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Andrey tsvetkov forex

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Mariya Ponarina1, Andrey Okhrimchuk1,2, Grigory Alagashev2, Trikshev A. I., Kamynin V. A., Tsvetkov V. B. and Itrin P. A. Quantum Electron. Oleg Tsvetkov, Corporate Secretary, Sberbank, Сhairman of the Board, NCSA Andrey Yakushin, Head of the Division of the Corporate Affairs Department. Viktoriia Degtereva, Andrey Zaytsev, Ekaterina Mihel Andrey Zaytsev, Viktoriia Degtereva, Nikolay Dmitriev Nina Olinder, Aleksej Tsvetkov. FOREX USD INDICATORS Some people need the best value supported devices that you are permanently as a brief. Page 73 WEP EXEC mode, use. Web Expand child. Audio Troubleshooting If the first time in Python, it will not be to a record of class "Customer".

Editors: view affiliations Ivan A. Buying options eBook EUR Softcover Book EUR Hardcover Book EUR Learn about institutional subscriptions. Table of contents 50 papers Search within book Search. Page 1 Navigate to page number of 3. Front Matter Pages i-xxv. Reznichenko, I. Verbenko, L. Shilkina, A. Pavlenko, S. Dudkina, I. Andryushina et al. Pages Zhilin, G. Karapetyan, M. Kutepov, T. Minasyan, V. Yatsenko, E.

Kaidashev Pages Shvetsov, E. Petrova, M. Lugovaya, N. Shvetsova, S. Shcherbinin, A. Rybyanets Pages Lugovaya, I. Shvetsov, N. Shvetsova, A. Reznichenko, A. Belenov, Vladislav S. Menshchikov, Alina K. Nevelskaya, Vasiliy V. Pryadchenko, Daria B. Shemet, Vasiliy V. Srabionyan et al. Bayan, Timofey G.

Lupeiko, Maria G. Volkova, Anna S. Kostenikova, Larisa E. Pustovaya, Aleksey G. Fedorenko Pages Bunin, Valentine A. Chanturiya, Nataliya E. Anashkina, Galina K. Khachatryan, Mariya V. Ryazantseva, Elizaveta V. Koporulina Pages Migal, Vladimir I. Kolesnikov Pages Ilyasov, B. Meshi, D. Pham, Ch. Nguyen, O. Holodova, T.

Zhdanova et al. Bondarev Pages Sakhnenko, Yu. Zakharov, I. Parinov, A. Lutokhin, E. Were there any sex-specific effects? As cite in that work, there were several other previously published papers suggesting a connection of autophagy to G4 nucleic acid metabolism as probed by G4 ligands: Orlotti et al. While all these papers delved more into the relationships of G4 and autophagy in cancer, it would be useful to discuss these works in a single paragraph in the Discussion and place the current work in light of those findings.

Is DNA damage accumulation in neurons also observed in the current work? How are the results and findings from the two studies related, if at all? In this paper, the authors rather convincingly show that the ATG7 gene, which is critical for the initiation of autophagy and whose transcription decreases with aging, does contain a bona fide G-quadruplex G4 in its first intron and that stabilization of G4 using pyridostatin PDS , a well-known benchmark G4 ligand, downregulates this ATG7 gene.

All this suggest that stabilization of ATG7 G4 does interfere with the transcription of this gene, thereby inhibiting induction of autophagy. In good agreement, the authors found that mice treated with PDS develop memory deficits and accumulation of lipofuscin, suggesting premature aging and deficient autophagy.

Moreover, brain samples from aged mice contain G4-DNA which are absent in brain samples from young mice. Finally, the authors showed that overexpressing the helicase Pif1, which is known to resolve G4, in neurons exposed to PDS improves the various phenotypes associated with PDS treatment, thereby suggesting that G4-DNA may represent an interesting and relevant intervention point for boosting autophagy and thereby interfering with neurodegeneration.

