Affinage

GMEB1

Glucocorticoid modulatory element-binding protein 1 · UniProt Q9Y692

Length
573 aa
Mass
62.6 kDa
Annotated
2026-06-10
29 papers in source corpus 22 papers cited in narrative 22 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

GMEB1 is a dual-function regulator that operates both as a sequence-specific DNA-binding transcriptional modulator and as a cytoplasmic anti-apoptotic factor. It was first defined biochemically as a subunit of a ~550 kDa heteromeric complex with GMEB2 that binds the glucocorticoid modulatory element (GME) and reshapes glucocorticoid receptor transactivation—shifting the agonist dose-response curve and the partial agonist activity of antisteroids (PMID:7665613, PMID:10894151). Sequence-specific DNA recognition is mediated by its SAND domain, whose 1.55 Å crystal structure positions the conserved KDWK motif on an exposed α-helix for DNA contact and contains a zinc-binding motif that sets the domain's C-terminal conformation without being required for binding (PMID:12702733). GMEB1 carries intrinsic transactivation activity through a domain separable from its GR-modulation domain, and it modulates GR not by directly altering GR–GRE binding but through parallel cofactor recruitment, engaging CBP and the SUMO-conjugating enzyme Ubc9 (PMID:10894151, PMID:11934901, PMID:11812797). As a transcription factor in its own right, GMEB1 controls midbrain dopamine neuron identity by driving tyrosine hydroxylase and dopamine transporter expression, with knockdown producing motor deficits (PMID:31175277), and it directs context-specific gene programs through partners such as FOXL2 and promoters including YAP1 (PMID:22544055, PMID:37389116). In the cytoplasm, GMEB1 is an endogenous inhibitor of initiator caspase activation: it binds the prodomains of procaspase-2, -8, and -9 to block their oligomerization-dependent activation, protecting cells against diverse stress stimuli and limiting ischemic brain injury in vivo (PMID:15555560, PMID:16497673, PMID:18455874). It additionally suppresses death-receptor signaling by bridging the deubiquitinase USP40 to CFLARL, stabilizing CFLARL and inhibiting DISC formation upon TRAIL stimulation (PMID:31046799). GMEB1 abundance and activity are tuned by ubiquitin-dependent turnover via the E3 ligase MIB2, which suppresses GMEB1-dependent HSP27 phosphorylation (PMID:34751796).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 1995 High

    Established the existence and biochemical identity of GME-binding activity, defining GMEB1/GMEB2 as a novel heteromeric complex distinct from known CRE-binding factors that modulates glucocorticoid receptor behavior.

    Evidence Partial protein purification, gel shift, size exclusion chromatography and peptide sequencing from cell cytosol

    PMID:7665613

    Open questions at the time
    • Component proteins not yet cloned
    • Molecular mechanism of GR modulation undefined
  2. 1998 High

    Cloning of GMEB2 and demonstration of cooperative GME binding with GMEB1 placed both proteins in a new KDWK-family and reconstituted the heteromeric DNA-binding complex.

    Evidence cDNA cloning, in vitro translation, gel shift with co-incubation

    PMID:9651376

    Open questions at the time
    • Structural basis of cooperativity unknown
    • In vivo functional consequence not addressed
  3. 1999 High

    Cloning of human GMEB1 and identification of HSP27 as a partner provided the human reagent and an early protein interaction beyond the GMEB2 complex.

    Evidence Yeast two-hybrid (HSP27 bait), cloning, EMSA/supershift, co-IP

    PMID:10386584

    Open questions at the time
    • Functional role of HSP27 interaction not established
    • Subcellular partitioning not resolved
  4. 2000 High

    Defined how GMEB1 modulates GR transactivation—via intrinsic transactivation activity, direct GR and CBP interactions, and a dose-response shift—rather than altering GR-GRE occupancy.

    Evidence Mammalian one/two-hybrid, GST pull-down, reporter assays, HAT assays; positional GME reporter mutants

    PMID:10692587 PMID:10854715 PMID:10894151

    Open questions at the time
    • Cofactor recruitment mechanism not yet molecular
    • Endogenous target genes beyond TAT reporter unknown
  5. 2002 High

    Structure-function mapping separated GMEB1 activities into distinct domains and identified Ubc9 as a functional cofactor, providing a mechanistic basis for independent control of EC50 versus total GR-induced expression.

