocopying CTCF motif deletions. Genome-wide CRISPR KO screen, Co-IP (MAZ-RAD21), ChIP-seq (MAZ/CTCF co-localization), MAZ motif deletion in mouse (CRISPR), gene expression analysis Nature genetics High 35145304
2022 MAZ transcriptionally activates FTH1 (ferritin heavy chain 1, a negative regulator of ferroptosis) by binding to the FTH1 promoter, as confirmed by ChIP assay. The lncRNA TUG1 directly targets MAZ (confirmed by luciferase assay), and TUG1 downregulation or FTH1 inhibition enhances dihydroartemisinin-induced ferroptosis in glioma cells. ChIP assay (MAZ binding FTH1 promoter), luciferase assay (TUG1-MAZ interaction), ferroptosis assays, in vitro and in vivo experiments Oxidative medicine and cellular longevity Medium 36164395
2024 G-quadruplexes (G4s) in the CCND1 promoter recruit MAZ and promote motility within MAZ phase-separated condensates to activate CCND1 transcription. Zinc finger 2 of MAZ is responsible for G4 binding, while zinc fingers 3–5 (not the disordered region) are critical for MAZ condensation. MAZ nuclear puncta colocalize with G4 signals and coactivators (BRD4, MED1, CDK9, active RNAPII, active histone markers). MAZ mutants lacking either G4 binding or phase separation ability fail to form nuclear puncta and show deficiencies in promoting hepatocellular carcinoma proliferation and xenograft tumor formation. Domain mutagenesis (ZF2 deletion, ZF3-5 deletion), phase-separation/condensate imaging, ChIP for coactivators, xenograft tumor formation assay, G4 co-localization Nature communications High 38316778
2024 MAZ is confirmed as the major upstream transcription factor directly regulating BCKDK expression in triple-negative breast cancer by binding to the BCKDK promoter, as validated by ChIP and luciferase assays. BCKDK interacts with glucose-6-phosphate dehydrogenase (G6PD) to increase pentose phosphate pathway flux, and forced G6PD expression rescues growth defects in BCKDK-deficient cells. ChIP assay, luciferase reporter assay, Co-IP (BCKDK-G6PD), isotope tracer metabolomics, cell growth assays, patient-derived xenograft Cell death & disease Medium 39025830
2024 MAZ transcriptionally activates NEIL3 expression in lung adenocarcinoma by binding to its promoter, as confirmed by dual-luciferase and ChIP assays. The MAZ/NEIL3 axis represses DNA damage to advance cisplatin resistance and promotes cell migration and invasion in LUAD. ChIP assay, dual-luciferase reporter assay, siRNA knockdown, DNA damage assays, cell migration and invasion Pulmonary pharmacology & therapeutics Medium 37121465
2024 MAZ promotes osteosarcoma cell migration and invasion downstream of PTX3/STAT3 signaling. PTX3 knockdown reduces MAZ promoter activity and MAZ expression via STAT3, and MAZ overexpression rescues migration suppressed by PTX3 knockdown. Luciferase reporter (MAZ promoter), western blot, STAT3 overexpression rescue, transwell migration/invasion, xenograft tail vein metastasis model Cancer cell international Medium 41107857
2025 MAZ binds to and recruits the transcriptional inhibitory complex containing HDAC1, RBBP7, and CUL4B. MAZ and HDAC1 cooperatively repress CSK gene expression; knockdown of either MAZ or HDAC1 activates CSK expression and subsequently inhibits MAPK/ERK, STAT3, and PI3K/AKT signaling. MAZ/HDAC1 complex-mediated histone deacetylation at the CSK promoter is the proposed mechanism. Immunoaffinity purification + silver-stain mass spectrometry (MAZ interactome), RNA-seq, ChIP assay, EdU, colony formation, transwell, in vivo xenograft and bioluminescence metastasis assay Molecular carcinogenesis Medium 40618395
2025 MAZ occupies the MYB promoter and transcriptionally activates MYB expression; MAZ depletion reduces MYB levels and leads to significant induction of γ-globin (HBG) expression and increased fetal hemoglobin in HUDEP-2 and patient-derived β-thalassemia erythroid cells. Restoration of MYB re-silences HBG levels in MAZ-depleted cells, establishing the MAZ-MYB-HBG axis. HUDEP-2 and primary erythroid cell MAZ knockdown, MYB re-expression rescue, HbF FACS quantification, qRT-PCR Scientific reports Medium 41331317
