Affinage

MAX

Protein max · UniProt P61244

Length
160 aa
Mass
18.3 kDa
Annotated
2026-04-28
100 papers in source corpus 27 papers cited in narrative 27 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

MAX is a constitutively expressed, stable nuclear bHLH-leucine zipper transcription factor that serves as the obligate dimerization hub of the MYC-MAX-MAD/MXD network, controlling cell proliferation, apoptosis, and differentiation through competitive heterodimerization at CACGTG E-box elements (PMID:1730411, PMID:1406956, PMID:8425218). MAX homodimers and MAD/MXD/MNT-MAX heterodimers repress E-box target genes—partly through mSin3-HDAC corepressor recruitment—while MYC-MAX heterodimers activate the same targets; the switch between repressive and activating complexes is dynamically regulated during cell cycle entry and differentiation (PMID:8224841, PMID:15866886, PMID:9308234). MAX activity is further tuned by alternative splicing that generates isoforms with distinct DNA-binding and transformation properties, by Casein Kinase II phosphorylation of its disordered N-terminus that modulates DNA-binding kinetics and E-box specificity, and by direct sensing of cytosine modification state at E-box CpGs via Arg36 (PMID:1566084, PMID:9211884, PMID:36174765, PMID:27903915). Germline loss-of-function mutations in MAX cause hereditary pheochromocytoma, and somatic MAX inactivation drives gastrointestinal stromal tumors (GISTs) and blocks MYC-dependent lymphomagenesis, establishing MAX as a context-dependent tumor suppressor (PMID:21685915, PMID:28270683, PMID:31395740).

Mechanistic history

Synthesis pass · year-by-year structured walk · 12 steps
  1. 1992 High

    Identification of MAX as the obligate, constitutively expressed, nuclear dimerization partner of c-Myc resolved how Myc, which cannot homodimerize efficiently, accesses DNA: MAX provides the stable bHLH-LZ scaffold for CACGTG E-box recognition.

    Evidence Reciprocal co-IP, DNA-binding assays, pulse-chase, subcellular fractionation, cross-linking, NLS mapping, and deletion mutagenesis in mammalian cells and with recombinant proteins

    PMID:1730411 PMID:1730412

    Open questions at the time
    • No genome-wide target identification at this stage
    • Mechanism of MAX nuclear import beyond NLS identification not resolved
  2. 1992 High

    Demonstration that MAX homodimers repress while MYC-MAX heterodimers activate E-box reporters, and that an alternatively spliced delta-MAX isoform lacking the NLS and C-terminal region converts MAX from a transformation suppressor to a cooperating oncogene, established the competitive-dimerization model and revealed isoform-specific functional divergence.

    Evidence Transient transfection reporter assays with domain mutants; Myc-Ras cotransformation in rat embryo fibroblasts with delta-MAX and full-length MAX constructs

    PMID:1406956 PMID:1566084

    Open questions at the time
    • Relative abundance of MAX isoforms in vivo unknown
    • No structural basis for isoform-specific differences
  3. 1993 High

    Discovery of MAD and MXI1 as MAX-specific dimerization partners that repress E-box transcription completed the tripartite network model: MYC-MAX activates, MAD/MXI1-MAX represses, and the ratio of these complexes determines transcriptional output.

    Evidence Lambda gt11 library screens, yeast two-hybrid, EMSA, reporter assays; co-IP showing MAD-MAX replaces MYC-MAX during monocyte differentiation

    PMID:8224841 PMID:8425218 PMID:8425219

    Open questions at the time
    • Mechanism of MAD-mediated repression (corepressor identity) not yet identified
    • Genome-wide extent of complex switching unknown
  4. 1993 High

    Characterization of MAX long and short isoforms showed phosphorylation-dependent regulation of DNA binding is isoform-specific, with the 9-amino-acid N-terminal insertion acting as a regulatory element, and ODC was identified as a direct MYC-MAX transcriptional target.

    Evidence Recombinant protein EMSA with multiple E-box variants and phosphorylation conditions; ODC promoter-CAT assays with antisense Myc knockdown

    PMID:8262968 PMID:8430110

    Open questions at the time
    • Kinase responsible for isoform-specific phosphorylation effects not definitively assigned in vivo
    • Full target gene repertoire uncharacterized
  5. 1994 High

    Showing that MAX homodimers bind nucleosomal DNA while Myc homodimers cannot established that dimerization partner identity controls chromatin accessibility, providing a mechanistic basis for how the network operates on packaged DNA.

