Tunda Hidvegi

1.6k total citations
20 papers, 1.2k citations indexed

About

Tunda Hidvegi is a scholar working on Molecular Biology, Cell Biology and Epidemiology. According to data from OpenAlex, Tunda Hidvegi has authored 20 papers receiving a total of 1.2k indexed citations (citations by other indexed papers that have themselves been cited), including 8 papers in Molecular Biology, 6 papers in Cell Biology and 5 papers in Epidemiology. Recurrent topics in Tunda Hidvegi's work include Endoplasmic Reticulum Stress and Disease (6 papers), Autophagy in Disease and Therapy (5 papers) and HIV Research and Treatment (4 papers). Tunda Hidvegi is often cited by papers focused on Endoplasmic Reticulum Stress and Disease (6 papers), Autophagy in Disease and Therapy (5 papers) and HIV Research and Treatment (4 papers). Tunda Hidvegi collaborates with scholars based in United States, Hungary and Germany. Tunda Hidvegi's co-authors include Pamela Hale, David H. Perlmutter, David H. Perlmutter, Michael Ewing, Béla Z. Schmidt, Caroline S. Beckett, Amitava Mukherjee, Christine Dippold, Carolyn Kemp and Simon C. Watkins and has published in prestigious journals such as Science, Journal of Biological Chemistry and Journal of Clinical Investigation.

In The Last Decade

Tunda Hidvegi

20 papers receiving 1.2k citations

Peers

Tunda Hidvegi
Sayan Chakraborty United States
Ji-An Pan United States
Akiyuki Hada Japan
Carol A. Mercer United States
Norimasa Matsushita Japan
Liu-Ya Tang United States
Lakshmi Reddy Palam United States
Honglin Li United States
Joonsung Hwang South Korea
Wei Jia United States
Sayan Chakraborty United States
Tunda Hidvegi
Citations per year, relative to Tunda Hidvegi Tunda Hidvegi (= 1×) peers Sayan Chakraborty

Countries citing papers authored by Tunda Hidvegi

Since Specialization
Citations

This map shows the geographic impact of Tunda Hidvegi's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by Tunda Hidvegi with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Tunda Hidvegi more than expected).

Fields of papers citing papers by Tunda Hidvegi

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Tunda Hidvegi. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by Tunda Hidvegi. The network helps show where Tunda Hidvegi may publish in the future.

Co-authorship network of co-authors of Tunda Hidvegi

This figure shows the co-authorship network connecting the top 25 collaborators of Tunda Hidvegi. A scholar is included among the top collaborators of Tunda Hidvegi based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with Tunda Hidvegi. Tunda Hidvegi is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