2025 Zip7 (zinc transporter) interacts with MAZ in the cytoplasm and facilitates MAZ nuclear import. Nuclear MAZ is upregulated in metastatic prostate cancer. Zip7 silencing inhibits PCa cell migration and invasion in vitro and bone metastasis in vivo; RNA-seq reveals Zip7 facilitates MAZ nuclear import to promote MYBL2 transcription. Co-IP (Zip7-MAZ cytoplasmic interaction), nuclear/cytoplasmic fractionation, Zip7 siRNA KD, intracardiac bone metastasis model, RNA-seq Communications biology Medium 42010154
2000 ZF87/MAZ overexpression in NIH3T3 fibroblasts causes a growth suppressor phenotype: significant reduction in colony formation, slow growth, delayed G1 transit, decreased endogenous c-myc expression, and reduced cyclin A and cyclin E protein levels. Retroviral transduction, colony formation assay, growth curve analysis, flow cytometry cell cycle analysis, western blot for cyclins Biochemistry and cell biology Medium 11012087

Source papers

Stage 0 corpus · 92 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1992 MAZ, a zinc finger protein, binds to c-MYC and C2 gene sequences regulating transcriptional initiation and termination. Proceedings of the National Academy of Sciences of the United States of America 290 1502157
1996 The serotonin 1a receptor gene contains a TATA-less promoter that responds to MAZ and Sp1. The Journal of biological chemistry 201 8626793
2019 Therapeutic targeting of circ-CUX1/EWSR1/MAZ axis inhibits glycolysis and neuroblastoma progression. EMBO molecular medicine 133 31709724
1992 Pur-1, a zinc-finger protein that binds to purine-rich sequences, transactivates an insulin promoter in heterologous cells. Proceedings of the National Academy of Sciences of the United States of America 107 1454839
1994 MAZ-dependent termination between closely spaced human complement genes. The EMBO journal 104 7988563
2012 Myc-associated zinc finger protein (MAZ) is regulated by miR-125b and mediates VEGF-induced angiogenesis in glioblastoma. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 102 22415301
2000 Unusual DNA structure of the diabetes susceptibility locus IDDM2 and its effect on transcription by the insulin promoter factor Pur-1/MAZ. Proceedings of the National Academy of Sciences of the United States of America 94 11070077
2014 HRAS is silenced by two neighboring G-quadruplexes and activated by MAZ, a zinc-finger transcription factor with DNA unfolding property. Nucleic acids research 82 25013182
2013 MAZ-binding G4-decoy with locked nucleic acid and twisted intercalating nucleic acid modifications suppresses KRAS in pancreatic cancer cells and delays tumor growth in mice. Nucleic acids research 82 23471001
2022 CRISPR and biochemical screens identify MAZ as a cofactor in CTCF-mediated insulation at Hox clusters. Nature genetics 71 35145304
2019 MAZ promotes prostate cancer bone metastasis through transcriptionally activating the KRas-dependent RalGEFs pathway. Journal of experimental & clinical cancer research : CR 65 31488180
1997 Activation of the adenovirus major late promoter by transcription factors MAZ and Sp1. Journal of virology 63 9371624
2002 Effect of the ubiquitous transcription factors, SP1 and MAZ, on NMDA receptor subunit type 1 (NR1) expression during neuronal differentiation. Brain research. Molecular brain research 62 12425938
2021 The Myc-associated zinc finger protein (MAZ) works together with CTCF to control cohesin positioning and genome organization. Proceedings of the National Academy of Sciences of the United States of America 61 33558242
2014 Hypoxia-inducible factor/MAZ-dependent induction of caveolin-1 regulates colon permeability through suppression of occludin, leading to hypoxia-induced inflammation. Molecular and cellular biology 61 24891620
2001 Independent repression of a GC-rich housekeeping gene by Sp1 and MAZ involves the same cis-elements. The Journal of biological chemistry 61 11259406
1998 Genomic organization and expression of a human gene for Myc-associated zinc finger protein (MAZ). The Journal of biological chemistry 61 9685418