    Evidence In vitro nucleosome binding assays with reconstituted chromatin templates

    PMID:8196648

    Open questions at the time
    • In vivo chromatin access not tested
    • No information on histone modification context
  6. 1997 High

    MNT was identified as a MAX-interacting repressor that recruits mSin3 corepressors via a discrete SID domain, and MAX(L) but not MAX(S) was shown to repress transcription and modulate proliferation and apoptosis, adding mechanistic resolution to repressor-complex assembly and isoform function.

    Evidence Co-IP, reporter assays, Myc-Ras transformation, deletion mutagenesis of MNT SID; stable MAX(L)/MAX(S) overexpression in NIH3T3 with growth factor deprivation apoptosis assays

    PMID:9211884 PMID:9308234

    Open questions at the time
    • HDAC identity within the mSin3 complex recruited by MNT-MAX not specified
    • Structural basis for isoform-specific repression unknown
  7. 2005 High

    NMR and biophysical analyses of full-length MAX revealed that flanking disordered regions destabilize homodimerization (~7 µM KD) relative to the bHLH-LZ fragment, and ChIP/genetic epistasis showed MNT-MAX to MYC-MAX switching on shared promoters controls cell cycle entry.

    Evidence NMR, CD, sedimentation equilibrium, mutagenesis of MAX; ChIP plus conditional double-KO of MNT and c-Myc in MEFs with flow cytometry

    PMID:15866886 PMID:16171389

    Open questions at the time
    • No in vivo measurement of MAX monomer-dimer equilibrium
    • Signaling pathway triggering the complex switch not identified
  8. 2006 High

    Crystal structures of MAX homodimer, MYC-MAX, and MAD-MAX heterodimers provided the atomic-level framework for understanding DNA recognition, differential complex assembly, and Sin3-mediated repression.

    Evidence X-ray crystallography of multiple MAX-containing complexes

    PMID:16620027

    Open questions at the time
    • No structure of full-length MAX including disordered termini
    • No structure of MAX with post-translational modifications
  9. 2011 High

    Discovery that germline loss-of-function MAX mutations cause hereditary pheochromocytoma, with LOH and protein loss in tumors, established MAX as a bona fide tumor suppressor in neural-crest-derived tissues.

    Evidence Exome sequencing of pheochromocytoma families, IHC for MAX protein, LOH by uniparental disomy analysis, PC12 cell characterization

    PMID:21685915

    Open questions at the time
    • Mechanism by which MAX loss drives tumorigenesis in chromaffin cells not elucidated
    • Penetrance and genotype-phenotype correlations incomplete
  10. 2017 High

    Structural and biochemical work showed MAX discriminates cytosine modification states at E-box CpGs—preferring unmodified C and 5-carboxylcytosine via an Arg36-mediated triad—and somatic MAX inactivation in ~21% of GISTs was linked to p16 silencing, with rescue restoring p16 expression, extending the tumor-suppressor role to a new cancer type.

    Evidence Fluorescence polarization with modified oligonucleotides, X-ray crystallography of MAX:5caC-E-box, mutagenesis; GIST sequencing, IHC, MAX re-expression rescue of p16 and proliferation

    PMID:27903915 PMID:28270683

    Open questions at the time
    • In vivo relevance of 5caC sensing at endogenous loci not demonstrated
    • Mechanism linking MAX loss to p16 epigenetic silencing not resolved
  11. 2019 High

    Conditional B-cell-specific MAX deletion completely blocked Eµ-Myc lymphomagenesis and reduced MYC protein levels, revealing a MAX-dependent MYC autoregulatory loop in which MYC-MAX activates genes controlling MYC stability.

    Evidence Conditional Cre-Lox MAX deletion, RNA-seq, ChIP-seq, Western blot, pharmacological MYC-MAX inhibitors

    PMID:31395740

    Open questions at the time
    • Identity of specific MYC-stability regulators within the autoregulatory loop not fully resolved
    • Whether the autoregulatory loop operates in non-B-cell contexts unknown
  12. 2022 High

    NMR and kinetic analyses showed the disordered MAX N-terminus makes intramolecular electrostatic contacts with the MYC:MAX DNA-binding domain that accelerate DNA-binding kinetics and confer E-box specificity, with CK2 phosphorylation of two N-terminal serines further enhancing these effects, providing a mechanistic explanation for decades of phosphorylation observations.