In general, I think this is a very interesting study based on well-designed and well-conducted experiments that deserves to be published in eLife. In particular, revealing that G4 may represent a new putative intervention point to interfere with autophagy-related neurodegeneration represents an important discovery. However, I have a few comments that need to be addressed before this paper could be deemed for publication in eLife. The analysis performed by the authors indicates that all the autophagy genes contain putative G4-DNA.

It would be important to precise the percentage of total genes that contain, or not putative G4-DNA to assess how specific is this correlation. The authors should comment on this. The authors argue that the presence of dehydrating agents PEG, CH 3 CN reduces the polymorphism and indeed the CD looks better but this effect has been reported only for telomeric sequences and is not fully admitted.

The TDS spectrum without dehydrating agents should also be shown. Also, another classical control for CD which is missing is the use of scrambled G runs. Finally, as for the experiments with N-TASQ, I have some problem to understand them because, as this fluorescent molecule is also a G4-ligand, one may imagine a competition between this compound and PDS for the binding on G4.

Should a compound that efficiently bind G4 without any effect on their stability exist, then it would represent an ideal control to further validate their findings. To finish, and importantly, in my view the main message of this manuscript is that G4-DNA may represent an interesting and relevant intervention point for boosting autophagy and thereby interfering with neurodegeneration, rather than the discovery of a novel pathway that regulates autophagy in neurons, as stated by the authors already in the title.

Therefore, I suggest that the authors down tune their message, especially in the Title but also in the discussion. I guess that revealing a new and relevant intervention point for modulating autophagy in neurons is per se sufficiently interesting in addition to be of biomedical relevance. They used biophysical methods to demonstrate accumulation of G4-DNA in the Atg7 gene and immunostaining methods to illustrate an age-dependent global increase of G4-DNA.

The authors further show that the majority of phenotypes induced by PDS were partially rescued by overexpression of fhe Pif1 helicase. The manuscript is clearly written, and data are well presented. The implication of G4-DNA in autophagy and age-related neurological deficit is novel and will be of interest to a broad readership.

Also, Pif1, as acknowledged by the authors, impacts telomere length, so how can the authors be sure that the reported partial improvements of neuronal phenotypes are solely due to resolving G4-DNA structures? Is the partial rescue specific to G4s in the Atfg7 gene? Performing a classical epistasis experiments is critical in this manuscript. For example, repeating key experiments in presence and absence of Atg7 will confirm that the reported phenotypes are due to direct modulation of G4-DNA in the Atg7 gene, hence supports the conclusion of a novel pathway as stated in the Title.

For the huntingtin experiments in Figure 4, I suggest using patient derived fibroblasts or iPS-derived striatal neurons instead of ectopic expression of the exon-1 fragment of the poly-Q huntingtin. Although, in silico predictions using the QGRS mapper rule out G4-DNA, it is important to experimentally rule it out in the native genomic environment.

The protein p62 is a known hallmark of perturbed autophagy. Is p62 aggregation also modulated by PDS in an Atg7 dependent manner? In the opinion of this reviewer, this is a better hallmark of perturbed autophagy given its clinical relevance. Overall, the concept is novel and exciting but the data in its present form do not support the main conclusion. Thank you for submitting your article "Small-molecule G-quadruplex stabilizers reveal a novel pathway of autophagy regulation in neurons" for consideration by eLife.

The following individuals involved in review of your submission have agreed to reveal their identity: Sherif El-Khamisy Reviewer 1. The reviewers have discussed the reviews with one another and the Reviewing Editor has drafted this decision to help you prepare a revised submission. This manuscript is a resubmission of a previous one in which authors show that the G-quadruplex G4 ligand pyridostatin PDS was found to downregulate expression of the Atg7 gene in neurons.

Mice treated with PDS develop memory deficits and accumulation of lipids and proteins previously observed to accumulate in aged brains. Brain samples from aged mice, but not young mice, contained G4 DNA, and overexpression of the G4-resolving helicase Pif1 in neurons improved the phenotypes associated with PDS treatment. The authors have satisfactorily responded to the concerns raised by the referees, but q few points need to be taken before the manuscript can be accepted. Hence it follows that the Atg sequence is most probably highly dynamic and may form several secondary structures that exist in equilibrium various G4, hairpins etc.