2018 The MAZ transcription factor is a downstream target of the oncoprotein Cyr61/CCN1 and promotes pancreatic cancer cell invasion via CRAF-ERK signaling. The Journal of biological chemistry 49 29414775
2018 16p11.2 transcription factor MAZ is a dosage-sensitive regulator of genitourinary development. Proceedings of the National Academy of Sciences of the United States of America 46 29432158
2024 G-quadruplexes promote the motility in MAZ phase-separated condensates to activate CCND1 expression and contribute to hepatocarcinogenesis. Nature communications 43 38316778
2003 Regulation of the rat phenylethanolamine N-methyltransferase gene by transcription factors Sp1 and MAZ. Molecular pharmacology 43 14573768
1999 Transcriptional repression from the c-myc P2 promoter by the zinc finger protein ZF87/MAZ. The Journal of biological chemistry 43 10383467
2004 MAZ elements alter transcription elongation and silencing of the fibroblast growth factor receptor 2 exon IIIb. The Journal of biological chemistry 42 15126509
2008 Quantitative proteomic identification of MAZ as a transcriptional regulator of muscle-specific genes in skeletal and cardiac myocytes. Molecular and cellular biology 41 18710939
2001 Two consecutive zinc fingers in Sp1 and in MAZ are essential for interactions with cis-elements. The Journal of biological chemistry 41 11395515
2017 Dual function of MAZ mediated by FOXF2 in basal-like breast cancer: Promotion of proliferation and suppression of progression. Cancer letters 40 28577976
2013 The prostate cancer-up-regulated Myc-associated zinc-finger protein (MAZ) modulates proliferation and metastasis through reciprocal regulation of androgen receptor. Medical oncology (Northwood, London, England) 40 23609189
2007 MAZ drives tumor-specific expression of PPAR gamma 1 in breast cancer cells. Breast cancer research and treatment 39 17902047
2015 miR-34c regulates the permeability of blood-tumor barrier via MAZ-mediated expression changes of ZO-1, occludin, and claudin-5. Journal of cellular physiology 38 25201524
2003 Transcriptional regulation by zinc-finger proteins Sp1 and MAZ involves interactions with the same cis-elements. International journal of molecular medicine 38 12684688
1996 Binding of THZif-1, a MAZ-like zinc finger protein to the nuclease-hypersensitive element in the promoter region of the c-MYC protooncogene. The Journal of biological chemistry 36 8940139
1997 MAZ, a Myc-associated zinc finger protein, is essential for the ME1a1-mediated expression of the c-myc gene during neuroectodermal differentiation of P19 cells. Oncogene 35 9294605
2000 Fetal Alz-50 clone 1 (FAC1) protein interacts with the Myc-associated zinc finger protein (ZF87/MAZ) and alters its transcriptional activity. Biochemistry 32 10727212
2014 Induction of Ras by SAF-1/MAZ through a feed-forward loop promotes angiogenesis in breast cancer. Cancer medicine 29 25449683
1996 Members of the MAZ family: a novel cDNA clone for MAZ from human pancreatic islet cells. Biochemical and biophysical research communications 26 8831693
2012 Regulation of neural stem cell differentiation by transcription factors HNF4-1 and MAZ-1. Molecular neurobiology 25 22944911
2025 MAZ-mediated tumor progression and immune evasion in hormone receptor-positive breast cancer: Targeting tumor microenvironment and PCLAF+ subtype-specific therapy. Translational oncology 22 39805182
2024 MAZ promotes thyroid cancer progression by driving transcriptional reprogram and enhancing ERK1/2 activation. Cancer letters 22 39197582
2021 MicroRNA-29b-3p Inhibits the Migration and Invasion of Gastric Cancer Cells by Regulating the Autophagy-Associated Protein MAZ. OncoTargets and therapy 22 34040389
2022 TUG1/MAZ/FTH1 Axis Attenuates the Antiglioma Effect of Dihydroartemisinin by Inhibiting Ferroptosis. Oxidative medicine and cellular longevity 20 36164395
2000 The transcription factors SP1 and MAZ regulate expression of the parathyroid hormone/parathyroid hormone-related peptide receptor gene. Journal of molecular endocrinology 19 11116210