20 of 20 papers shown
1.
Li, Jie, Francesca Moretti, Tunda Hidvegi, et al.. (2024). Multiple Genes Core to ERAD, Macroautophagy and Lysosomal Degradation Pathways Participate in the Proteostasis Response in α1-Antitrypsin Deficiency. Cellular and Molecular Gastroenterology and Hepatology. 17(6). 1007–1024. 1 indexed citations
2.
Tafaleng, Edgar N., Jie Li, Yan Wang, et al.. (2024). Variants in autophagy genes MTMR12 and FAM134A are putative modifiers of the hepatic phenotype in α1-antitrypsin deficiency. Hepatology. 80(4). 859–871. 3 indexed citations
3.
Wang, Yan, Murat Can Çobanoğlu, Jie Li, et al.. (2019). An analog of glibenclamide selectively enhances autophagic degradation of misfolded α1-antitrypsin Z. PLoS ONE. 14(1). e0209748–e0209748. 15 indexed citations
4.
Mukherjee, Amitava, et al.. (2018). NFκB mitigates the pathological effects of misfolded α1-antitrypsin by activating autophagy and an integrated program of proteostasis mechanisms. Cell Death and Differentiation. 26(3). 455–469. 14 indexed citations
5.
Hidvegi, Tunda, Donna B. Stolz, John F. Alcorn, et al.. (2015). Enhancing Autophagy with Drugs or Lung-directed Gene Therapy Reverses the Pathological Effects of Respiratory Epithelial Cell Proteinopathy. Journal of Biological Chemistry. 290(50). 29742–29757. 24 indexed citations
6.
Li, Jie, Stephen C. Pak, Linda P. O’Reilly, et al.. (2014). Fluphenazine Reduces Proteotoxicity in C. elegans and Mammalian Models of Alpha-1-Antitrypsin Deficiency. PLoS ONE. 9(1). e87260–e87260. 34 indexed citations
7.
Ding, Jianqiang, Govardhana Rao Yannam, Namita Roy‐Chowdhury, et al.. (2011). Spontaneous hepatic repopulation in transgenic mice expressing mutant human α1-antitrypsin by wild-type donor hepatocytes. Journal of Clinical Investigation. 121(5). 1930–1934. 61 indexed citations
8.
Hidvegi, Tunda, Amitava Mukherjee, Michael Ewing, Carolyn Kemp, & David H. Perlmutter. (2011). The Role of Autophagy in Alpha-1-Antitrypsin Deficiency. Methods in enzymology on CD-ROM/Methods in enzymology. 499. 33–54. 14 indexed citations
9.
Hidvegi, Tunda, Michael Ewing, Pamela Hale, et al.. (2010). An Autophagy-Enhancing Drug Promotes Degradation of Mutant α 1 -Antitrypsin Z and Reduces Hepatic Fibrosis. Science. 329(5988). 229–232. 463 indexed citations
10.
Hidvegi, Tunda, Károly Mirnics, Pamela Hale, et al.. (2007). Regulator of G Signaling 16 Is a Marker for the Distinct Endoplasmic Reticulum Stress State Associated with Aggregated Mutant α1-Antitrypsin Z in the Classical Form of α1-Antitrypsin Deficiency. Journal of Biological Chemistry. 282(38). 27769–27780. 58 indexed citations
11.
Kamimoto, Takahiro, Shisako Shoji, Tunda Hidvegi, et al.. (2005). Intracellular Inclusions Containing Mutant α1-Antitrypsin Z Are Propagated in the Absence of Autophagic Activity. Journal of Biological Chemistry. 281(7). 4467–4476. 207 indexed citations
12.
Hidvegi, Tunda, Béla Z. Schmidt, Pamela Hale, & David H. Perlmutter. (2005). Accumulation of Mutant α1-Antitrypsin Z in the Endoplasmic Reticulum Activates Caspases-4 and -12, NFκB, and BAP31 but Not the Unfolded Protein Response. Journal of Biological Chemistry. 280(47). 39002–39015. 189 indexed citations
13.
14.
Hidvegi, Tunda, Lilian Varga, F. Marañón, et al.. (1997). Comparative study of the complement-activating and specific IgE-binding properties of ragweed pollen allergen. Clinical & Experimental Immunology. 108(1). 122–127. 4 indexed citations
15.
Prohászka, Zoltán, Tunda Hidvegi, Eszter Újhelyi, et al.. (1995). Interaction of complement and specific antibodies with the external glycoprotein 120 of HIV-1.. PubMed. 85(2). 184–9. 18 indexed citations
16.
Füst, George, Zoltán Prohászka, Tunda Hidvegi, et al.. (1994). Competition of complement proteins and specific antibodies for binding to HIV-1 envelope antigens.. PubMed. 41 Suppl. 27–31. 2 indexed citations
17.
Hidvegi, Tunda, Zoltán Prohászka, Eszter Újhelyi, et al.. (1993). Studies on the mechanism of complement-mediated inhibition of antibody binding to HIV gp41. Clinical & Experimental Immunology. 94(3). 490–493. 13 indexed citations
18.
Füst, George, Eszter Újhelyi, Tunda Hidvegi, et al.. (1991). The Complement System in HIV Disease. Immunological Investigations. 20(2). 231–241. 12 indexed citations
19.
20.
Hidvegi, Tunda, et al.. (1985). Non-covalently bound C3 enhances lysis of rabbit erythrocytes through the alternative pathway.. PubMed. 56(4). 735–41. 3 indexed citations

Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.

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