    Evidence Deletion mutagenesis with two-hybrid/DNA-binding/reporter readouts; co-IP and SUMO-transfer-dead Ubc9 mutants; in vitro MURF-1 binding

    PMID:11812797 PMID:11927605 PMID:11934901

    Open questions at the time
    • Functional relevance of MURF-1 interaction untested
    • How Ubc9 local concentration alters transcription not directly shown
  6. 2003 High

    The SAND domain crystal structure resolved the DNA-recognition surface (KDWK motif) and a zinc-binding motif, establishing the atomic basis of sequence-specific DNA binding.

    Evidence X-ray crystallography (1.55 Å), NMR, site-directed mutagenesis, DNA binding assays

    PMID:12702733

    Open questions at the time
    • Structure of full-length complex on DNA absent
    • Role of zinc conformation in vivo not defined
  7. 2006 High

    Extended GMEB1's anti-apoptotic role from procaspase-2 to procaspase-8 and -9 and demonstrated physiological protection in vivo, revealing a cytoplasmic function distinct from its transcriptional role.

    Evidence Co-IP, in vitro prodomain binding, caspase activation assays, siRNA, neurospecific transgenic mice with focal ischemia

    PMID:15555560 PMID:16497673

    Open questions at the time
    • Determinants of cytoplasmic versus nuclear localization unknown
    • Stoichiometry of caspase prodomain blockade unresolved
  8. 2008 Medium

    Confirmed GMEB1 inhibits initiator caspase activation across hypoxic and oxidative stress, generalizing its cytoprotective mechanism.

    Evidence Caspase activation and viability assays under hypoxia and oxidative stress in neuroblastoma cells

    PMID:18455874

    Open questions at the time
    • Single cell-line context
    • Upstream regulators of GMEB1 under stress not identified here
  9. 2011 Medium

    Placed GMEB1 downstream of IL-12/PI3K/Akt signaling as the effector mediating anti-apoptotic protection against glucocorticoid-induced T-cell death.

    Evidence siRNA knockdown, apoptosis flow cytometry, qPCR, PI3K inhibition

    PMID:21840619

    Open questions at the time
    • Direct biochemical link to PI3K/Akt not shown
    • Whether transcriptional or caspase-binding function mediates the effect unclear
  10. 2012 Medium

    Identified FOXL2 as a transcriptional partner and showed GMEB1 acts mainly as a repressor but enhances activity of an oncogenic FOXL2 variant, broadening its transcriptional partnerships.

    Evidence Yeast two-hybrid, co-IP, immunofluorescence (aggregate sequestration), luciferase reporters

    PMID:22544055

    Open questions at the time
    • Endogenous co-regulated genes not mapped
    • Mechanism of promoter-specific switch from repression to activation unknown
  11. 2019 High

    Defined a death-receptor-specific anti-apoptotic mechanism (USP40-mediated CFLARL stabilization via GMEB1 bridging) and established GMEB1 as a master transcriptional regulator of dopaminergic neuron identity.

    Evidence Co-IP/pull-down, ubiquitination assays, shRNA, xenograft; nuclear capture RNA-seq/DNase-seq with in vivo AAV knockdown and behavioral readout

    PMID:31046799 PMID:31175277

    Open questions at the time
    • Direct DNA-binding sites at Th/Dat loci not structurally defined
    • Cross-talk between transcriptional and DISC-inhibitory functions unexplored
  12. 2020 Medium

    Identified TRAF3 as a partner that potentiates GMEB1's anti-apoptotic function, adding a regulatory input to caspase-inhibitory activity.

    Evidence Yeast two-hybrid, co-IP with domain mapping, siRNA, apoptosis assays

    PMID:32514408

    Open questions at the time
    • Domain on GMEB1 mediating TRAF3 binding not mapped
    • Mechanism by which TRAF3 enhances protection unclear
  13. 2021 Medium

    Revealed ubiquitin-dependent control of GMEB1 levels through MIB2, linking GMEB1 turnover to suppression of HSP27 phosphorylation.

    Evidence RNA pull-down, co-IP, Western blot for stability/ubiquitination, gain/loss of function

    PMID:34751796

    Open questions at the time
    • Ubiquitination sites on GMEB1 not mapped
    • How GMEB1 drives HSP27 phosphorylation mechanistically unknown
  14. 2023 Medium

    Showed GMEB1 directly activates YAP1 transcription in hepatocellular carcinoma, extending its DNA-binding transcriptional role to a cancer-relevant target.

