!!Tibor Vellai - Publications
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__10 major publications (number of citations based on Google Scholar):__\\
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1. Sturm Á, Saskői É, Hotzi B, Tarnóci A, Barna J, Bodnár F, Sharma H, Kovács T, Ari E, Weinhardt N, Kerepesi C, Perczel A, Ivics Z, Vellai T. Downregulation of transposable elements extends lifespan in Caenorhabditis elegans. Nat. Commun. 14(1):5278 (2023). (PMID: 37644049, IF: 16.6, D1, citations: 3) [[Uncovering the role of transposable elements in aging and the role of N6-adenine methylation in the progressive mobilization of transposable elements during aging. These data may lead to the exploration of the mechanism of aging: transposable elements are effectively inhibited in non-aging cells, while become increasingly mobilized in aging cells during lifespan, causing a significant level of genomic instability at advanced ages.]\\
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2. Csabai L, Fazekas D, Kadlecsik T, Szalay-Bekő M, Bohár B, Madgwick M, Módos D, Ölbei M, Gul L, Sudhakar P, Kubisch J, Oyeyemi OJ, Liska O, Ari E, Hotzi B, Billes VA, Molnár E, Földvári-Nagy L, Csályi K, Demeter A, Pápai N, Koltai M, Varga M, Lenti K, Farkas IJ, Türei D, Csermely P, Vellai T, Korcsmáros T. SignaLink3: a multi-layered resource to uncover tissue-specific signaling networks. Nucleic Acids Res. 50(D1):D701-D709 (2021). (PMID: 34634810, IF: 16.971, D1, citations: 19) [[SignaLink database was developed to identify tissue-specific signalling networks and novel signalling crosstalk.]\\
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3. Kovács T, Szinyákovics J, Billes V, Murányi G, Varga VB, Bjelik A, Légrádi Á, Szabó M, Sándor S, Kubinyi E, Szekeres-Paracky C, Szocsics P, Lőke J, Mulder J, Gulyás B, Renner É, Palkovits M, Gulya K, Maglóczky Z, Vellai T. A conserved MTMR lipid phosphatase increasingly suppresses autophagy in brain neurons during aging. Sci. Rep. 12(1):21817 (2022). (PMID: 36528685, IF: 4.6, D1, citations: 3) [[According to the study, neuronal aging is genetically determined because endogenous pro-aging factors such as MTMR14-like lipid phosphatases and Rubicon gradually lower the activity of autophagy during adulthood.]\\
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4. Vellai T. How the amino acid leucine activates the key cell-growth regulator mTOR. Nature 596(7871):192-194 (2021). (PMID: 34290413, IF: 69.504, D1, citations: 29) [[Recognizing that TOR – target-of rapamycin – kinase senses the intracellular levels of amino acids only that are used in the highest quantities in proteins. These amino acids, Ser, Leu and Arg, are determined by the largest number of codons, six in total.]\\
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5. Billes V, Kovács T, Manzéger A, Lőrincz P, Szincsák S, Regős Á, Kulcsár PI, Korcsmáros T, Lukácsovich T, Hoffmann G, Erdélyi M, Mihály J, Takács-Vellai K, Sass M, Vellai T. Developmentally regulated autophagy is required for eye formation in Drosophila. Autophagy 14(9):1499-1519 (2018). (PMID: 29940806, IF: 11.1, D1, citations: 20) The paper shows that certain autophagy genes are regulated by specific Hox proteins, master regulators of early development, during eye development in Drosophila. In addition, a compensatory mechanism was explored by which autophagy gene mutants can survive and develop normally.]\\
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6. Sturm Á, Saskői É, Kovács T, Weinhardt N, Vellai T. Highly efficient RNAi and Cas9-based auto-cloning systems for C. elegans research. Nucleic Acids Res. 46(17):e105 (2018). (PMID: 29924347, IF: 11.561, D1, citations: 40) [[A novel, highly efficient RNA interference method for C. elegans genetics was developed, and also an auto-cloning method that is free of in vitro enzymatic reaction was created.]\\
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7. Hargitai B, Kutnyánszky V, Blauwkamp TA, Steták A, Csankovszki G, Takács-Vellai K, Vellai T. xol-1, the master sex switch gene in C. elegans, is a transcriptional target of the terminal sex-determining factor TRA-1/GLI. Development 136(23):3881-3887 (2009). (PMID: 19906855, IF: 7.194, D1, citations: 30) [[Dosage compensation enigma in the nematode Caenorhabditis elegans: if the master sex switch gene xol-1 is inhibited by X-linked genes in individuals with two X chromosomes (hermaphrodites), but not in individual with one X chromosome (males), and this repression allows the dosage compensation machinery to reduce the activity of X-linked genes by half, how xol-1 repression could be maintained in hermaphrodites during the entire life. The authors demonstrated that xol-1 is transcriptionally repressed by TRA-1, the terminal effector of the sex-determining pathway, which is autosomally encoded.]\\
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8. Tóth ML, Sigmond T, Borsos É, Barna J, Erdélyi P, Takács-Vellai K, Orosz L, Kovács AL, Csikós G, Sass M, Vellai T. Longevity pathways converge on autophagy genes to regulate life span in Caenorhabditis elegans. Autophagy 4(3):330-338 (2008). (PMID: 18219227, IF: 5.479, D1, citations: 480) [[Here the central role of autophagy in aging control is demonstrated. The authors show  that distinct longevity pathways including TOR signaling, insulin/IGF1 signaling and mitochondrial respiration converge on the autophagic gene cascade to modulate the rate at which cells age.]\\
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9. Takács-Vellai K, Vellai T, Puoti A, Passannante M, Wicky C, Streit A, Kovács AL, Müller F. Inactivation of the autophagy gene bec-1 triggers apoptotic cell death in C. elegans. Curr. Biol. 15(16):1513-1517 (2005). (PMID: 16111945, IF: 11.732, D1, citations: 289) [[The authors isolated the first autophagy defective C. elegans mutant strains, and showed that BEC-1, the nematode ortholog of human Beclin 1 (Bcl2-interacting) autophagy protein, influences apoptotic cell death by interacting with CED-9/Bcl2, the major pro-apoptotic factor in nematodes. Hence, the apoptotuic and autophagic pathways are interconnected by BEC-1/Beclin 1 proteins.]\\
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10. Vellai T, Takács-Vellai K, Zhang Y, Kovács AL, Orosz L, Müller F. Influence of TOR kinase on lifespan in C. elegans. Nature 426(6967):620 (2003). (PMID: 14668850, IF: 30.979, D1, citations: 1280) The authors revealed the role of TOR – target-of-rapamycin – kinase in the regulation of aging in C. elegans. Until now, TOR is the only protein whose aging function has been proven in all major aging models, yeast, nematodes, flies and mice. They also showed that TOR kinase and the insulin/IGF-1 genetic pathway form a shared signaling axis to determine lifespan.]\\
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__Number of peer reviewed articles in referred journals:__ 99\\
__Number of D1 articles: 56, and number of Q1 articles:__ 22\\
__Number of book chapters:__ 2\\
__Number of citations:__ 18598 (Google Scholar)\\
__H-index:__ 38 (Google Scholar)\\ \\[{ALLOW view All}][{ALLOW edit tvellai}][{ALLOW upload tvellai}][{ALLOW comment All}]