Affinage

MAZ

Myc-associated zinc finger protein · UniProt P56270

Length
477 aa
Mass
48.6 kDa
Annotated
2026-04-28
92 papers in source corpus 35 papers cited in narrative 34 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MAZ is a Cys2His2 zinc finger transcription factor that binds GA-box (GGGAGGG), GC-rich, and G-quadruplex DNA elements to regulate transcription initiation, termination, RNA polymerase II pausing, and three-dimensional chromatin organization. It activates diverse promoters — including c-MYC, insulin, KRAS, HRAS, MYB, and muscle-specific genes — by recognizing G-rich sequences and G-quadruplex structures (via zinc finger 2), and can form phase-separated nuclear condensates (via zinc fingers 3–5) that compartmentalize coactivators such as BRD4, MED1, and CDK9 to drive transcription (PMID:1502157, PMID:1454839, PMID:23471001, PMID:25013182, PMID:38316778). MAZ also functions as a transcriptional repressor through its N-terminal proline/alanine-rich domain, recruits HDAC1 to silence targets such as CSK, autorepresses its own promoter, and represses p53 transcription in an Akt-phosphorylation-dependent manner (PMID:10383467, PMID:26902421, PMID:40618395). At a higher-order level, MAZ physically interacts with the cohesin subunit RAD21, independently arrests cohesin sliding, colocalizes with CTCF at topologically associating domain boundaries, and pauses elongating RNA polymerase II to influence co-transcriptional alternative splicing and chromatin insulation, with loss of MAZ causing homeotic transformations at Hox clusters and congenital kidney/urinary tract anomalies in mice (PMID:33558242, PMID:35145304, PMID:29432158). Its DNA-binding activity is positively regulated by casein kinase II phosphorylation at Ser480 and negatively regulated by Akt phosphorylation at Thr385 (PMID:10448092, PMID:26902421).

Mechanistic history

Synthesis pass · year-by-year structured walk · 15 steps
  1. 1992 High

    The identity of the factor binding GA-box elements in the c-MYC promoter was unknown; cloning of MAZ revealed a six-zinc-finger protein recognizing GGGAGGG motifs at both initiation and termination elements, establishing that a single factor could participate in both processes.

    Evidence cDNA cloning from HeLa library with in vitro DNA-binding and mutational analysis

    PMID:1502157

    Open questions at the time
    • No in vivo demonstration of termination function
    • Mechanism of termination versus initiation distinction unclear
  2. 1992 High

    Whether MAZ could function as a bona fide transcriptional activator at endogenous promoters beyond c-MYC was unresolved; demonstration that Pur-1/MAZ activates the insulin promoter via GAGA boxes in nonpancreatic cells established it as a general transcriptional activator of purine-rich elements.

    Evidence cDNA cloning from insulinoma library, transient transfection/transactivation in HeLa and beta-cell lines

    PMID:1454839

    Open questions at the time
    • No chromatin context demonstrated
    • No loss-of-function for insulin expression
  3. 1994 High

    How transcription terminates between closely spaced genes was mechanistically opaque; showing that MAZ binding sites are required for termination between complement genes C2/Factor B, and that MAZ bends DNA, provided a physical model for termination at gene boundaries.

    Evidence In vitro binding, DNA bending assay, in vivo termination assay with site mutations

    PMID:7988563

    Open questions at the time
    • No structural data on MAZ-induced DNA bend
    • Mechanism linking bending to polymerase release not established
  4. 1996 High

    Whether MAZ and Sp1 share or compete for regulatory elements was unclear; footprinting of the serotonin 1a receptor and later the PNMT promoter revealed overlapping MAZ/Sp1 binding sites, establishing competitive co-occupancy as a regulatory mechanism at GC-rich promoters.

    Evidence DNase I footprinting, EMSA competition, reporter assays across multiple promoters

    PMID:14573768 PMID:8626793

    Open questions at the time
    • Genome-wide extent of MAZ/Sp1 competition unknown at this stage
    • Whether competition is cell-type-specific not addressed
  5. 1997 High

    MAZ had been characterized only as an activator; demonstrating GAL4-fusion-mediated repression mapped to the N-terminal proline/alanine-rich domain established MAZ as a bifunctional transcription factor capable of both activation and repression.