Hence this analysis does not allow the authors to firmly conclude the existence of a stable G4. Therefore, the authors should down-tune, or at least modulate their G4 hypothesis. This observation is interesting but somehow a bit surprising and rather counter-intuitive as it is not fully consistent with numerous studies reported in the literature that show that the G4 unwinding activity of most of the G4 helicases is indeed prevented by G4 ligands.

This has been shown in particular for Pif1 see Mendoza et al. The authors should discuss the results of their experiment with Pif1 in light of all the published data indicating that Pif1 G4 unwinding activity is inhibited by various G4 ligands that include PDS, or alternatively they could test their hypothesis by performing a functional in vitro assay e.

We thank the reviewer for this comment. We revised the manuscript to describe the results in greater detail, including quantitative statements for all of the results in the revised Results section. We thought this was an excellent suggestion, and we collected new data, which were added to the revised manuscript, to address this issue Figure 8F. Indeed, the mutant Pif1 failed to affect PDS-associated neuronal phenotypes—strong evidence that wild-type Pif1 activates coping mechanisms in PDS-treated degenerating neurons, leading to improved neuronal phenotypes, such as enhanced autophagy.

The referee correctly points out that we only briefly described how protein or organelle half-life is measured with photoswitchable proteins and optical pulse-chase labeling OPL. A number of studies used Dendra2 or other photoswitchable proteins, such as EOS2, and the OPL method to study protein or organelle dynamics in live cells.

For example, mouse cell lines that express a mitochondrially localized Dendra2 mito-Dendra2 were created to study mitochondrial dynamics and mitophagy Pham, McCaffery and Chan, The journal Autophagy published a review paper, which recommended using Dendra2-LC3 to study autophagic flux in neurons Klionsky et al. To measure autophagic flux in live neurons, we used the OPL method and longitudinal imaging Barmada et al.

We can then track how the red signal e. We thank the reviewer for these questions. We apologize for this delay. Regarding sex differences, we only used male mice in the original submission. This is a very important point and thus we prepared new cohorts of male and female mice that were injected with PDS.

Previously, a G4-binding small molecule MM41 was used as an anti-cancer therapy Kulkarni, Chen and Maday, ; we therefore used a comparable dosage and schedule of PDS. We also used old male and female mice 25 months with a leaky blood brain barrier BBB Haeusle, Donnelly and Rothstein, We examined these mice in 1 the novel object recognition test NORT , 2 a fear conditioning test.

We worked in collaboration with Dr. Second, mice were tested in the fear conditioning assay. The latter proved extremely stressful for old mice: they would frequently not move, making it difficult to analyze the data. Nevertheless, male mice performed worse in the fear conditioning assay. There was also a trend showing worse performance in the female cohort, although the data did not achieve statistical significance see Author response image 1.

That is an excellent suggestion, as we indeed only briefly mentioned that a prior study investigated whether there is a relationship between G4-DNA, autophagy, and cancer. Critically, we did not emphasize that G4 ligands stimulate autophagy in cancer cells. In our study, we show the opposite: G4-DNA ligands downregulate autophagy in post-mitotic neurons, which comes as no surprise since the autophagic pathways in neurons differ from those in other cell types Kulkarni, Chen and Maday, Therefore, we have taken this opportunity to review our discussion of the literature and to revise the manuscript to more effectively elaborate on the involvement of G4-DNA in autophagy and, importantly, on potential differences between neurons and cancer cells.

We added a reference to illustrate that the G4 structures play a role in frontotemporal dementia and ALS Haeusler, Donnelly and Rothstein, The experiments to address this question were technically challenging because our bioinformatics analyses revealed the presence of putative G4-DNA motifs in virtually all autophagy genes. However, importantly, many autophagy genes contain just a few putative G4-DNA motifs, whereas the Rattus norvegicus Atg7 gene contains As a result, transcription of Atg7 , which diminishes with aging Lipinski et al.