    Evidence ChIP-qPCR, dual-luciferase reporter, qRT-PCR, gain/loss of function

    PMID:37389116

    Open questions at the time
    • Binding motif at YAP1 promoter not defined
    • Whether GMEB2/cofactors participate not addressed

Open questions

Synthesis pass · forward-looking unresolved questions
  • How GMEB1's nuclear transcriptional functions and cytoplasmic caspase/DISC-inhibitory functions are partitioned, coordinated, and switched within a cell remains unresolved.
  • No determinant of nucleo-cytoplasmic localization identified
  • No unified model linking transcriptional and anti-apoptotic roles
  • Genome-wide direct targets largely undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0003677 DNA binding 4 GO:0098772 molecular function regulator activity 4 GO:0140110 transcription regulator activity 4 GO:0060090 molecular adaptor activity 1
Localization
GO:0005634 nucleus 3 GO:0005829 cytosol 3
Pathway
R-HSA-5357801 Programmed Cell Death 3 R-HSA-74160 Gene expression (Transcription) 3 GO:0140110 transcription regulator activity 2 R-HSA-162582 Signal Transduction 2
Complex memberships
GMEB1-GMEB2 GME-binding complex

Evidence

Reading pass · 22 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1995 GMEB1 (88 kDa) and GMEB2 (67 kDa) were partially purified and characterized as two novel proteins that bind the glucocorticoid modulatory element (GME/CRE) as a heteromeric macromolecular complex of ~550 kDa (dissociable by deoxycholate), distinct from CREB/CREM/ATF family members, and capable of modulating glucocorticoid receptor transactivation properties (EC50 shift and partial agonist activity of antagonists). Partial protein purification, gel shift assays, size exclusion chromatography, molecular weight determination, partial peptide sequencing The Journal of biological chemistry High 7665613
1998 GMEB2 (67 kDa, cloned by PCR/RACE) binds GME DNA in gel shift assays; its binding to GME DNA increases markedly when mixed with authentic GMEB-1, forming a heteromeric complex similar to that from HTC cell cytosol. GMEB2 shares the KDWKR domain with Drosophila DEAF-1, rat Suppressin, and C. elegans ORFs, defining a novel protein family. cDNA cloning, in vitro transcription/translation, gel shift assay, co-incubation with GMEB-1 The Journal of biological chemistry High 9651376
1999 Human GMEB1 (hGMEB1, 573 aa, 85 kDa) was cloned using HSP27 as bait in a yeast two-hybrid screen. In vitro translated hGMEB1 bound specifically to GME oligonucleotides, forming a complex of similar size to that from rat liver nuclear extracts (confirmed by supershift with anti-hGMEB1 antibody). Co-immunoprecipitation confirmed the in vivo interaction of HSP27 with hGMEB1. Yeast two-hybrid screening, cDNA cloning, in vitro translation, EMSA/gel shift with supershift, co-immunoprecipitation FEBS letters High 10386584
2000 GMEB-1 interacts with glucocorticoid receptor (GR) as shown by mammalian two-hybrid and pull-down assays. GMEB-1 possesses intrinsic transactivation activity in mammalian one-hybrid assays. Overexpression of GMEB-1 (alone or with GMEB-2) causes a reversible right shift in the GR dose-response curve and decreased partial agonist activity of antisteroids. Both GMEBs interact with CREB-binding protein (CBP) in two-hybrid assays; neither possesses histone acetyltransferase (HAT) activity. GMEB-1 and -2 share a 90-aa region (~80% identical) containing the KDWK core. Mammalian two-hybrid assay, GST pull-down, mammalian one-hybrid transactivation assay, reporter gene assay, HAT activity assay Molecular endocrinology (Baltimore, Md.) High 10894151
2000 GME activity requires positioning within ~250 bp upstream of a tandem GRE driving a complex promoter; phasing between GME and downstream GREs is unimportant (unlike GREs); the GME does not affect GR binding to a single GRE. Changes in GME activity did not correlate with fold induction from the GRE, indicating that GME and GRE activities utilize parallel rather than common pathways. Transient transfection reporter gene assays with positional/distance mutants, gel shift assays Molecular and cellular endocrinology Medium 10854715