    Evidence GAL4 fusion repressor assay, deletion mapping, reporter assay in COS cells

    PMID:10383467

    Open questions at the time
    • Cofactors mediating repression not identified at this stage
    • No in vivo repression data
  6. 1999 High

    Post-translational regulation of MAZ DNA-binding activity was unknown; identification of CKII-mediated phosphorylation at Ser480 as required for maximum DNA binding and transactivation established phosphorylation as a key regulatory switch.

    Evidence In vitro kinase assay, Ser480Ala mutagenesis, EMSA, luciferase reporter

    PMID:10448092

    Open questions at the time
    • In vivo phosphorylation dynamics not characterized
    • Other kinase inputs not explored
  7. 2004 High

    Whether MAZ could affect post-transcriptional gene regulation was unknown; showing that MAZ elements pause elongating RNA polymerase II within FGFR2 and thereby influence co-transcriptional alternative splicing linked MAZ to RNA processing.

    Evidence Minigene reporter, RT-PCR elongation assay, in vitro transcription

    PMID:15126509

    Open questions at the time
    • Direct protein requirement (versus DNA element requirement) not fully separated
    • Genome-wide scope of MAZ-dependent splicing unknown
  8. 2013 High

    The relationship between MAZ and non-canonical DNA structures was unexplored; demonstrating that MAZ binds and activates transcription through G-quadruplex structures in the KRAS promoter, and that G4-decoy oligonucleotides block this, established G-quadruplex recognition as a functional mode of MAZ action.

    Evidence G4 competitive binding assay, reporter assay, xenograft mouse model

    PMID:23471001

    Open questions at the time
    • Structural basis of MAZ–G4 interaction unresolved
    • Whether G4 binding is separable from duplex binding not determined
  9. 2014 High

    Whether MAZ simply bound or actively remodeled G-quadruplexes was unknown; reconstitution showing MAZ unfolds HRAS promoter G-quadruplexes and promotes duplex formation established MAZ as a G4-resolving factor that activates transcription by unwinding inhibitory structures.

    Evidence In vitro G-quadruplex unfolding assay with MAZ-GST, mutagenesis, reporter assay

    PMID:25013182

    Open questions at the time
    • Energy source for unfolding not identified
    • In vivo G4 resolution not demonstrated
  10. 2016 Medium

    A second kinase input to MAZ was undefined; showing that Akt phosphorylates MAZ at Thr385 to release it from the p53 promoter, thereby derepressing p53, revealed a phosphorylation-dependent toggle between MAZ occupancy and gene activation.

    Evidence In vitro kinase assay, ChIP, site-directed mutagenesis, reporter assay

    PMID:26902421

    Open questions at the time
    • Single lab finding
    • Interplay between CKII (Ser480) and Akt (Thr385) phosphorylation not examined
  11. 2018 High

    The in vivo developmental requirement for MAZ was unknown; CRISPR knockout of Maz in mice caused perinatal lethality with kidney and urinary tract anomalies (CAKUT) and haploinsufficiency for bladder development, while knockdown in human cells disrupted S-phase entry and Wnt morphogen expression.

    Evidence CRISPR-Cas9 mouse model, siRNA knockdown with transcriptome analysis, cell cycle assay

    PMID:29432158

    Open questions at the time
    • Direct transcriptional targets mediating CAKUT not delineated
    • Human genetic CAKUT association not established
  12. 2021 High

    Whether MAZ functioned in higher-order chromatin organization was entirely open; demonstrating that MAZ physically interacts with cohesin, independently arrests cohesin sliding, pauses RNA polymerase II, and insulates enhancer–promoter communication established MAZ as a chromatin architectural protein analogous to CTCF.

