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Eugene Tulchinsky

Researcher at University of Leicester

Publications -  45
Citations -  4466

Eugene Tulchinsky is an academic researcher from University of Leicester. The author has contributed to research in topics: Regulation of gene expression & Transcription factor. The author has an hindex of 29, co-authored 44 publications receiving 4021 citations. Previous affiliations of Eugene Tulchinsky include Nazarbayev University & Karolinska Institutet.

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SIP1/ZEB2 induces EMT by repressing genes of different epithelial cell–cell junctions

TL;DR: It is shown that expression of SIP1 in human epithelial cells results in a clear morphological change from an epithelial to a mesenchymal phenotype, and repression occurs by a general mechanism mediated by Smad Interacting Protein 1 (SIP1)-binding sites.
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A switch in the expression of embryonic EMT-inducers drives the development of malignant melanoma.

TL;DR: It is found that regulation and functions of EMT-TFs are different in malignant melanoma and this switch results in E-cadherin loss, enhanced invasion, and constitutes an independent factor of poor prognosis in melanoma patients.
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Tumor suppressor p53 protein is a new target for the metastasis-associated Mts1/S100A4 protein: functional consequences of their interaction.

TL;DR: The ability of Mts1 to enhance p53-dependent apoptosis might accelerate the loss of wild type p53 function in tumors and contribute to the development of a more aggressive phenotype during tumor progression.
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The metastasis-associated Mts1(S100A4) protein could act as an angiogenic factor.

TL;DR: It is shown that an oligomeric, but not a dimeric form of the Mts1(S100A4) protein was capable of enhancing the endothelial cell motility in vitro and stimulate the corneal neovascularization in vivo and might induce tumor progression via stimulation of angiogenesis.
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ZEB/miR-200 feedback loop: at the crossroads of signal transduction in cancer.

TL;DR: Crosstalk between the ZEB/miR‐200 axis and several signal transduction pathways activated at different stages of tumor development is reviewed and suggests that ZEB1 and ZEB2 may have different, possibly even opposing, roles in some forms of human cancer.