Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot keyword mapping
Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara
Gene Ontology annotation of human sequence-specific DNA binding transcription factors (DbTFs) based on the TFClass database
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
EGR2 induces apoptosis in various cancer cell lines by direct transactivation of BNIP3L and BAK.
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EGR2 directly transactivates expression of BNIP3L and BAK through binding to their promoter regions, inducing apoptosis in cancer cell lines.
"EGR2 could induce apoptosis in a large proportion of these lines by altering the permeability of mitochondrial membranes, releasing cytochrome c and activating caspase-3, -8, and -9. Analysis by cDNA microarray and subsequent functional studies revealed that EGR2 directly transactivates expression of BNIP3L and BAK."
HCF-1 functions as a coactivator for the zinc finger protein Krox20.
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HCFC1 functions as a coactivator for EGR2/Krox20. The HCF-binding motif (DHLY at residues 162-165) in EGR2 mediates interaction with the HCFC1 beta-propeller domain. Mutation of this motif diminishes both transactivation and HCFC1 association.
"Krox20, a zinc finger transcription factor required for Schwann cell differentiation, and E2F4, a cell cycle regulator, showed a strong requirement for functional HCF-1 to activate transcription ... In Krox20, the HCF-binding motif lies within the N-terminal activation domain and mutation of this sequence diminishes both transactivation and association with the HCF-1 beta-propeller"
Functional, histopathologic and natural history study of neuropathy associated with EGR2 mutations.
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Characterization of EGR2 mutations causing CMT1D/CHN/DSS. R359W and E412K mutations cause loss of DNA binding and transactivation. I268N affects the NAB repressor binding site. Cranial nerve dysfunction and respiratory compromise are common features.
"Mutations in the EGR2 gene cause a spectrum of Charcot-Marie-Tooth disease and related inherited peripheral neuropathies ... respiratory compromise and cranial nerve dysfunction are commonly associated with EGR2 mutations"
The HECT-type E3 ubiquitin ligase AIP2 inhibits activation-induced T-cell death by catalyzing EGR2 ubiquitination.
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WWP2/AIP2 interacts with and ubiquitinates EGR2, promoting its proteasomal degradation. EGR2 regulates FasL expression in T cells during activation-induced cell death. AIP2-mediated EGR2 degradation protects against T cell apoptosis.
"AIP2 interacts with and promotes ubiquitin-mediated degradation of EGR2, a zinc finger transcription factor that has been found to regulate Fas ligand (FasL) expression during activation-induced T-cell death"
The transcription factor Krox20 is an E3 ligase that sumoylates its Nab coregulators.
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EGR2/Krox20 functions as an E3 SUMO ligase, catalyzing SUMO1 conjugation to its NAB coregulators. This requires interaction with the SUMO-conjugating enzyme UBC9. NAB sumoylation negatively modulates EGR2 transcriptional activity.
"we show that Krox20 functions as a SUMO ligase for its coregulators--the Nab proteins--and that Nab sumoylation negatively modulates Krox20 transcriptional activity in vivo"
Impact of cytosine methylation on DNA binding specificities of human transcription factors.
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Systematic SELEX analysis of 542 human TFs including EGR2 characterized binding specificities on both unmethylated and CpG-methylated DNA.
"By analysis of 542 human TFs with methylation-sensitive SELEX (systematic evolution of ligands by exponential enrichment), we found that there are also many TFs that prefer CpG-methylated sequences"
Mutations in the early growth response 2 (EGR2) gene are associated with hereditary myelinopathies.
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First identification of EGR2 mutations causing human myelinopathies. Recessive and dominant missense mutations found in patients with CHN and CMT1. Egr2 knockout mice show disrupted hindbrain development and a block in Schwann cell differentiation.
"Stable expression of Egr2 is specifically associated with the onset of myelination in the peripheral nervous system (PNS). Egr2(-/-) mice display disrupted hindbrain segmentation and development, and a block of Schwann-cell differentiation at an early stage"
NGF- and MAPK-dependent EGR1, EGR2 and EGR4 expression
EGR1,2,3 bind the NAB2 promoter
EGR1, EGR2 bind the RRAD promoter
NAB2 and CHD4 bind and repress EGR-mediated RRAD gene expression
EGR2:NAB2 and CHD4 bind the ID2 and ID4 promoter regions
EGR2 and SOX10 bind the MAG gene
EGR2, SOX10 and TEAD1 bind enhancers in the PMP22 gene
SOX10, EGR2 and NAB proteins bind the GJB1 promoter
EGR2 and SREBF2 dimer bind SCD5 gene
EGR2 and SREBF2 dimer bind CYP51A1 gene
EGR2 and SREBF2(1-484) dimer bind HMGCR gene
Deep research report on EGR2 function (Falcon provider)