These questions were not addressed in the current study and are currently being pursued in our lab. We applied single-cell longitudinal analysis to gain spatiotemporal resolution and to simultaneously visually monitor the accumulation of p62, an autophagy substrate and autophagic marker, and neuronal toxicity in neurons expressing ATG7-mApple treated with a vehicle or PDS.

We added the data to the revised manuscript Figure 5—figure supplement 3. We thank the referee for this comment. We think this is a very important one. In our manuscript, we did not aim to conclude that the only way G4-DNA causes neurodegeneration is by downregulating autophagy. At the same time, we cannot exclude the possibility that more factors may contribute to neurodegeneration. With that in mind, we agree with the reviewer and have discussed this issue in the manuscript. Autophagic genes can be epigenetically silenced Artal-Martinez de Narvajaset al.

However, epigenetic silencing is a common mechanism in aged cells and affects the genes well beyond the autophagy pathway genes. In many models, the DNA damage repair genes and other gene types are epigenetically silenced in cancer and during aging Lahtz and Pfeifer, ; Langie et al. Our work suggests that an age-associated change in DNA conformation could be a novel epigenetic-like mechanism of gene expression in aging neurons; therefore, the results from our two studies are related.

Please see the fourth paragraph in the Discussion section that describes this issue. In general I think this is a very interesting study based on well-designed and well-conducted experiments that deserves to be published in eLife.

That means that other genes, even those that can potentially regulate autophagy directly or indirectly, were not taken into account in our analyses. We would like to point out that all of those genes were already analyzed for putative G4-DNA motifs by other labs Chambers, This point has been added to the discussion please see the fifth paragraph in the Discussion section.

The reviewer is correct, of course: we should have used the BRACO19 ligand in other experiments as well please see Figure 2, Figure 3 and Figure 4—figure supplement 1, Figure 5—figure supplement 1. We agree that the use of dehydrating conditions to improve the CD signature of a quadruplex structure has not been examined thoroughly despite an initial impetus provided by Chaires et al.

However, we also reported this effect for non-telomeric quadruplexes, extending this observation to quadruplex-forming sequences in the promoter of human genes e. Monchaud et al. The results seen in Author response image 2 clearly indicated that ATG folds into a complex structure comprising both a quadruplex core 1 H-NMR signals between 10 and 12 ppm and duplex stems 1 H-NMR signals between Of note, the polymorphism of the ATG quadruplex is also obvious, given the low resolution of the signal in the region of the NMR signals typical of the quadruplex core.

We added the data to the revised manuscript Figure 3, Figure 4—figure supplement 1. We agree and apologize for this oversight. The results seen in Figure 3 indicate clearly the topological differences between ATG and its mutated counterpart, the latter being characterized by both a CD signature cf. Vorlickova et al. Mergny et al. We fear, however, that it is not easy to address their concern.

First, the precise mode of binding of the antibody HF2 to G4s is not known. HF2 might discriminate between various quadruplexes from the KIT gene cf. Balasubramanian et al. Second, it has also been demonstrated with another quadruplex-selective antibody, BG4, that the concomitant binding of both an antibody BG4 and a ligand cPDS is possible cf.

Third, examples of quadruplex-destabilizing agents are still very sparse in the literature, and reported examples e. Pearson et al. Therefore, performing experiments in presence of both antibodies and ligands is possible, but the many possible outcomes e. Nevertheless, we again thank the reviewer for this comment and will address this in future experiments.

We thank the reviewer for this comment and apologize if our explanation was not clear in the initial manuscript. Briefly, the most important parameters to control are the live-cell incubation of the quadruplex ligand e. This protocol, which allows for assessing the extent and modification of the quadruplex landscape upon ligand treatment, was developed with MCF7 cells cf.

Importantly, this protocol was used with cancer cells but never with neurons, and the collected results presented here lend further credence to its reliability and broad applicability. As discussed above, there are no reliable examples of small molecules reported as quadruplex-destabilizing agents, apart from somewhat debatable candidates. We thank the reviewer for their comments. We substantially expanded the Discussion section.

