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My research interest is a cancer cell biology. My PhD project was focused on the regilation of alternative splicing regulation by mutant p53 in breast cancer. Currently I'm working on the role of ubiquitin-proteasome system in tumor proteom regulation.
In my work I apply many basic molecular biology techniques, different methods to analyse protein-protein and protein-RNA interations and confocal microscopy. I'm also familiar with Zebrafish model organism and its applications in cancer research.
This project will be the first attempt to systematically understand the impact of the proteasome on proteome and transcriptome of several cancer types, as well as how this effect can be taken advantage of therapeutically. The clinically approved therapies involving proteasome inhibitors – such as bortezomib and carfilzomib -successful in hematologic neoplasias, are facing a growing resistance problem, while their use is not effective in solid tumors for unknown reasons. The proposed research will enrich the knowledge of basic cellular mechanisms controlled by the proteasome and will uncover novel routes of extending or bypassing the proteasome inhibitor-based therapies and combating resistance to the approved proteasome inhibitors.
I advise you to order predesigned validated siRNA. The optimal solution is to use pooled siRNA - a mix of 3-4 sequences. Using a mix enchances efficiency of a knock down and reduces off target effect because concentration of individual sequences is lower than when you use single siRNA.
Gain-of-function (GOF) mutations in the TP53 gene lead to acquisition of new functions by the mutated tumor suppressor p53 protein. A number of the over-represented 'hot spot' mutations, including the ones in codons 175, 248 or 273, convey GOF phenotypes. Such phenotypes may include resistance to chemotherapeutics or changes in motility and invasiv...
The protein is not degraded in the cell lysate. The cells degrade it in normal conditions to stop expression of genes regulated by HIF1 alpha. In the lysis buffer you have proteases inhibitors and denaturating agents so nothing can be degraded.
Human p53 protein acts as a transcription factor predominantly in a tetrameric
form. Single residue changes, caused by hot-spot mutations of the TP53 gene in
human cancer, transform wild-type (wt) p53 tumor suppressor proteins into potent
oncoproteins - with gain-of-function, tumor-promoting activity. Oligomerization of p53
allows for a direct inte...
As crucial regulators of the immune response against pathogens, macrophages have been extensively shown also to be important players in several diseases, including cancer. Specifically, breast cancer macrophages tightly control the angiogenic switch and progression to malignancy. ID4, a member of the ID (inhibitors of differentiation)...
The abundant, nuclear-retained, metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been associated with a poorly differentiated and aggressive phenotype of mammary carcinomas. This long non-coding RNA (lncRNA) localizes to nuclear speckles, where it interacts with a subset of splicing factors and modulates their activity. In this s...
Despite decades of cancer research, the search for key oncogenesis regulators as potential targets for novel therapies continues. Proteins, belonging to ID family, may be such promising candidates. They are DNA binding inhibitors, mainly of the bHLH transcription factor subfamily, which regulate genes related to cell differentiation. ID genes are n...