2000 Mouse GMEB-1 was identified by yeast two-hybrid screening using the activation domain 2 of nuclear receptor coactivator TIF2 as bait. In vitro translated mGMEB-1 bound specifically to GME oligonucleotides alone and as a heterodimer with rGMEB-2. Transient transfection with TAT promoter reporter genes indicated a role as a transcriptional regulator of the TAT promoter. Yeast two-hybrid screening, in vitro translation, EMSA/gel shift, transient transfection reporter assay FEBS letters Medium 10692587
2002 GMEB-1 domains were mapped for distinct activities: homooligomerization, heterooligomerization, DNA binding, binding to GR, binding to CBP, and GR modulation each require defined regions. The domain for GR modulation and the domain for intrinsic transactivation activity do not overlap, providing a structural basis for the independence of dose-response curve modulation from total levels of GR-induced gene expression. Deletion/truncation mutagenesis, mammalian two-hybrid assay, DNA binding assays, reporter gene assays The Journal of biological chemistry High 11934901
2002 MURF-1 binds GMEB-1 (a transcriptional regulator) in vitro. Endogenous MURF-1 was detected in nuclei of some myocytes, suggesting that MURF-1's interaction with GMEB-1 may link myofibril signaling to muscle gene expression. In vitro binding assay, immunofluorescence/subcellular fractionation The Journal of cell biology Medium 11927605
2002 GMEBs contact Ubc9 (mammalian E2 SUMO-conjugating enzyme), which also binds GR. Ubc9 modifies GR-induced gene expression (amount, fold induction, EC50, partial agonist activity) in a manner independent of its SUMO-1 transfer activity. The GME is proposed to act by increasing the local concentration of Ubc9 near the transcription machinery. Co-immunoprecipitation, reporter gene assay, transfection with Ubc9 mutants (SUMO-transfer deficient) The Journal of biological chemistry Medium 11812797
2003 The 1.55 Å crystal structure of the GMEB1 SAND domain was determined. NMR and binding studies mapped DNA recognition to an alpha-helical region exposing the conserved KDWK motif. Site-directed mutagenesis identified key residues for DNA binding. The GMEB1 SAND domain also contains a zinc-binding motif (absent in Sp100b SAND domain); zinc is not required for DNA binding but determines C-terminal conformation of the domain. X-ray crystallography (1.55 Å), NMR spectroscopy, site-directed mutagenesis, DNA binding assays Molecular endocrinology (Baltimore, Md.) High 12702733
2004 GMEB1 binds to the prodomain (CARD) of procaspase-2 and inhibits its autoproteolytic activation by oligomerization in a chemical compound-dependent system, identifying GMEB1 as an endogenous inhibitor of procaspase-2 autoactivation. Co-immunoprecipitation, in vitro binding to procaspase-2 prodomain, caspase activation assay Biochemical and biophysical research communications Medium 15555560
2004 GMEB-2 structure/activity relationships mirror those of GMEB-1: homo- and heterooligomerization, GR binding, CBP binding, DNA binding, and GR transactivation modulation each require large regions of the protein; only intrinsic transactivation activity could be localized to a small region. Quantitative differences between GMEB-1 and -2 activities arise from amino acid sequence variation rather than global structural differences. Deletion/truncation mutagenesis, mammalian two-hybrid assay, DNA binding assays, reporter gene assays Biochemistry Medium 14705952
2006 GMEB1 binds to procaspase-8 and procaspase-9 (in addition to procaspase-2) via their prodomains. GMEB1 attenuates Fas-mediated caspase-8 and -9 activation and subsequent apoptosis. siRNA knockdown of endogenous GMEB1 renders cells more sensitive to stress-induced apoptosis. Transgenic mice with neurospecific GMEB1 overexpression exhibit smaller cerebral infarcts and less brain swelling after transient focal ischemia. Co-immunoprecipitation, siRNA knockdown, caspase activation assays, transgenic mouse model with focal ischemia The Journal of biological chemistry High 16497673
2008 GMEB1 prevents caspase activation and apoptosis in human neuroblastoma SK-N-MC cells subjected to hypoxia or oxidative stress, confirming its role as an endogenous inhibitor of initiator caspase activation in response to diverse stress stimuli. Caspase activation assays, cell viability/apoptosis assays under hypoxia and oxidative stress Neuroscience letters Medium 18455874