    Evidence NMR spectroscopy, SPR kinetics, in vitro CK2 phosphorylation, DNA-binding assays

    PMID:36174765

    Open questions at the time
    • In vivo CK2-MAX phosphorylation dynamics not measured
    • Whether phosphorylation differentially affects MAX homodimer vs. MYC-MAX heterodimer kinetics in cells remains untested

Open questions

Synthesis pass · forward-looking unresolved questions
  • The structural basis for how full-length MAX (including disordered termini and post-translational modifications) assembles with different partners in a chromatin context, and the precise mechanism by which MAX loss drives tumorigenesis in specific tissues (pheochromocytoma, GIST) while being dispensable for some lymphocyte functions, remain unresolved.
  • No structure of full-length, phosphorylated MAX in complex on nucleosomal DNA
  • Tissue-specific determinants of MAX tumor-suppressor function unknown
  • Genome-wide, modification-state-aware map of MAX occupancy in vivo not available

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003677 DNA binding 8 GO:0140110 transcription regulator activity 7 GO:0098772 molecular function regulator activity 4
Localization
GO:0005634 nucleus 2
Pathway
R-HSA-74160 Gene expression (Transcription) 6 R-HSA-1643685 Disease 3 R-HSA-1640170 Cell Cycle 2 R-HSA-4839726 Chromatin organization 2 R-HSA-5357801 Programmed Cell Death 2
Partners
MAD1MAD4MLXMNTMXI1MYCSIN3A
Complex memberships
MAD-MAX heterodimerMAX homodimerMNT-MAX heterodimerMYC-MAX heterodimer