    Evidence Co-IP, Hi-C, insulator reporter assay, siRNA depletion, RNAPII pausing assay

    PMID:33558242

    Open questions at the time
    • Structural basis of cohesin arrest unknown
    • Whether MAZ and CTCF act redundantly or synergistically at all shared sites unclear
  13. 2022 High

    The functional consequence of MAZ at CTCF boundaries in developmental gene regulation was untested; a genome-wide CRISPR screen and MAZ motif deletions at Hox clusters showed that MAZ cooperates with CTCF to insulate posterior Hox genes, with loss causing homeotic transformations in mice.

    Evidence CRISPR KO screen, MAZ motif deletions, Hi-C, biochemical Co-IP with RAD21, mouse phenotyping

    PMID:35145304

    Open questions at the time
    • Whether MAZ insulation extends beyond Hox clusters genome-wide not fully mapped
    • Mechanism distinguishing MAZ-dependent from CTCF-only boundaries undefined
  14. 2024 High

    How MAZ concentrates transcriptional machinery at target promoters was mechanistically unexplained; showing that MAZ forms phase-separated condensates via ZF3-5, that G-quadruplex binding by ZF2 mobilizes MAZ into these condensates to colocalize with BRD4/MED1/CDK9, and that both activities are required for target gene activation, unified G4 recognition with phase separation as a transcriptional activation mechanism.

    Evidence Zinc finger mutagenesis, in vitro phase separation, immunofluorescence colocalization, xenograft model

    PMID:38316778

    Open questions at the time
    • In vivo dynamics of MAZ condensates not resolved
    • Whether phase separation contributes to insulator or repressor functions not tested
  15. 2025 High

    The cofactor basis for MAZ-mediated transcriptional repression was largely uncharacterized; immunoaffinity purification identified an MAZ–HDAC1–RBBP7–CUL4B complex that cooperatively silences CSK by catalyzing histone deacetylation at its promoter, providing a mechanistic basis for MAZ repressor function.

    Evidence Immunoaffinity purification/mass spectrometry, ChIP, Co-IP, RNA-seq, xenograft model

    PMID:40618395

    Open questions at the time
    • Whether HDAC1 recruitment is general to all MAZ-repressed targets unknown
    • Structural basis of MAZ–HDAC1 interaction not determined

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the structural basis of MAZ–cohesin interaction and cohesin arrest, the genome-wide rules distinguishing MAZ-activated from MAZ-repressed targets, whether MAZ phase separation contributes to its insulator and repressor functions, and whether human MAZ mutations cause developmental syndromes analogous to mouse CAKUT/Hox phenotypes.
  • No crystal or cryo-EM structure of MAZ bound to DNA or cohesin
  • No human Mendelian disease formally attributed to MAZ variants in the literature
  • Interplay between CKII and Akt phosphorylation in regulating MAZ chromatin occupancy not investigated

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003677 DNA binding 15 GO:0140110 transcription regulator activity 11 GO:0008092 cytoskeletal protein binding 2 GO:0098772 molecular function regulator activity 2
Localization
GO:0005634 nucleus 10 GO:0005654 nucleoplasm 2 GO:0005694 chromosome 2
Pathway
R-HSA-74160 Gene expression (Transcription) 13 R-HSA-1266738 Developmental Biology 3 R-HSA-162582 Signal Transduction 3 R-HSA-4839726 Chromatin organization 3
Partners
CTCFCUL4BEWSR1HDAC1RAD21RBBP7SLC39A7SP1
Complex memberships
MAZ–HDAC1–RBBP7–CUL4B repressive complex