Please see the fifth paragraph of the Discussion section. We thank the referee for these comments. In our original submission, we showed that 1 stabilizing G4s downregulates Atg7 , ATG7, and autophagy; 2 old brains contain more G4s but young brains hardly any; 3 Atg7 is downregulated in old brains; 4 Pif1 rescues phenotypes associated with PDS treatment e.

We, therefore, speculated in the Discussion section that in addition to histone acetyltransferases facilitating chromatin decondensation and promoting the expression of autophagy-related genes Baek and Kim, ; Lapierre et al. Mutated Pif1 was not able to rescue autophagic phenotypes in neurons. Our conclusions reflect the prevailing views in the autophagy field Lapierre et al. Reviewer 1 raised a similar question. However, analyses of the aged brain samples with no neurodegenerative pathologies led to a surprising and serendipitous finding—that the G4 structures are present in the aged brains and could be a marker of senescence in aging cells e.

Therefore, at a larger scale, we view our data on an age-associated change in DNA conformation as a novel epigenetic-like mechanism of gene expression in aging neurons. Recently, transposable elements were found to be epigenetic regulators of the genome, opening a new avenue of exciting research in neurodegeneration Sun et al. We believe that G4-DNA is an additional layer for such epigenetic-like regulation. As an autophagy lab interested in neuronal autophagy Moruno Manchon et al.

Please see the fourth paragraph in Discussion section, which discusses this important issue. Neurons are post-mitotic and how telomere length could be affected by Pif1 is not exactly clear. Indeed, cell-cycle activity is a driving force for telomere shortening. In some neurodegenerative diseases and in advanced aging, post-mitotic neurons re-enter the cell cycle, leading to various DNA abnormalities Mosch et al.

Neurons with a shorter telomere length can be generated from aged fibroblasts Huh et al. We believe it is unlikely that Pif1 is neuroprotective due to a telomere effect. Indeed, in the revised manuscript, we show that a helicase dead mutant lost its effect Figure 8F. Nevertheless, we cannot fully exclude the possibility that Pif1 may have additional unknown functions besides being a G4-DNA helicase.

Briefly, among ATG-related genes, Atg7 contains one of the highest amount of putative G4 motifs, and it works at the very beginning of the initiation of autophagy. We thought this was an excellent suggestion. As we study autophagy in the lab, we frequently use mutant huntingtin as a marker of autophagic clearance effectiveness. PDS promoted accumulation of mutant huntingtin indicating that the degradative pathways in neurons are affected by PDS Figure 5—figure supplement 2.

We thought this was a great suggestion. We collected new data, which are now added to the revised manuscript Figure 5—figure supplement 3. We are pleased that this reviewer accepts the novelty of our study and hope that the new data support the conclusions of our manuscript. Dempsey, W. PhOTO zebrafish: a transgenic resource for in vivo lineage tracing during development and regeneration.

PLoS One 7, e The referees correctly point out that we only briefly described how Atg may fold into several secondary structures that likely exist in an equilibrium. Therefore, we reviewed our explanation of the results and revised the manuscript to more effectively elaborate on how Atg may form various structures. In particular, we re-wrote the paragraph that explains the observed data and it now reads as the following.

These signals indicate that Atg may fold into a variety of G4-DNA topologies, including both 3- and 4-G-quartet G4s with both short 2-nt and long 9-nt hairpin-forming loops Figure 3B , which were also detected earlier in non-neuronal cells 3,40 or computationally predicted 41, We also thank the referees for the references. In addition to citing Bedrat et al. Please see the new Figure 3B that illustrates these possibilities. We thank the referees for this comment.

That is an excellent suggestion, as we indeed did not discuss that several prior studies investigated how an unwinding activity of G4 helicases is affected by G4-ligands e. We did not emphasize that several previous studies reported that, in general, G4-ligands impede helicase functions.