Evidence

Reading pass · 27 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1992 MAX (bHLH-Zip protein) heterodimerizes with c-Myc in vivo, forming a complex that binds CACGTG DNA sequences; MAX is a nuclear phosphoprotein phosphorylated by casein kinase II, is highly stable, and is constitutively expressed regardless of cell cycle status, while Myc is rapidly degraded during or after association with MAX. Co-immunoprecipitation with anti-Myc and anti-Max antibodies, DNA binding assays, subcellular fractionation, pulse-chase Genes & development High 1730411
1992 MAX overexpression represses transcription of a reporter gene containing CACGTG sites, requiring an intact DNA-binding domain; c-Myc overexpression activates the same reporter, requiring both the N-terminal transactivation and C-terminal dimerization domains; Myc-induced activation reverses Max-mediated repression. Transient transfection reporter assays in mammalian cells with deletion mutants Nature High 1406956
1992 MAX contains a nuclear localization signal (PQSRKKLR) in its carboxy-terminal region and lacks a transcriptional activation domain functional in mammalian cells; MAX interacts with c-Myc intracellularly in a manner dependent on the helix-loop-helix and leucine zipper motifs; MAX and c-Myc/MAX complexes bind DNA as dimers to a GGGCAC(G/A)TGCCC sequence. Fusion protein analysis in CHO cells, chemical and photo-cross-linking, bacterially produced recombinant proteins, deletion mutagenesis Genes & development High 1730412
1993 MAD heterodimerizes specifically with MAX in vitro to form a sequence-specific DNA binding complex at CACGTG sites with properties similar to MYC-MAX; both MYC-MAX and MAD-MAX heterocomplexes are favored over MAX homodimers; DNA binding activity of MAD-MAX heterodimers (unlike MAX homodimers) is unaffected by CKII phosphorylation; MAD-MAX and MYC-MAX have opposing transcriptional activities (MAD-MAX represses, MYC-MAX activates). Lambda gt11 library screen with radiolabeled MAX protein, in vitro binding, transient transfection reporter assays, EMSA Cell High 8425218
1993 MXI1 interacts specifically with MAX via bHLH-Zip motifs to form heterodimers that efficiently bind the Myc-Max consensus CACGTG recognition site; MXI1-MAX heterodimers do not stimulate transcription in yeast, consistent with a model where MXI1-MAX sequesters MAX from MYC-MAX complexes and competes for target sites. Yeast interaction trap (two-hybrid), DNA binding assays Cell High 8425219
1993 During monocyte-to-macrophage differentiation, MAX complexes switch from MYC-MAX to MAD-MAX; MAD is a nuclear phosphoprotein with very short half-life (15-30 min) detectable in complex with MAX in vivo; undifferentiated U937 cells contain MYC-MAX, whereas after TPA-induced differentiation only MAD-MAX complexes are detectable. Co-immunoprecipitation, Western blot, kinetics of differentiation with TPA Genes & development High 8224841
1992 An alternatively spliced form of MAX (delta MAX, truncated at the C-terminus) retains DNA binding in complex with c-Myc but lacks the nuclear localization signal and putative regulatory domain; delta MAX enhances Myc-Ras cotransformation whereas full-length MAX suppresses it, indicating MAX can encode both negative and positive regulators of c-Myc function. Myc-Ras cotransformation assay in rat embryo fibroblasts, transfection of delta MAX and full-length MAX constructs Science High 1566084
1993 The c-Myc-MAX protein complex binds to a CACGTG element in the human ornithine decarboxylase (ODC) promoter and transactivates ODC expression; antisense oligonucleotides against c-myc reduced complex formation and endogenous ODC mRNA, identifying ODC as a direct transcriptional target of MYC-MAX. EMSA, methylation interference, transient transfection of ODC promoter-CAT constructs, antisense oligonucleotides, antibody supershifts The Journal of biological chemistry High 8262968
1992 c-Myc and MAX homodimers bend DNA in opposite orientations at CACGTG sequences; c-Myc-MAX heterodimers cause a smaller bend in an orientation similar to MAX homodimers; no specific DNA unwinding is caused by either protein. Circular permutation assay and phasing analysis (gel mobility-shift), DNA unwinding assay Proceedings of the National Academy of Sciences of the United States of America Medium 1323849
1994 MAX homodimers can bind to nucleosomal DNA, while truncated c-Myc homodimers cannot; changing c-Myc's dimerization partner to MAX or modifying its dimerization interface enables nucleosomal DNA binding, demonstrating that dimerization partner identity influences access to chromatin. In vitro nucleosome binding assays with reconstituted chromatin templates, EMSA Molecular and cellular biology High 8196648
1996 Drosophila homologs dMyc and dMax heterodimerize, recognize the same CACGTG DNA sequence as vertebrate homologs, and activate transcription; dMyc is likely encoded by the diminutive (dm) gene, mutation of which causes small body size and female sterility. Cloning, heterodimerization assays, DNA-binding assays, genetic analysis of diminutive mutants Science High 8929412
1997 MAX(L) isoform is much more effective at homodimeric DNA binding than MAX(S); MAX(L) represses a c-Myc-responsive reporter gene while MAX(S) does not; MAX(L)-overexpressing cells grow more slowly, have higher growth factor requirements, and show accelerated apoptosis after growth factor deprivation, demonstrating isoform-specific roles in proliferation and apoptosis. In vitro DNA binding assays, reporter gene assays, stable overexpression in NIH3T3 cells, growth factor deprivation apoptosis assays The Journal of biological chemistry High 9211884
1997 MNT (a novel Max-interacting protein) interacts with MAX in vivo and represses transcription through E-box sites; repression maps to a 13-amino-acid SID domain that interacts with mSin3 corepressors; deleting this domain converts MNT from a repressor to an activator and from a Myc transformation suppressor to a cooperating oncogene. Co-immunoprecipitation, reporter gene assays, Myc-Ras transformation assays, deletion mutagenesis Current topics in microbiology and immunology High 9308234
1997 MAX dimerization and DNA binding promote alpha-helix formation; at low protein concentration MAX exists as a monomer with low helical content, at high concentration it forms dimers with increased helical content, and addition of CACGTG-containing DNA further increases helical content. Circular dichroism (CD) spectroscopy, sedimentation equilibrium experiments Journal of biochemistry Medium 9399572