Evidence

Reading pass · 34 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1992 MAZ (MYC-associated zinc finger protein) was cloned as a 477-amino acid zinc finger protein containing six Cys2His2-type zinc fingers, an N-terminal proline-rich domain, and polyalanine tracts. It binds specifically to the GA box sequence (GGGAGGG) found 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. cDNA cloning from HeLa lambda gt11 library, in vitro DNA-binding assay with fusion protein, mutational analysis of binding sites Proceedings of the National Academy of Sciences of the United States of America High 1502157
1992 Pur-1 (MAZ) binds specifically to purine-rich GAGA boxes in the insulin gene promoter and acts as a potent transcriptional activator in both pancreatic and nonpancreatic cells, activating an intact insulin promoter in HeLa cells where it is normally inactive. cDNA cloning from insulinoma library, DNA-binding assay, transient transfection/transactivation assay Proceedings of the National Academy of Sciences of the United States of America High 1454839
1994 MAZ binds to a consensus sequence G5AG5 in transcriptional termination regions between closely spaced human complement genes C2 and Factor B; mutation of MAZ binding sites severely reduces termination activity, and MAZ induces DNA bending, which is proposed to be important for termination function. In vitro protein-DNA binding, in vivo termination assay, mutational analysis of MAZ binding sites, DNA bending assay The EMBO journal High 7988563
1996 MAZ binds to four GC-rich sites in the serotonin 1a receptor gene promoter (identified by DNase I footprinting), three of which overlap Sp1 binding sites, and overproduction of MAZ in transient transfection substantially increases expression from the human serotonin 1a receptor promoter. One GC-rich sequence was also shown to function as a transcription initiator in vitro. cDNA cloning, DNase I footprinting, transient transfection/reporter assay, in vitro transcription initiation 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 Kd ~0.077 µM; binding is enhanced by methylated cytosine on single-stranded DNA and is mediated primarily by the amino-terminal second zinc finger motif. It does not bind the purine-rich strand. EMSA with GST-fusion proteins, deletion mutant analysis, methylation analysis The Journal of biological chemistry Medium 8940139
1997 Overexpression of ZF87/MAZ in COS cells significantly represses transcription from the murine c-myc P2 promoter through the ME1a2 element at -86 relative to the P2 start site. MAZ functions as a true transcriptional repressor independently of the c-myc promoter context (shown via GAL4 fusion), with the repressive domain mapping to the N-terminal proline/alanine-rich region. Transient transfection/reporter assay, GAL4 fusion repressor assay, deletion mapping The Journal of biological chemistry High 10383467
1997 MAZ is essential for ME1a1-mediated expression of c-myc during retinoic acid-induced neuroectodermal differentiation of P19 cells; MAZ DNA-binding activity kinetics closely correlated with changes in c-myc promoter activity during differentiation, and a construct lacking the ME1a1 site failed to show the MAZ-dependent transient increase. Reporter gene assay in P19 cells, EMSA with ME1a1 probe Oncogene Medium 9294605
1997 MAZ and Sp1 both activate expression from the adenovirus type 5 major late promoter by binding to GC-rich sequences flanking the TATA box (MAZ at -18 and -36; Sp1 at -18) and distal sites. Both transcription factors interact with adenovirus E1A protein as demonstrated by immunoprecipitation, and E1A enhances their activation. DNase I footprinting, transient transfection/reporter assay, mutational analysis, immunoprecipitation Journal of virology High 9371624
1999 MAZ is phosphorylated by casein kinase II (CKII) at serine 480 (the major site), and this phosphorylation is required for maximum DNA binding of MAZ to the pyrimidine-rich NHE of the c-myc promoter. Mutation of Ser480 to alanine eliminates DNA-binding activity and abolishes MAZ-mediated enhancement of c-myc promoter-driven luciferase expression in the presence of CKII. Site-specific mutagenesis, in vitro phosphorylation assay, EMSA, luciferase reporter assay Biochemical and biophysical research communications High 10448092