Therefore, the relevance of their findings to our study is not that straightforward. For example, these in vitro studies used an excess of the G4-ligands that may have a strong effect on the outcome. Critically, these studies used a G4-forming sequence without its complementary sequence in the in vitro assays.

Our in vivo context and low concentrations of PDS may explain why our data are different from those generated in vitro. We have taken this opportunity to review our discussion of the literature and to revise the manuscript to meticulously explain the main conclusions, as follows. In addition, the in vitro experiments assayed the activity of Pif1 using an excess of G4 ligands 84 , and therefore, the data are not easy to extrapolate to our neuronal in vivo model.

Published online Feb Author information Article notes Copyright and License information Disclaimer. Andrey S Tsvetkov: ude. Received Sep 29; Accepted Jan 7. This article is distributed under the terms of the Creative Commons Attribution License , which permits unrestricted use and redistribution provided that the original author and source are credited. This article has been cited by other articles in PMC. Transparent reporting form. Research organism: Mouse, Rat.

Open in a separate window. Figure 1. PQFS in the gene and the promoter sequence of autophagy genes. Figure 1—source data 1. Click here to view. Figure 2. Figure 3. Figure 4. Figure 4—figure supplement 1. PDS inhibits neuronal autophagy To confirm that autophagy is downregulated by PDS, we measured autophagic flux in live neurons.

Figure 5. PDS inhibits autophagy in cultured primary neurons. Figure 5—figure supplement 1. BRACO19 inhibits autophagy in cultured primary neurons. Figure 5—figure supplement 2. PDS induces accumulation of mutant huntingtin in cultured primary neurons from Huntington disease mice. Figure 5—figure supplement 3.

Figure 6. Mice treated with PDS develop memory deficits and aged-related symptoms. Figure 7. Brain samples from aged mice exhibit elevated levels of G4-DNA. Figure 8. The helicase Pif1 restores autophagy in PDS-treated neurons. Monchaud lab. Survival analysis We used automated microscopy and longitudinal analysis to determine neuronal survival.

HF2 binding assay HF2 antibody expression and purification were carried out as described Fernando et al. DNA-dynabeads affinity purification of proteins DNA-Dynabeads affinity purification of proteins was carried out as described Gao et al. Immunohistochemistry To determine and analyze G4 quadruples in brain samples from young and aged mice, frozen floating brain sections were incubated with antibodies against G4 BG4 overnight.

Novel object recognition test NORT The test is a standard test for recognition memory that is sensitive to aging. Statistical analysis For longitudinal survival analysis, neurons that died during the imaging interval were assigned a survival time the period between transfection and their disappearance from an image.

Funding Statement The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication. Additional information Competing interests No competing interests declared. Data curation, Formal analysis, Investigation, Methodology.

Resources, Data curation, Formal analysis, Investigation. Additional files Transparent reporting form Click here to view. Data availability All data generated or analysed during this study are included in the manuscript and supporting files. References Antunes M, Biala G. The novel object recognition memory: neurobiology, test procedure, and its modifications. Cognitive Processing. Inclusion body formation reduces levels of mutant huntingtin and the risk of neuronal death.

Automated microscope system for determining factors that predict neuronal fate. Epigenetic regulation of autophagy by the methyltransferase G9a. Molecular and Cellular Biology. Epigenetic control of autophagy: nuclear events gain more attention. Molecular Cell. Nature Chemical Biology. Nucleic Acids Research. Re-evaluation of G-quadruplex propensity with G4Hunter. Quantitative visualization of DNA G-quadruplex structures in human cells. Nature Chemistry.

DNA secondary structures: stability and function of G-quadruplex structures. Nature Reviews Genetics. Lipofuscin: mechanisms of age-related accumulation and influence on cell function. Polyethylene glycol binding alters human telomere G-quadruplex structure by conformational selection. Structure and function of Pif1 helicase. Biochemical Society Transactions. Spatial parkin translocation and degradation of damaged mitochondria via mitophagy in live cortical neurons.