1993 The two MAX protein isoforms (long and short, differing by a 9-amino-acid N-terminal insertion) display distinct DNA-binding preferences across multiple Myc-related E-box sequences; phosphorylation strongly affects DNA binding by MAX(long) but not MAX(short), identifying the 9-amino-acid segment as a regulatory element. Recombinant protein production, EMSA with multiple oligonucleotide sequences, phosphorylation in reticulocyte lysate Proceedings of the National Academy of Sciences of the United States of America Medium 8430110
1999 MLX (Max-like protein X) forms heterodimers with MAD1 and MAD4 (but not with other MAD family members or MYC) that bind CACGTG DNA; MLX-MAD1 heterodimers repress transcription via recruitment of the mSin3A-HDAC corepressor complex, dependent on dimerization and DNA binding. Yeast two-hybrid, co-immunoprecipitation, DNA binding assays, reporter gene assays The Journal of biological chemistry High 10593926
1999 Adrenomedullin and CGRP induce MAX expression in rat endothelial cells; MAX overexpression rescues serum-deprivation-induced apoptosis; antisense knockdown of MAX mRNA abolishes adrenomedullin's anti-apoptotic effect, identifying MAX upregulation as a mechanism for adrenomedullin-mediated endothelial cell survival. Transfection of Max expression plasmid, antisense oligodeoxynucleotides, real-time PCR, reporter assay, apoptosis assay Molecular endocrinology Medium 10446908
2005 NMR and thermodynamic analysis of full-length p21 MAX shows its N-terminal and C-terminal regions are unstructured in the absence of DNA; the p21 MAX KD for homodimerization is ~7×10⁻⁶ M (37°C), 10-100-fold weaker than the bHLH-LZ fragment alone due to electrostatic repulsions from flanking disordered regions; a double mutant stabilizes the dimer to KD ~3×10⁻¹⁰ M. NMR spectroscopy, circular dichroism, sedimentation equilibrium, thermodynamic measurements Biochemistry High 16171389
2005 During cell cycle entry, c-Myc induction causes a transient decrease in MNT-MAX complexes and a switch in the ratio of MNT-MAX to c-Myc-MAX on shared target gene promoters; MNT overexpression suppresses cell cycle entry; Cre-Lox deletion of both MNT and c-Myc in MEFs rescues the cell cycle and proliferative block caused by c-Myc ablation alone, establishing MNT-MAX to MYC-MAX switching as a mechanism regulating cell cycle entry. Co-immunoprecipitation, ChIP, conditional knockout MEFs, flow cytometry The Journal of cell biology High 15866886
2006 Crystal structures of MAX homodimer and MYC-MAX and MAD-MAX heterodimers reveal molecular basis for complex assembly, DNA recognition, and transcriptional regulation; structural determinants of Mad-mediated Sin3 repression pathway recruitment are illuminated. X-ray crystallography Current topics in microbiology and immunology High 16620027
2011 Germline loss-of-function mutations in MAX cause hereditary pheochromocytoma; absence of MAX protein in tumors and loss of heterozygosity by uniparental disomy support a tumor suppressor role; the lack of functional MAX in PC12 cells suggests MAX loss promotes neural crest tumor development. Exome sequencing, loss of heterozygosity analysis, immunohistochemistry for MAX protein, functional analysis of PC12 cells Nature genetics High 21685915
2017 MAX exhibits the greatest DNA-binding affinity for E-box elements containing unmodified cytosine or 5-carboxylcytosine (5caC), and greatly reduced affinity for 5mC, 5hmC, or 5fC forms; crystal structure of MAX with 5caC-modified E-box reveals recognition via a 5caC-Arg36-Guanine triad; mutations of Arg35, Arg36, and Arg60 (found in multiple myeloma patients) abolish or reduce DNA binding. Fluorescence polarization binding assays, X-ray crystallography, mutagenesis, in vitro binding with modified E-box oligonucleotides Nucleic acids research High 27903915
2017 MAX inactivation (hemizygous or homozygous mutations) occurs in ~21% of GISTs and is associated with p16 silencing (without p16 coding sequence deletion); re-introduction of MAX restores p16 expression and inhibits GIST cell proliferation, placing MAX upstream of p16 in a tumor-suppressive pathway. Sequencing, MAX protein loss confirmed by IHC, MAX re-expression in cell lines with proliferation and p16 expression assays Nature communications High 28270683
2019 B-cell-specific deletion of MAX completely abrogates Eµ-Myc-driven lymphomagenesis; MAX loss leads to a significant reduction in MYC protein levels and down-regulation of MYC direct transcriptional targets including regulators of MYC stability; MAX-MYC dimerization inhibitors also reduce MYC protein levels, uncovering a MAX-dependent MYC autoregulatory mechanism. Conditional Cre-Lox B-cell-specific MAX deletion, RNA-seq, ChIP-seq, Western blot, pharmacological MYC-MAX inhibitors Genes & development High 31395740
2018 In B lymphocytes, c-Myc requires MAX for its full function; B lymphocytes lacking MAX show impaired responses and upregulation of B-cell receptor signaling pathways; some key processes such as initial cell differentiation and DNA replication can proceed without c-Myc/MAX heterodimers, revealing context-dependent dispensability. In vivo and ex vivo conditional deletion models, flow cytometry, proliferation assays EMBO reports Medium 30126925
2019 LncEGFL7OS interacts with MAX protein in endothelial cells; MAX regulates histone acetylation at the EGFL7/miR-126 promoter/enhancer; lncEGFL7OS silencing impairs angiogenesis and reduces EGFL7/miR-126 expression, while overexpression has the opposite effect. RNA pulldown/co-IP identifying MAX as lncRNA-binding protein, ChIP for histone acetylation, in vitro/in vivo angiogenesis assays, siRNA knockdown and overexpression eLife Medium 30741632
2022 The disordered MAX N-terminus binds the MYC:MAX DNA-binding domain via electrostatic interactions competitive with DNA binding; this intramolecular interaction accelerates DNA binding kinetics and provides E-box specificity; Casein Kinase 2-mediated phosphorylation of two serine residues in the MAX N-terminus further enhances these effects. NMR spectroscopy, Surface Plasmon Resonance (SPR), in vitro CK2 phosphorylation assays, DNA binding kinetics Journal of molecular biology High 36174765