1996 Selenite supplementation decreases expression of MAZ in HT29 human colon adenocarcinoma cells. Nutrition and cancer 19 8844723
2016 MAZ mediates the cross-talk between CT-1 and NOTCH1 signaling during gliogenesis. Scientific reports 18 26867947
2016 Akt phosphorylates myc-associated zinc finger protein (MAZ), releases P-MAZ from the p53 promoter, and activates p53 transcription. Cancer letters 18 26902421
2008 Gastrin activates paracrine networks leading to induction of PAI-2 via MAZ and ASC-1. American journal of physiology. Gastrointestinal and liver physiology 18 19074642
1999 The DNA-binding and transcriptional activities of MAZ, a myc-associated zinc finger protein, are regulated by casein kinase II. Biochemical and biophysical research communications 18 10448092
2010 Antioxidant liposomes protect against CEES-induced lung injury by decreasing SAF-1/MAZ-mediated inflammation in the guinea pig lung. Journal of biochemical and molecular toxicology 17 20583300
2020 The transcription factor Maz is essential for normal eye development. Disease models & mechanisms 16 32571845
2024 MAZ-mediated up-regulation of BCKDK reprograms glucose metabolism and promotes growth by regulating glucose-6-phosphate dehydrogenase stability in triple-negative breast cancer. Cell death & disease 15 39025830
2014 23S rRNA as an a-Maz-ing new bacterial toxin target. RNA biology 15 24525465
1999 Structural organization and expression of the mouse gene for Pur-1, a highly conserved homolog of the human MAZ gene. European journal of biochemistry 15 10092852
2024 MAZ promotes tumor proliferation and immune evasion in lung adenocarcinoma. Oncogene 14 39424990
2021 Identification of the transcription factor MAZ as a regulator of erythropoiesis. Blood advances 14 34351390
2017 MAZ induces MYB expression during the exit from quiescence via the E2F site in the MYB promoter. Nucleic acids research 14 28973440
2024 Transcription Factor MAZ Potentiates the Upregulated NEIL3-mediated Aerobic Glycolysis, thereby Promoting Angiogenesis in Hepatocellular Carcinoma. Current cancer drug targets 13 38347781
2003 The MAZ protein is an autoantigen of Hodgkin's disease and paraneoplastic cerebellar dysfunction. Annals of neurology 13 12509857
2009 SAF-3, a novel splice variant of the SAF-1/MAZ/Pur-1 family, is expressed during inflammation. The FEBS journal 12 19583771
2023 Transcriptional factor MAZ promotes cisplatin-induced DNA damage repair in lung adenocarcinoma by regulating NEIL3. Pulmonary pharmacology & therapeutics 11 37121465
2024 Genome-wide functional integration identified MAZ-controlled RPS14 dysregulation in hepatocellular carcinoma. Archives of toxicology 10 38189915
2018 Association of SHMT1, MAZ, ERG, and L3MBTL3 Gene Polymorphisms with Susceptibility to Multiple Sclerosis. Biochemical genetics 9 30456721
1993 Physical characteristics of a factor related to the c-myc/insulin promoter binding protein ZF87/Pur-1. Biochemical and biophysical research communications 9 8507192
2024 Calycosin inhibits the proliferation and metastasis of renal cell carcinoma through the MAZ/HAS2 signaling pathway. Phytotherapy research : PTR 8 39120474
2025 Single-cell and spatial transcriptome analyses reveal MAZ(+) NPC-like clusters as key role contributing to glioma recurrence and drug resistance. Journal of translational medicine 7 40524155
2025 MAZ-mediated N6-methyladenosine modification of ZEB1 promotes hepatocellular carcinoma progression by regulating METTL3. Journal of translational medicine 6 40038747
2022 Qingdu decoction can reduce LPS induced ACLF endotoxemia by regulating microRNA-34c/MAZ/TJs and microRNA-122a/Zonulin/EGFR signal pathway. Journal of ethnopharmacology 6 36414212
2000 The ZF87/MAZ transcription factor functions as a growth suppressor in fibroblasts. Biochemistry and cell biology = Biochimie et biologie cellulaire 6 11012087
1998 Human genes for KNSL4 and MAZ are located close to one another on chromosome 16p11.2. Genomics 6 9790757