2000 FAC1 protein interacts with ZF87/MAZ, as identified by yeast two-hybrid and confirmed in vitro with recombinant proteins. The FAC1-MAZ interaction domain maps to the NLS/NES region of FAC1, while FAC1 recognizes a conformational interface including the proline/alanine-rich domain and first zinc finger of MAZ. Co-expression of FAC1 reduces ZF87/MAZ-induced transcriptional activation of an SV40 promoter in a dose-dependent manner. Yeast two-hybrid, recombinant protein pulldown, transient co-transfection/reporter assay, deletion mapping Biochemistry Medium 10727212
2000 G-quartet structures formed by the insulin-linked polymorphic region (ILPR) in the insulin gene promoter influence Pur-1/MAZ-dependent transcriptional activity; inter- and intramolecular G-quartet formation correlates with changes in insulin transcription activity associated with IDDM2 diabetes susceptibility. G-quartet formation assay, transient transfection/reporter assay with mutant ILPR sequences Proceedings of the National Academy of Sciences of the United States of America Medium 11070077
2001 MAZ and Sp1 both interact with the same GC-rich cis-elements in the human MAZ gene promoter. The DNA-binding activities of Sp1 and MAZ depend mainly on consecutive zinc fingers: third and fourth zinc fingers of MAZ (zinc fingers 2 and 3 of Sp1). MAZ autorepresses its own promoter, with histone deacetylases involved in MAZ autorepression, while Sp1-mediated repression involves DNA methyltransferase 1. EMSA, deletion and mutational analysis, transient transfection/reporter assay, zinc finger domain mapping The Journal of biological chemistry High 11259406 11395515
2002 SP1 and MAZ bind to a 27 bp GC-rich region in the NR1 (NMDA receptor subunit 1) gene promoter; mutations in the SP1 and MAZ binding sites impair binding of both proteins and decrease NR1 promoter activity during neuronal differentiation of P19 cells, indicating both factors mediate enhancement of NR1 promoter activity. EMSA, mutational analysis, transient transfection/reporter assay Brain research. Molecular brain research Medium 12425938
2003 MAZ and Sp1 competitively bind to overlapping sequences at -48 and -38 bp in the rat PNMT gene promoter; MAZ displaces Sp1 binding in a concentration-dependent manner, and their binding is mutually exclusive. Phosphorylation of both factors (shown by phosphatase treatment) is required for DNA binding. Despite higher affinity, MAZ is a less effective activator than Sp1, and MAZ preferentially increases intron-retaining mRNA. Gel mobility shift assay (EMSA) with in vitro translated proteins and nuclear extracts, phosphatase treatment, transient transfection/reporter assay, mutational analysis Molecular pharmacology High 14573768
2004 MAZ elements in the FGFR2 gene act as RNA polymerase II pause sites; insertion of a MAZ4 element at positions 5' of upstream silencing elements or between exon IIIb and downstream silencing elements decreases silencing of exon IIIb, while insertion 3' of downstream silencing elements has no effect. An RT-PCR elongation assay confirmed MAZ4 is a RNAPII pause site, and promoter identity alters the MAZ4 effect, linking MAZ-dependent RNAPII pausing to co-transcriptional alternative splicing decisions. Minigene transfection reporter assay, RT-PCR elongation assay, in vitro transcribed RNA transfection The Journal of biological chemistry High 15126509
2008 MAZ binds the muscle creatine kinase (MCK) promoter element MPEX in vitro and in vivo (ChIP), transactivates the MCK promoter, and occupies promoters of multiple muscle genes (Skeletal alpha-actin, Desmin, alpha-Myosin heavy chain, Six4) in skeletal and cardiac myocytes. MAZ DNA-binding activity and transcript levels are upregulated during skeletal myocyte differentiation. MAZ also binds sequences diverging from its canonical GA box (e.g., CTCCTCCC) in muscle promoters. ICAT-based quantitative proteomics, in vitro DNA binding, chromatin immunoprecipitation (ChIP), transient transfection/reporter assay Molecular and cellular biology High 18710939