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2005 Feature selection based on mutual information: criteria of max-dependency, max-relevance, and min-redundancy. IEEE transactions on pattern analysis and machine intelligence 2590 16119262
1993 Mxi1, a protein that specifically interacts with Max to bind Myc-Max recognition sites. Cell 747 8425219
1993 Mad: a heterodimeric partner for Max that antagonizes Myc transcriptional activity. Cell 690 8425218
2010 RNA-Seq Atlas of Glycine max: a guide to the soybean transcriptome. BMC plant biology 486 20687943
1992 Myc and Max proteins possess distinct transcriptional activities. Nature 471 1406956
2011 Exome sequencing identifies MAX mutations as a cause of hereditary pheochromocytoma. Nature genetics 413 21685915
1992 Myc and Max associate in vivo. Genes & development 412 1730411
2006 The Arabidopsis MAX pathway controls shoot branching by regulating auxin transport. Current biology : CB 335 16546078
1993 A switch from Myc:Max to Mad:Max heterocomplexes accompanies monocyte/macrophage differentiation. Genes & development 289 8224841
1992 Max: functional domains and interaction with c-Myc. Genes & development 281 1730412
2012 MAX mutations cause hereditary and sporadic pheochromocytoma and paraganglioma. Clinical cancer research : an official journal of the American Association for Cancer Research 257 22452945
2010 Evidence of the differential biotransformation and genotoxicity of ZnO and CeO2 nanoparticles on soybean (Glycine max) plants. Environmental science & technology 253 20384348
2016 Biology of VO2 max: looking under the physiology lamp. Acta physiologica (Oxford, England) 226 27888580
2014 Soybean (Glycine max) expansin gene superfamily origins: segmental and tandem duplication events followed by divergent selection among subfamilies. BMC plant biology 195 24720629
2007 Improved low molecular weight Myc-Max inhibitors. Molecular cancer therapeutics 183 17876039
2015 Soybean (Glycine max) SWEET gene family: insights through comparative genomics, transcriptome profiling and whole genome re-sequence analysis. BMC genomics 168 26162601
1996 Myc and Max homologs in Drosophila. Science (New York, N.Y.) 157 8929412
1992 Alternative forms of Max as enhancers or suppressors of Myc-ras cotransformation. Science (New York, N.Y.) 141 1566084
1992 Myc and Max function as a nucleoprotein complex. Current opinion in genetics & development 119 1638116
1993 Regulation of human ornithine decarboxylase expression by the c-Myc.Max protein complex. The Journal of biological chemistry 112 8262968
2009 A second function of gamma frequency oscillations: an E%-max winner-take-all mechanism selects which cells fire. The Journal of neuroscience : the official journal of the Society for Neuroscience 105 19515917
2013 The use and misuse of V(c,max) in Earth System Models. Photosynthesis research 101 23564478
2014 Functional interactions among members of the MAX and MLX transcriptional network during oncogenesis. Biochimica et biophysica acta 93 24857747
1999 Mlx, a novel Max-like BHLHZip protein that interacts with the Max network of transcription factors. The Journal of biological chemistry 88 10593926
1999 Induction of max by adrenomedullin and calcitonin gene-related peptide antagonizes endothelial apoptosis. Molecular endocrinology (Baltimore, Md.) 87 10446908
2007 The glycine max xylem sap and apoplast proteome. Journal of proteome research 71 17696379
2017 MAX is an epigenetic sensor of 5-carboxylcytosine and is altered in multiple myeloma. Nucleic acids research 69 27903915
1993 Differential patterns of DNA binding by myc and max proteins. Proceedings of the National Academy of Sciences of the United States of America 69 8430110
2005 Mnt-Max to Myc-Max complex switching regulates cell cycle entry. The Journal of cell biology 68 15866886
2019 Multiple GmWRI1s are redundantly involved in seed filling and nodulation by regulating plastidic glycolysis, lipid biosynthesis and hormone signalling in soybean (Glycine max). Plant biotechnology journal 61 31161718
2006 Identification and characterization of a novel heat shock transcription factor gene, GmHsfA1, in soybeans (Glycine max). Journal of plant research 60 16570125
1995 Carboxypeptidase M is identical to the MAX.1 antigen and its expression is associated with monocyte to macrophage differentiation. The Journal of biological chemistry 60 7797563
2020 Genome-wide identification and characterization of GRAS genes in soybean (Glycine max). BMC plant biology 56 32891114
2017 Soybean (Glycine max) WRINKLED1 transcription factor, GmWRI1a, positively regulates seed oil accumulation. Molecular genetics and genomics : MGG 56 29138932