2009 GMEB1/PIF p96 interacts with the N-terminal domain of RAG1 as identified by yeast two-hybrid assay. A WW-like motif within RAG1's N-terminal domain mediates this interaction; point mutations at conserved WW residues abolished binding. A luciferase reporter assay demonstrated that a protein complex containing RAG proteins and GMEB1 can assemble in cells. Yeast two-hybrid assay, point mutagenesis, luciferase reporter assay Nucleic acids research Medium 19324890
2011 IL-12 induces GMEB1 expression in human T cells. siRNA knockdown of GMEB1 reverses the protective effect of IL-12 on dexamethasone-induced T cell apoptosis, placing GMEB1 downstream of IL-12/PI3K/Akt signaling as a mediator of anti-apoptotic protection against glucocorticoid-induced apoptosis. siRNA knockdown, apoptosis assays (flow cytometry), qPCR, PI3K inhibitor treatment Immunobiology Medium 21840619
2012 GMEB1 was identified as a novel binding partner of FOXL2 transcription factor by yeast two-hybrid screening and confirmed by co-immunoprecipitation. GMEB1 is sequestered in aggregates formed by BPES-causing FOXL2 mutants. On most promoters GMEB1 acts as a transcriptional repressor; it increases wild-type FOXL2 activity on the Per2 promoter and to a greater extent increases the activity of the oncogenic p.C134W FOXL2 variant. Yeast two-hybrid screening, co-immunoprecipitation, immunofluorescence (aggregate sequestration), luciferase reporter assays Human molecular genetics Medium 22544055
2019 GMEB1 interacts with CFLARL (c-FLIPL) in the cytosol and promotes its stability. The deubiquitinase USP40 catalyzes K48-linked deubiquitination of CFLARL; GMEB1 acts as a bridge protein promoting the binding of USP40 to CFLARL. USP40 knockdown abolishes GMEB1-mediated CFLARL stabilization. GMEB1 inhibits pro-caspase-8 activation and DISC formation upon TRAIL stimulation; CFLARL enhances the binding of GMEB1 to CASP8. GMEB1 knockdown inhibits A549 xenograft tumor growth in vivo. Co-immunoprecipitation, GST pull-down, Western blot (ubiquitination), immunofluorescence, flow cytometry (apoptosis), shRNA knockdown, xenograft mouse model Journal of experimental & clinical cancer research : CR High 31046799
2019 In midbrain dopamine (mDA) neurons, Gmeb1 was identified as a transcription factor regulating expression of Th (tyrosine hydroxylase) and Dat (dopamine transporter). Gmeb1 knockdown in mDA neurons caused downregulation of Th and Dat and severe motor deficits, establishing Gmeb1 as a master regulator of mDA gene expression and function. Virus-based nuclear capture, RNA-seq, DNase-seq (chromatin accessibility), predictive modeling, in vivo AAV-mediated Gmeb1 knockdown with behavioral readout Nature communications High 31175277
2020 TRAF3 interacts with GMEB1 as identified by yeast two-hybrid screening of a human B cell cDNA library and confirmed by co-immunoprecipitation in mammalian cells. TRAF3 overexpression enhances GMEB1's anti-apoptotic function; TRAF3 siRNA knockdown significantly reduces GMEB1-mediated inhibition of apoptosis. The RING and TRAF-C domains of TRAF3 are not required for this interaction. Yeast two-hybrid screening, co-immunoprecipitation, siRNA knockdown, cell viability/apoptosis assays Journal of biological research (Thessalonike, Greece) Medium 32514408
2021 CircGlis3 promotes the degradation of GMEB1 by facilitating the interaction between GMEB1 and the E3 ubiquitin ligase MIB2, thereby suppressing GMEB1-dependent phosphorylation of HSP27. RNA pull-down, co-immunoprecipitation, Western blot (protein stability/ubiquitination), gain/loss-of-function assays Diabetologia Medium 34751796
2023 GMEB1 binds to the YAP1 promoter region and positively regulates YAP1 expression in hepatocellular carcinoma cells. GMEB1 binding to the YAP1 promoter was confirmed by dual-luciferase reporter assay and chromatin immunoprecipitation-qPCR. Chromatin immunoprecipitation-qPCR, dual-luciferase reporter assay, Western blot, qRT-PCR, gain/loss-of-function (overexpression/knockdown) World journal of gastrointestinal oncology Medium 37389116