Current Biology. High-throughput sequencing of DNA G-quadruplex structures in the human genome. Nature Biotechnology. Selective molecular alterations in the autophagy pathway in patients with lewy body disease and in models of alpha-synucleinopathy. Autophagy and aging: keeping that old broom working. Trends in Genetics. G-quadruplexes as novel cis-elements controlling transcription during embryonic development. Genome-wide analysis reveals regulatory role of G4 DNA in gene transcription.

Genome Research. Gene function correlates with potential for G4 DNA formation in the human genome. Induction of autophagy by spermidine promotes longevity. Nature Cell Biology. Nucleocytosolic depletion of the energy metabolite acetyl-coenzyme a stimulates autophagy and prolongs lifespan. Cell Metabolism. RNA G-Quadruplexes in biology: principles and molecular mechanisms. Journal of Molecular Biology.

Disruption of the beclin 1-BCL2 autophagy regulatory complex promotes longevity in mice. Selective recognition of a DNA G-quadruplex by an engineered antibody. Changes in neuronal DNA content variation in the human brain during aging.

Aging Cell. Journal of Neuroscience. Cracking the survival code: autophagy-related histone modifications. Molecular definitions of autophagy and related processes. Chemical Communications. Full-length human mutant huntingtin with a stable polyglutamine repeat can elicit progressive and selective neuropathogenesis in BACHD mice.

Guanines are a quartet's best friend: impact of base substitutions on the kinetics and stability of tetramolecular quadruplexes. The expanding biology of the C9orf72 nucleotide repeat expansion in neurodegenerative disease. Nature Reviews Neuroscience.

G-quadruplex structures mark human regulatory chromatin. Nature Genetics. Autophagy as a promoter of longevity: insights from model organisms. Nature Reviews Molecular Cell Biology. Regulation mechanisms and signaling pathways of autophagy. Annual Review of Genetics. G-quadruplexes in promoters throughout the human genome. A sensitive and quantitative technique for detecting autophagic events based on lysosomal delivery.

FEBS Journal. The interplay between G-quadruplex and transcription. Current Medicinal Chemistry. Guidelines for the use and interpretation of assays for monitoring autophagy 3rd edition Autophagy. Loss of autophagy in the central nervous system causes neurodegeneration in mice. Neuronal autophagy and intercellular regulation of homeostasis in the brain.

Current Opinion in Neurobiology. Autophagy-monitoring and autophagy-deficient mice. Silencing c-MYC expression by targeting quadruplex in P1 promoter using locked nucleic acid trap. Zinc-finger transcription factors are associated with guanine quadruplex motifs in human, chimpanzee, mouse and rat promoters genome-wide. Visualization of RNA-Quadruplexes in live cells. Journal of the American Chemical Society.

Scientific Reports. Transcriptional and epigenetic regulation of autophagy in aging. Genome-wide analysis reveals mechanisms modulating autophagy in normal brain aging and in Alzheimer's disease. From autophagy to mitophagy: the roles of P62 in neurodegenerative diseases. Journal of Bioenergetics and Biomembranes. Gene regulation and DNA damage in the ageing human brain.

EMBO Reports. The G4 genome. PLOS Genetics. G-quadruplexes and helicases. Thermal difference spectra: a specific signature for nucleic acid structures.

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His professional practice is connected with setting up and structuring of businesses. He also is a highly experienced expert in project finance and capital markets. Tzvetkov advised a number of large foreign and transnational corporations operating in Russia in the fuel and energy sector, processing and iron and steel industry. In particular, he participated in their restructuring, rendered support in major stock sales and purchases, structured management procedures with participation of several investors, advised on foreign direct investments and other corporate governance issues.

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Tzvetkov has considerable hands-on-experience in dispute resolution and handles real property disputes and bankruptcy proceedings before Russian courts at all levels. Yuri Tzvetkov is a member of the Moscow Bar Association. Contributed to the formation of foreign-owned companies and joint ventures in Russia, specifically a building materials JV and a crude transport equipment JV. Contributed to the legal support for a project of a major Russian manufacturer to set up joint ventures in the CIS.

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