1998 Regulation of GmNRT2 expression and nitrate transport activity in roots of soybean (Glycine max). Planta 56 9715532
2020 Soybean (Glycine max) Haplotype Map (GmHapMap): a universal resource for soybean translational and functional genomics. Plant biotechnology journal 55 32794321
2006 Determination of amino acid composition of soybeans (Glycine max) by near-infrared spectroscopy. Journal of agricultural and food chemistry 54 19127714
1992 Opposite orientations of DNA bending by c-Myc and Max. Proceedings of the National Academy of Sciences of the United States of America 54 1323849
2011 Premetazoan ancestry of the Myc-Max network. Molecular biology and evolution 53 21571926
2019 The Ethylene Signaling Pathway Negatively Impacts CBF/DREB-Regulated Cold Response in Soybean (Glycine max). Frontiers in plant science 51 30853961
1994 Differential binding of c-Myc and Max to nucleosomal DNA. Molecular and cellular biology 50 8196648
2019 Max deletion destabilizes MYC protein and abrogates Eµ-Myc lymphomagenesis. Genes & development 49 31395740
2013 Metabolic and Transcriptional Reprogramming in Developing Soybean (Glycine max) Embryos. Metabolites 48 24957996
2017 MAX inactivation is an early event in GIST development that regulates p16 and cell proliferation. Nature communications 47 28270683
1997 Distinct roles for MAX protein isoforms in proliferation and apoptosis. The Journal of biological chemistry 47 9211884
1995 The mycN/max protein complex in neuroblastoma. Short review. European journal of cancer (Oxford, England : 1990) 47 7576956
2013 Coordination of nutrient availability and utilization by MAX- and MLX-centered transcription networks. Cold Spring Harbor perspectives in medicine 45 24003245
2011 Protein and metabolite composition of xylem sap from field-grown soybeans (Glycine max). Planta 45 21246215
2017 Isoflavone Malonyltransferases GmIMaT1 and GmIMaT3 Differently Modify Isoflavone Glucosides in Soybean (Glycine max) under Various Stresses. Frontiers in plant science 43 28559900
2021 A combinatorial action of GmMYB176 and GmbZIP5 controls isoflavonoid biosynthesis in soybean (Glycine max). Communications biology 42 33742087
2023 Polystyrene micro and nanoplastics attenuated the bioavailability and toxic effects of Perfluorooctane sulfonate (PFOS) on soybean (Glycine max) sprouts. Journal of hazardous materials 40 36860033
2021 Dissecting the transcriptional regulation of proanthocyanidin and anthocyanin biosynthesis in soybean (Glycine max). Plant biotechnology journal 39 33539645
2021 Genome-wide characterization and analysis of the CCT motif family genes in soybean (Glycine max). Planta 37 33392793
2014 Expression of root-related transcription factors associated with flooding tolerance of soybean (Glycine max). International journal of molecular sciences 36 25268626
2011 Combined analysis of transcriptome and metabolite data reveals extensive differences between black and brown nearly-isogenic soybean (Glycine max) seed coats enabling the identification of pigment isogenes. BMC genomics 36 21801362
2017 Strigolactones promote rhizobia interaction and increase nodulation in soybean (Glycine max). Microbial pathogenesis 34 29191709
2015 Distribution and evolution of the lectin family in soybean (Glycine max). Molecules (Basel, Switzerland) 34 25679048
2020 Crop Management Impacts the Soybean (Glycine max) Microbiome. Frontiers in microbiology 33 32582080
2023 Physiological and transcriptome analysis of response of soybean (Glycine max) to cadmium stress under elevated CO2 concentration. Journal of hazardous materials 32 36860078
2008 Hypocotyl-based Agrobacterium-mediated transformation of soybean (Glycine max) and application for RNA interference. Plant cell reports 32 18347801
1997 Mnt: a novel Max-interacting protein and Myc antagonist. Current topics in microbiology and immunology 32 9308234
1992 Transcriptional activities of the Myc and Max proteins in mammalian cells. Current topics in microbiology and immunology 32 1490382
2011 Evolution of the Max and Mlx networks in animals. Genome biology and evolution 31 21859806
2009 Myc's secret life without Max. Cell cycle (Georgetown, Tex.) 31 19887915
1993 Expression of the soybean (Glycine max) glutamate 1-semialdehyde aminotransferase gene in symbiotic root nodules. Plant physiology 31 8278535
2012 Effect of tannic acid on properties of soybean (Glycine max) seed ferritin: a model for interaction between naturally-occurring components in foodstuffs. Food chemistry 30 25683413
2006 The potential allergenicity of two 2S albumins from soybean (Glycine max): a protein microarray approach. International archives of allergy and immunology 30 16837790