Source papers

Stage 0 corpus · 29 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2002 Muscle-specific RING finger-1 interacts with titin to regulate sarcomeric M-line and thick filament structure and may have nuclear functions via its interaction with glucocorticoid modulatory element binding protein-1. The Journal of cell biology 200 11927605
2002 Ubc9 is a novel modulator of the induction properties of glucocorticoid receptors. The Journal of biological chemistry 78 11812797
1995 The factor binding to the glucocorticoid modulatory element of the tyrosine aminotransferase gene is a novel and ubiquitous heteromeric complex. The Journal of biological chemistry 47 7665613
2000 Properties of the glucocorticoid modulatory element binding proteins GMEB-1 and -2: potential new modifiers of glucocorticoid receptor transactivation and members of the family of KDWK proteins. Molecular endocrinology (Baltimore, Md.) 44 10894151
2012 Discovery of novel protein partners of the transcription factor FOXL2 provides insights into its physiopathological roles. Human molecular genetics 41 22544055
2003 Crystal structure and nuclear magnetic resonance analyses of the SAND domain from glucocorticoid modulatory element binding protein-1 reveals deoxyribonucleic acid and zinc binding regions. Molecular endocrinology (Baltimore, Md.) 39 12702733
1998 Cloning and characterization of a novel binding factor (GMEB-2) of the glucocorticoid modulatory element. The Journal of biological chemistry 34 9651376
2019 Glucocorticoid modulatory element-binding protein 1 (GMEB1) interacts with the de-ubiquitinase USP40 to stabilize CFLARL and inhibit apoptosis in human non-small cell lung cancer cells. Journal of experimental & clinical cancer research : CR 27 31046799
2000 Ability of the glucocorticoid modulatory element to modify glucocorticoid receptor transactivation indicates parallel pathways for the expression of glucocorticoid modulatory element and glucocorticoid response element activities. Molecular and cellular endocrinology 27 10854715
2021 Lipotoxicity-induced circGlis3 impairs beta cell function and is transmitted by exosomes to promote islet endothelial cell dysfunction. Diabetologia 26 34751796
2006 Glucocorticoid modulatory element-binding protein 1 binds to initiator procaspases and inhibits ischemia-induced apoptosis and neuronal injury. The Journal of biological chemistry 25 16497673
2022 Fatty acid metabolism-related genes are associated with flavor-presenting aldehydes in Chinese local chicken. Frontiers in genetics 22 36035160
1999 Cloning and characterization of hGMEB1, a novel glucocorticoid modulatory element binding protein. FEBS letters 22 10386584
2000 Genomic organization of human GMEB-1 and rat GMEB-2: structural conservation of two multifunctional proteins. Nucleic acids research 18 10734202
2011 IL-12 inhibits glucocorticoid-induced T cell apoptosis by inducing GMEB1 and activating PI3K/Akt pathway. Immunobiology 17 21840619
2002 Structure/activity elements of the multifunctional protein, GMEB-1. Characterization of domains relevant for the modulation of glucocorticoid receptor transactivation properties. The Journal of biological chemistry 17 11934901
2000 Cloning of a mouse glucocorticoid modulatory element binding protein, a new member of the KDWK family. FEBS letters 15 10692587
2008 GMEB1, a novel endogenous caspase inhibitor, prevents hypoxia- and oxidative stress-induced neuronal apoptosis. Neuroscience letters 14 18455874
2004 Regulation of procaspase-2 by glucocorticoid modulatory element-binding protein 1 through the interaction with caspase recruitment domain. Biochemical and biophysical research communications 12 15555560
2009 A WW-like module in the RAG1 N-terminal domain contributes to previously unidentified protein-protein interactions. Nucleic acids research 10 19324890
2020 TRAF3 can interact with GMEB1 and modulate its anti-apoptotic function. Journal of biological research (Thessalonike, Greece) 9 32514408
2019 In vivo nuclear capture and molecular profiling identifies Gmeb1 as a transcriptional regulator essential for dopamine neuron function. Nature communications 9 31175277
2004 Structure/activity relationships for GMEB-2: the second member of the glucocorticoid modulatory element-binding complex. Biochemistry 7 14705952
2023 Withdrawn: Z. Cui, Q. Sun, W. Yan, Q. Han, G. Wang, Y. Hu. The role of miR-320a and its target gene GMEB1 in epithelial-mesenchymal transition and invasion of colorectal cancer, published in The Journal of Gene Medicine. The journal of gene medicine 6 33617082
2023 Chromatin Accessibility and Transcriptional Landscape during Inhibition of Salmonella enterica by Lactobacillus reuteri in IPEC-J2 Cells. Cells 5 36980306
2022 Identification of functionally important miRNA targeted genes associated with child obesity trait in genome-wide association studies. BMC genomics 4 35546387
2023 Transcription factor glucocorticoid modulatory element-binding protein 1 promotes hepatocellular carcinoma progression by activating Yes-associate protein 1. World journal of gastrointestinal oncology 2 37389116
2018 From Matrices to Knowledge: Using Semantic Networks to Annotate the Connectome. Frontiers in neuroanatomy 2 30581382
2026 Genome-wide profiling of salivary promoter-region DNA methylation in periodontitis: the Tromsø Study. BMC medical genomics 0 41652412

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