2025 MAZ-induced lncRNA H19 regulates proliferation and differentiation of porcine skeletal muscle satellite cells via sponge miR-935/miR-296-5p and the p38 MAPK pathway. International journal of biological macromolecules 5 40164245
2023 PCGF6/MAX/KDM5D facilitates MAZ/CDK4 axis expression and pRCC progression by hypomethylation of the DNA promoter. Epigenetics & chromatin 5 36890610
2024 Molecular mechanisms of MAZ targeting up-regulation of NDUFS3 expression to promote malignant progression in melanoma. Communications biology 4 39532991
2017 miRNA Enriched in Human Neuroblast Nuclei Bind the MAZ Transcription Factor and Their Precursors Contain the MAZ Consensus Motif. Frontiers in molecular neuroscience 4 28878619
1994 Analysis of the C-myc promoter-binding factor zf87/pur1 in transformed and nontransformed cell-lines. International journal of oncology 4 21559684
2019 Revealing the alternative promoter usage of SAF/MAZ gene by bichromatic fluorescent reporter construct. Bioscience reports 3 30610159
2025 A MAZ::NCOA2 Subcutaneous Small Round Cell Sarcoma of Infancy With Diffuse S100/SOX10 Positivity: A Novel Entity. Genes, chromosomes & cancer 2 39985329
2025 Dihydroartemisinin alleviates diethylnitrosamine-induced hepatocarcinogenesis by targeting a novel MAZ/TRIM50 axis. International immunopharmacology 2 40288151
2025 MAZ Coordinates With HDAC1 to Promote Hepatocarcinoma Proliferation and Metastasis Through Transcriptional Repression of CSK. Molecular carcinogenesis 2 40618395
2024 Decoding the synergistic potential of MAZ-51 and zingerone as therapy for melanoma treatment in alignment with sustainable development goals. Cell biochemistry and function 2 38348768
2025 ANKRD22 Induced by Transcription Factor MAZ Promotes Proliferation and Invasion of Nasopharyngeal Carcinoma. Journal of biochemical and molecular toxicology 1 40346905
2025 PUF60-Regulated Isoform Switching of MAZ Modulates Gastric Cancer Cell Migration. Cancer medicine 1 40411278
2025 Exploring Phytochemical Adjuvant Therapy in Melanoma Treatment: The Effects of MAZ-51 and Zingerone on Melanoma Cell Proliferation. Clinical and experimental pharmacology & physiology 1 40695356
2025 Suppression of pentraxin 3 inhibits human osteosarcoma cell metastasis by repressing MAZ through STAT3 pathway. Cancer cell international 1 41107857
2024 MAZ regulates ferroptosis, apoptosis and differentiation of oligodendrocyte precursor cells. Brain research 1 39581526
2023 Aquaporin 1 overexpression may enhance glioma tumorigenesis by interacting with the transcriptional regulation networks of Foxo4, Maz, and E2F families. Chinese neurosurgical journal 1 38057925
2026 Multi-Omics Analysis Reveals That the MAZ/HDGF Regulatory Axis Drives High-Grade Serous Ovarian Cancer Progression by Modulating Glycolysis and M2 Macrophage Polarization. IUBMB life 0 41467359
2026 MAZ-Mediated ubiquitin-conjugating enzyme E2C upregulation promotes breast cancer progression via the MAPK signaling pathway. Translational oncology 0 41496410
2026 Long non-coding RNA LINC00092 inhibits esophageal squamous cell carcinoma progression by promoting ferroptosis through the MAZ/NFE2L2 axis. Journal of thoracic disease 0 41660456
2026 Zinc-dependent Zip7-MAZ-MYBL2 axis promotes prostate cancer metastasis. Communications biology 0 42010154
2025 Transcription factor MAZ activates the transcription of hypomethylated TYMP in ccRCC. Functional & integrative genomics 0 39797954
2025 MAZ-mediated LAMA5 transcription activation promotes gastric cancer progression through the STAT3 signaling. Functional & integrative genomics 0 40072648
2025 Activation of ERK/MAPK signaling by MAZ through transcriptional repression of PPP3CA to promote osteoclastogenesis and osteoporosis progression: Functions and mechanisms. Tissue & cell 0 40602229
2025 Upregulation of SLC25A1 by MAZ reprograms fatty acid synthesis and fuels LUAD malignancy. General physiology and biophysics 0 41020326
2025 MAZ regulates fetal hemoglobin repression by activating MYB transcription. Scientific reports 0 41331317

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