2008 Enzyme-assisted aqueous extraction of oleosomes from soybeans (Glycine max). Journal of agricultural and food chemistry 29 18251501
2006 Structural aspects of interactions within the Myc/Max/Mad network. Current topics in microbiology and immunology 28 16620027
2022 Time-series transcriptome comparison reveals the gene regulation network under salt stress in soybean (Glycine max) roots. BMC plant biology 27 35361109
2019 Highly multiplexed AmpliSeq technology identifies novel variation of flowering time-related genes in soybean (Glycine max). DNA research : an international journal for rapid publication of reports on genes and genomes 27 31231761
2020 Progresses, Challenges, and Prospects of Genome Editing in Soybean (Glycine max). Frontiers in plant science 26 33193504
2002 Soybean (Glycine max) cell wall composition and availability to feed enzymes. Journal of agricultural and food chemistry 25 11902936
1999 Analysis of the Max-binding protein MNT in human medulloblastomas. International journal of cancer 25 10446446
2018 Recovery of Antimicrobials and Bioaccessible Isoflavones and Phenolics from Soybean (Glycine max) Meal by Aqueous Extraction. Molecules (Basel, Switzerland) 24 30587803
2004 The expression and processing of two recombinant 2S albumins from soybean (Glycine max) in the yeast Pichia pastoris. Biochimica et biophysica acta 24 15134653
2022 Soil and foliar exposure of soybean (Glycine max) to Cu: Nanoparticle coating-dependent plant responses. NanoImpact 23 35588596
2019 Effects of Different Oligochitosans on Isoflavone Metabolites, Antioxidant Activity, and Isoflavone Biosynthetic Genes in Soybean ( Glycine max) Seeds during Germination. Journal of agricultural and food chemistry 23 30933513
2018 RNA sequencing analysis of salt tolerance in soybean (Glycine max). Genomics 23 29626511
2016 Genetic background and environmental conditions drive metabolic variation in wild type and transgenic soybean (Glycine max) seeds. Plant, cell & environment 22 27038216
1997 Dimerization and DNA binding facilitate alpha-helix formation of Max in solution. Journal of biochemistry 22 9399572
2023 Functional characterization of Cinnamate 4-hydroxylase gene family in soybean (Glycine max). PloS one 21 37186600
2022 The Disordered MAX N-terminus Modulates DNA Binding of the Transcription Factor MYC:MAX. Journal of molecular biology 21 36174765
2011 Proteomic analysis of high protein soybean (Glycine max) accessions demonstrates the contribution of novel glycinin subunits. Journal of agricultural and food chemistry 21 21344854
2022 Fe-Based Nanomaterial-Induced Root Nodulation Is Modulated by Flavonoids to Improve Soybean (Glycine max) Growth and Quality. ACS nano 20 36479882
2020 Functional characterization of soybean (Glycine max) DIRIGENT genes reveals an important role of GmDIR27 in the regulation of pod dehiscence. Genomics 20 33144217
2019 LncEGFL7OS regulates human angiogenesis by interacting with MAX at the EGFL7/miR-126 locus. eLife 20 30741632
2016 Comprehensive Analysis of the Soybean (Glycine max) GmLAX Auxin Transporter Gene Family. Frontiers in plant science 20 27014306
2016 A Global Analysis of the Polygalacturonase Gene Family in Soybean (Glycine max). PloS one 19 27657691
2013 Changes in RNA Splicing in Developing Soybean (Glycine max) Embryos. Biology 19 24833227
2005 Structural and thermodynamical characterization of the complete p21 gene product of Max. Biochemistry 19 16171389
1998 Distinct apoptotic responses imparted by c-myc and max. Blood 19 9680370
2022 GmEIL4 enhances soybean (Glycine max) phosphorus efficiency by improving root system development. Plant, cell & environment 18 36419232
2018 Functional interplay between c-Myc and Max in B lymphocyte differentiation. EMBO reports 18 30126925
2018 Deciphering V̇O: limits of the genetic approach. The Journal of experimental biology 17 30381476
2019 Transcriptional landscape of soybean (Glycine max) embryonic axes during germination in the presence of paclobutrazol, a gibberellin biosynthesis inhibitor. Scientific reports 16 31270425
2018 Genomic, molecular evolution, and expression analysis of NOX genes in soybean (Glycine max). Genomics 16 29621573
2012 Pseudomonas fluorescens N21.4 metabolites enhance secondary metabolism isoflavones in soybean (Glycine max) calli cultures. Journal of agricultural and food chemistry 16 23039196
2010 Effect of drying on nutritional and functional quality and electrophoretic pattern of soyflour from sprouted soybean (Glycine max). Journal of food science and technology 15 23572675
2005 Evaluation of nonstarch polysaccharides and oligosaccharide content of different soybean varieties (Glycine max) by near-infrared spectroscopy and proteomics. Journal of agricultural and food chemistry 15 16277410