2012 miR-125b targets MAZ mRNA and is downregulated in glioblastoma-associated endothelial cells and upon VEGF exposure, resulting in increased MAZ expression. MAZ in turn transcriptionally activates VEGF, creating a feed-forward loop. Inhibition of MAZ accumulation by miR-125b or MAZ-specific shRNAs attenuates primary human brain endothelial cell migration and tubule formation in vitro. shRNA knockdown, miRNA overexpression, migration assay, tubule formation assay, transcriptional reporter assay 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 the NHE G-quadruplex competitively inhibit MAZ binding, suppress KRAS expression in pancreatic cancer cells, inhibit proliferation and colony formation, activate apoptosis, and reduce tumor xenograft growth by 64% in mice. Transcriptional reporter assay, G-quadruplex competitive binding assay, cell viability assay, xenograft mouse model Nucleic acids research High 23471001
2014 MAZ binds to two neighboring G-quadruplex structures in the HRAS promoter and unfolds them; in the presence of complementary strands, MAZ-GST promotes rapid transformation of HRAS quadruplexes into duplexes. Mutational dissection shows that the two neighboring G-quadruplexes synergistically repress HRAS transcription, and MAZ binding (unfolding) activates HRAS expression. In vitro G-quadruplex binding and unfolding assay with MAZ-GST fusion, mutational analysis of G-elements, transcriptional reporter assay Nucleic acids research High 25013182
2014 MAZ protein is essential for HIF2α-mediated activation of the Cav1 (caveolin-1) promoter in intestinal epithelial cells; HIF2α activates the Cav1 promoter in a HIF response element-independent manner, and MAZ is required for this activation. Hypoxic induction of CAV1 via HIF2α/MAZ suppresses occludin expression, disrupting intestinal barrier integrity and contributing to hypoxia-induced inflammation. Mouse models with intestine-specific HIF1α/HIF2α overexpression, promoter/reporter assay, siRNA knockdown Molecular and cellular biology Medium 24891620
2016 Akt phosphorylates MAZ at Thr385, and this phosphorylation releases MAZ from the p53 promoter, leading to transcriptional activation of p53. MAZ functions as a transcriptional repressor of the p53 promoter. In vitro kinase assay, ChIP assay, reporter gene assay, site-directed mutagenesis Cancer letters Medium 26902421
2017 MAZ purified from nuclear extracts (as the Myb-sp factor) directly binds the E2F element in the MYB promoter and activates transcription through it. Various MAZ isoforms are present in Myb-sp and activate MYB transcription. Co-expression of MAZ not only reverts RB/p130-mediated repression via the E2F element but activates transcription, and MAZ knockdown inhibits MYB expression during exit from quiescence. Protein purification, EMSA, luciferase reporter assay, ChIP, siRNA knockdown Nucleic acids research High 28973440
2018 MAZ promotes pancreatic cancer cell invasiveness by increasing CRAF-ERK signaling (not by directly affecting K-Ras expression); this activation is mediated via PAK and AKT/PKB signaling cascades. The oncoprotein Cyr61/CCN1 regulates MAZ expression via Notch-1-sonic hedgehog signaling. siRNA knockdown, invasion/migration assay, western blot, western blot of signaling components The Journal of biological chemistry Medium 29414775
2018 MAZ knockdown in HEK293 cells results in differential expression of WNT morphogens Wnt11 and Wnt4, prevents efficient S phase transition, and abrogates growth of human embryonic kidney cells. In mice, homozygous CRISPR-Cas9 Maz deletion results in perinatal lethality with high penetrance of congenital anomalies of the kidney and urinary tract (CAKUTs), and Maz is haploinsufficient for normal bladder development. siRNA knockdown with transcriptome analysis, CRISPR-Cas9 mouse model, cell cycle assay Proceedings of the National Academy of Sciences of the United States of America High 29432158
2019 circ-CUX1 binds to EWSR1 to facilitate EWSR1 interaction with MAZ, resulting in transactivation of MAZ and transcriptional alteration of CUX1 and other genes associated with neuroblastoma progression. This circ-CUX1/EWSR1/MAZ axis promotes aerobic glycolysis in neuroblastoma. RNA pulldown, co-immunoprecipitation, luciferase reporter assay, inhibitory peptide and lentiviral knockdown EMBO molecular medicine Medium 31709724
2019 MAZ promotes bone metastasis of prostate cancer through transcriptional upregulation of KRas (and HRas) expression, with RalGEF signaling selectively mediating the pro-metastatic effect of KRas. ChIP and luciferase assays demonstrated MAZ binding to and activation of KRAS promoter. ChIP assay, luciferase reporter assay, transwell invasion assay, mouse intracardiac bone metastasis model Journal of experimental & clinical cancer research Medium 31488180
