scholarly journals ETS Domain-Containing Protein Elk-4

2020 ◽  
Author(s):  
Keyword(s):  
Ets Domain

scholarly journals ETS-Domain Transcription Factor Elk-1 Regulates Stemness Genes in Brain Tumors and CD133+ BrainTumor-Initiating Cells

2021 ◽  
Vol 11 (2) ◽  
pp. 125
Author(s):  
Melis Savasan Sogut ◽  
Chitra Venugopal ◽  
Basak Kandemir ◽  
Ugur Dag ◽  
Sujeivan Mahendram ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Brain Tumor ◽  
Brain Tumors ◽  
System Development ◽  
Nervous System Development ◽  
Stem Cell Population ◽  
Tumor Initiating Cells ◽  
Specific Domain ◽  
Brain Tumor Initiating Cells ◽  
Ets Domain

Elk-1, a member of the ternary complex factors (TCFs) within the ETS (E26 transformation-specific) domain superfamily, is a transcription factor implicated in neuroprotection, neurodegeneration, and brain tumor proliferation. Except for known targets, c-fos and egr-1, few targets of Elk-1 have been identified. Interestingly, SMN, SOD1, and PSEN1 promoters were shown to be regulated by Elk-1. On the other hand, Elk-1 was shown to regulate the CD133 gene, which is highly expressed in brain-tumor-initiating cells (BTICs) and used as a marker for separating this cancer stem cell population. In this study, we have carried out microarray analysis in SH-SY5Y cells overexpressing Elk-1-VP16, which has revealed a large number of genes significantly regulated by Elk-1 that function in nervous system development, embryonic development, pluripotency, apoptosis, survival, and proliferation. Among these, we have shown that genes related to pluripotency, such as Sox2, Nanog, and Oct4, were indeed regulated by Elk-1, and in the context of brain tumors, we further showed that Elk-1 overexpression in CD133+ BTIC population results in the upregulation of these genes. When Elk-1 expression is silenced, the expression of these stemness genes is decreased. We propose that Elk-1 is a transcription factor upstream of these genes, regulating the self-renewal of CD133+ BTICs.

scholarly journals Epidermal Growth Factor-mediated Activation of the ETS Domain Transcription Factor Elk-1 Requires Nuclear Calcium

2002 ◽  
Vol 277 (30) ◽  
pp. 27517-27527 ◽  
Author(s):  
Thomas Pusl ◽  
Julie J. Wu ◽  
Tracy L. Zimmerman ◽  
Lei Zhang ◽  
Barbara E. Ehrlich ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Nuclear Calcium ◽  
Epidermal Growth ◽  
Ets Domain

scholarly journals The Role of the Ets Domain Transcription Factor Erm in Modulating Differentiation of Neural Crest Stem Cells

2002 ◽  
Vol 250 (1) ◽  
pp. 168-180 ◽  
Author(s):  
Christian Paratore ◽  
Guya Brugnoli ◽  
Hye-Youn Lee ◽  
Ueli Suter ◽  
Lukas Sommer
Keyword(s):  
Stem Cells ◽  
Transcription Factor ◽  
Neural Crest ◽  
Neural Crest Stem Cells ◽  
Ets Domain

scholarly journals Comparative structure analysis of the ETSi domain of ERG3 and its complex with the E74 promoter DNA sequence

2018 ◽  
Vol 74 (10) ◽  
pp. 656-663 ◽  
Author(s):  
Ruby Sharma ◽  
Shanti P. Gangwar ◽  
Ajay K. Saxena
Keyword(s):  
Transcription Factors ◽  
Dna Binding ◽  
Dna Sequence ◽  
Structure Analysis ◽  
Dna Sequences ◽  
Space Group ◽  
Class 1 ◽  
Comparative Structure ◽  
Ets Domain ◽  
Promoter Dna

ERG3 (ETS-related gene) is a member of the ETS (erythroblast transformation-specific) family of transcription factors, which contain a highly conserved DNA-binding domain. The ETS family of transcription factors differ in their binding to promoter DNA sequences, and the mechanism of their DNA-sequence discrimination is little known. In the current study, crystals of the ETSi domain (the ETS domain of ERG3 containing a CID motif) in space group P41212 and of its complex with the E74 DNA sequence (DNA9) in space group C2221 were obtained and their structures were determined. Comparative structure analysis of the ETSi domain and its complex with DNA9 with previously determined structures of the ERGi domain (the ETS domain of ERG containing inhibitory motifs) in space group P65212 and of the ERGi–DNA12 complex in space group P41212 were performed. The ETSi domain is observed as a homodimer in solution as well as in the crystallographic asymmetric unit. Superposition of the structure of the ETSi domain on that of the ERGi domain showed a major conformational change at the C-terminal DNA-binding autoinhibitory (CID) motif, while minor changes are observed in the loop regions of the ETSi-domain structure. The ETSi–DNA9 complex in space group C2221 forms a structure that is quite similar to that of the ERG–DNA12 complex in space group P41212. Upon superposition of the complexes, major conformational changes are observed at the 5′ and 3′ ends of DNA9, while the conformation of the core GGA nucleotides was quite conserved. Comparison of the ETSi–DNA9 structure with known structures of ETS class 1 protein–DNA complexes shows the similarities and differences in the promoter DNA binding and specificity of the class 1 ETS proteins.

Development of the Drosophila tracheal system occurs by a series of morphologically distinct but genetically coupled branching events

Development ◽  
1996 ◽  
Vol 122 (5) ◽  
pp. 1395-1407 ◽  
Author(s):  
C. Samakovlis ◽  
N. Hacohen ◽  
G. Manning ◽  
D.C. Sutherland ◽  
K. Guillemin ◽  
...  
Keyword(s):  
Tube Formation ◽  
The Body ◽  
Terminal Branch ◽  
Cellular Mechanisms ◽  
Morphological Marker ◽  
Tracheal System ◽  
Fgf Receptor ◽  
Restricted Domains ◽  
Gene Regulatory ◽  
Ets Domain

The tracheal (respiratory) system of Drosophila melanogaster is a branched network of epithelial tubes that ramifies throughout the body and transports oxygen to the tissues. It forms by a series of sequential branching events in each hemisegment from T2 to A8. Here we present a cellular and initial genetic analysis of the branching process. We show that although branching is sequential it is not iterative. The three levels of branching that we distinguish involve different cellular mechanisms of tube formation. Primary branches are multicellular tubes that arise by cell migration and intercalation; secondary branches are unicellular tubes formed by individual tracheal cells; terminal branches are subcellular tubes formed within long cytoplasmic extensions. Each level of branching is accompanied by expression of a different set of enhancer trap markers. These sets of markers are sequentially activated in progressively restricted domains and ultimately individual tracheal cells that are actively forming new branches. A clonal analysis demonstrates that branching fates are not assigned to tracheal cells until after cell division ceases and branching begins. We further show that the breathless FGF receptor, a tracheal gene required for primary branching, is also required to activate expression of markers involved in secondary branching and that the pointed ETS-domain transcription factor is required for secondary branching and also to activate expression of terminal branch markers. The combined morphological, marker expression and genetic data support a model in which successive branching events are mechanistically and genetically distinct but coupled through the action of a tracheal gene regulatory hierarchy.

Sign in / Sign up

Export Citation Format

Share Document