2020 Disruption of Maz in mice produces developmental eye defects, with significant upregulation of Wnt2b, Sfrp2, and Fzd4 in Maz-deficient eyes, along with downregulation of the Wnt reporter TCF-Lef1, indicating MAZ is required for activation of the Wnt/β-catenin pathway and ciliary margin patterning. Conditional mouse Maz knockout, gene expression analysis, Wnt reporter assay Disease models & mechanisms Medium 32571845
2021 MAZ, like CTCF, physically interacts with the cohesin subunit (Co-IP demonstrated) and can independently arrest cohesin sliding. MAZ also independently pauses the elongating form of RNA polymerase II and consequently affects RNA alternative splicing. CTCF/MAZ double sites are more effective at sequestering cohesin than CTCF-only sites. MAZ depletion disrupts local interactions within TADs and TAD boundaries, and MAZ binding between an enhancer and promoter results in down-regulation of reporter gene expression, supporting a role as an insulator protein. Co-immunoprecipitation, Hi-C, insulator reporter assay, siRNA depletion, RNAPII pausing assay, alternative splicing analysis Proceedings of the National Academy of Sciences of the United States of America High 33558242
2021 MAZ identified by DNA affinity purification/mass spectrometry as binding to the alpha-globin gene promoter in primary human erythroid cells. Genome-wide ChIP-seq showed MAZ occupies active promoters and GATA1-bound enhancers of key erythroid genes. MAZ knockdown reduces alpha-globin expression in K562 cells and impairs differentiation in primary human erythroid cells. DNA affinity purification, mass spectrometry, ChIP-seq, siRNA knockdown, erythroid differentiation assay Blood advances High 34351390
2022 MAZ colocalizes with CTCF at chromatin borders and interacts with the cohesin subunit RAD21 (biochemical assay). CRISPR KO screen and MAZ motif deletions lead to derepression of posterior Hox genes immediately after CTCF boundaries upon differentiation, causing homeotic transformations in mice, establishing MAZ as a cofactor in CTCF-mediated genomic insulation at Hox clusters. Genome-wide CRISPR knockout screen, biochemical Co-IP, MAZ motif deletion, Hi-C, CRISPR mouse model Nature genetics High 35145304
2024 G-quadruplexes in the CCND1 promoter recruit MAZ and propel motility in MAZ phase-separated condensates, activating CCND1 transcription. Zinc finger 2 of MAZ is responsible for G4 binding; ZF3-5 are critical for MAZ condensation. MAZ nuclear puncta overlap G4 signals and coactivators BRD4, MED1, CDK9, and active RNA polymerase II. MAZ mutants lacking either G4 binding or phase separation ability cannot form nuclear puncta and fail to promote hepatocellular carcinoma cell proliferation. Mutagenesis of MAZ zinc fingers, phase separation assay, co-localization (immunofluorescence), G4 binding assay, xenograft tumor model Nature communications High 38316778
2025 MAZ binds to the FTH1 promoter (confirmed by ChIP assay) to directly regulate FTH1 transcription. Long non-coding RNA TUG1 binds MAZ (confirmed by luciferase assay) and acts as a negative regulator of MAZ; downregulation of TUG1 upregulates MAZ, increasing FTH1 expression and attenuating ferroptosis in glioma cells treated with dihydroartemisinin. ChIP assay, dual-luciferase reporter assay, siRNA knockdown, ferroptosis assay Oxidative medicine and cellular longevity Medium 36164395
2025 MAZ binds to the MAZ promoter and interacts with HDAC1, RBBP7, and CUL4B as a transcriptional inhibitory complex. MAZ and HDAC1 cooperatively repress CSK gene expression; knockdown of either MAZ or HDAC1 activates CSK expression, subsequently inhibiting MAPK/ERK, STAT3, and PI3K/AKT signaling. MAZ recruits HDAC1 to catalyze histone deacetylation at the CSK promoter. Immunoaffinity purification with mass spectrometry, RNA-seq, ChIP assay, Co-IP, in vivo xenograft model Molecular carcinogenesis High 40618395
2026 Zip7 (a zinc transporter) mainly interacts with MAZ in the cytoplasm to facilitate MAZ nuclear import; nuclear MAZ is upregulated in metastatic prostate cancer and promotes MYBL2 transcription, driving prostate cancer bone metastasis. Co-immunoprecipitation, subcellular fractionation, RNA-seq, ChIP, in vivo intrarterial bone metastasis xenograft model Communications biology Medium 42010154

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 288 1502157
1996 The serotonin 1a receptor gene contains a TATA-less promoter that responds to MAZ and Sp1. The Journal of biological chemistry 200 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 103 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 99 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
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
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 81 25013182
2022 CRISPR and biochemical screens identify MAZ as a cofactor in CTCF-mediated insulation at Hox clusters. Nature genetics 68 35145304
2019 MAZ promotes prostate cancer bone metastasis through transcriptionally activating the KRas-dependent RalGEFs pathway. Journal of experimental & clinical cancer research : CR 63 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
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
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 60 33558242
1998 Genomic organization and expression of a human gene for Myc-associated zinc finger protein (MAZ). The Journal of biological chemistry 60 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 48 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
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
2024 G-quadruplexes promote the motility in MAZ phase-separated condensates to activate CCND1 expression and contribute to hepatocarcinogenesis. Nature communications 40 38316778
2017 Dual function of MAZ mediated by FOXF2 in basal-like breast cancer: Promotion of proliferation and suppression of progression. Cancer letters 39 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) 39 23609189
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
2007 MAZ drives tumor-specific expression of PPAR gamma 1 in breast cancer cells. Breast cancer research and treatment 38 17902047
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
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
2025 MAZ-mediated tumor progression and immune evasion in hormone receptor-positive breast cancer: Targeting tumor microenvironment and PCLAF+ subtype-specific therapy. Translational oncology 21 39805182
2024 MAZ promotes thyroid cancer progression by driving transcriptional reprogram and enhancing ERK1/2 activation. Cancer letters 21 39197582
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
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
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
2014 23S rRNA as an a-Maz-ing new bacterial toxin target. RNA biology 14 24525465
2003 The MAZ protein is an autoantigen of Hodgkin's disease and paraneoplastic cerebellar dysfunction. Annals of neurology 13 12509857
2024 Transcription Factor MAZ Potentiates the Upregulated NEIL3-mediated Aerobic Glycolysis, thereby Promoting Angiogenesis in Hepatocellular Carcinoma. Current cancer drug targets 12 38347781
2009 SAF-3, a novel splice variant of the SAF-1/MAZ/Pur-1 family, is expressed during inflammation. The FEBS journal 12 19583771
2024 MAZ promotes tumor proliferation and immune evasion in lung adenocarcinoma. Oncogene 11 39424990
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
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 6 40524155
2024 Calycosin inhibits the proliferation and metastasis of renal cell carcinoma through the MAZ/HAS2 signaling pathway. Phytotherapy research : PTR 6 39120474
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-mediated N6-methyladenosine modification of ZEB1 promotes hepatocellular carcinoma progression by regulating METTL3. Journal of translational medicine 4 40038747
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 4 40164245
2024 Molecular mechanisms of MAZ targeting up-regulation of NDUFS3 expression to promote malignant progression in melanoma. Communications biology 4 39532991
2023 PCGF6/MAX/KDM5D facilitates MAZ/CDK4 axis expression and pRCC progression by hypomethylation of the DNA promoter. Epigenetics & chromatin 4 36890610
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 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 Dihydroartemisinin alleviates diethylnitrosamine-induced hepatocarcinogenesis by targeting a novel MAZ/TRIM50 axis. International immunopharmacology 1 40288151
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 ANKRD22 Induced by Transcription Factor MAZ Promotes Proliferation and Invasion of Nasopharyngeal Carcinoma. Journal of biochemical and molecular toxicology 0 40346905
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