Matija Hedl

7.5k total citations · 1 hit paper
37 papers, 2.0k citations indexed

About

Matija Hedl is a scholar working on Immunology, Molecular Biology and Genetics. According to data from OpenAlex, Matija Hedl has authored 37 papers receiving a total of 2.0k indexed citations (citations by other indexed papers that have themselves been cited), including 30 papers in Immunology, 11 papers in Molecular Biology and 9 papers in Genetics. Recurrent topics in Matija Hedl's work include Immune cells in cancer (16 papers), Immune Cell Function and Interaction (13 papers) and Inflammatory Bowel Disease (9 papers). Matija Hedl is often cited by papers focused on Immune cells in cancer (16 papers), Immune Cell Function and Interaction (13 papers) and Inflammatory Bowel Disease (9 papers). Matija Hedl collaborates with scholars based in United States, Germany and Australia. Matija Hedl's co-authors include Clara Abraham, Judy H. Cho, Jing Li, Jie Yan, Amit Lahiri, Victor W. Rodwell, Wei Zhang, Lidia Bosurgi, Richard A. Flavell and David M. Valenzuela and has published in prestigious journals such as Nature, Proceedings of the National Academy of Sciences and Journal of Biological Chemistry.

In The Last Decade

Matija Hedl

37 papers receiving 1.9k citations

Hit Papers

align trajectories

What are hit papers?

Hit papers significantly outperform the citation benchmark for their cohort. A paper qualifies if it has ≥500 total citations, achieves ≥1.5× the top-1% citation threshold for papers in the same subfield and year (this is the minimum needed to enter the top 1%, not the average within it), or reaches the top citation threshold in at least one of its specific research topics.

IL-22BP is regulated by the inflammasome and modulates tumorigenesis in the intestine

2012 583 citations Samuel Huber, Nicola Gagliani et al. Nature profile →

Peers

Countries citing papers authored by Matija Hedl

Since Specialization

Citations

This map shows the geographic impact of Matija Hedl'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 Matija Hedl with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Matija Hedl more than expected).

Fields of papers citing papers by Matija Hedl

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Matija Hedl. 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 Matija Hedl. The network helps show where Matija Hedl may publish in the future.

Co-authorship network of co-authors of Matija Hedl

This figure shows the co-authorship network connecting the top 25 collaborators of Matija Hedl. A scholar is included among the top collaborators of Matija Hedl 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 Matija Hedl. Matija Hedl is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

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20 of 20 papers shown

#	Work	Indexed citations
1	The E3 ubiquitin ligase RNF186 and RNF186 risk variants regulate innate receptor-induced outcomes 2021 ·Proceedings of the National Academy of Sciences ·Kishu Ranjan, Matija Hedl, Clara Abraham	9
2	Ubiquitination of ATF6 by disease-associated RNF186 promotes the innate receptor-induced unfolded protein response 2021 ·Journal of Clinical Investigation ·Kishu Ranjan, Matija Hedl, (unknown), Xuchen Zhang, Clara Abraham	23
3	TNFSF15 Promotes Antimicrobial Pathways in Human Macrophages and These Are Modulated by TNFSF15 Disease-Risk Variants 2020 ·Cellular and Molecular Gastroenterology and Hepatology ·Rui Sun, Matija Hedl, Clara Abraham	17
4	Myeloid Cell–Intrinsic IRF5 Promotes T Cell Responses through Multiple Distinct Checkpoints In Vivo, and IRF5 Immune-Mediated Disease Risk Variants Modulate These Myeloid Cell Functions 2020 ·The Journal of Immunology ·Jie Yan, Matija Hedl, Clara Abraham	6
5	Disease Risk–Associated Genetic Variants in STAT1 and STAT4 Function in a Complementary Manner to Increase Pattern-Recognition Receptor–Induced Outcomes in Human Macrophages 2020 ·The Journal of Immunology ·Matija Hedl, Rui Sun, Clara Abraham	11
6	LACC1 Required for NOD2-Induced, ER Stress-Mediated Innate Immune Outcomes in Human Macrophages and LACC1 Risk Variants Modulate These Outcomes 2019 ·Cell Reports ·Chen Huang, Matija Hedl, Kishu Ranjan, Clara Abraham	25
7	Twist1 and Twist2 Induce Human Macrophage Memory upon Chronic Innate Receptor Treatment by HDAC-Mediated Deacetylation of Cytokine Promoters 2019 ·The Journal of Immunology ·Rui Sun, Matija Hedl, Clara Abraham	13
8	ErbB4 signaling stimulates pro-inflammatory macrophage apoptosis and limits colonic inflammation 2017 ·Cell Death and Disease ·Michael A. Schumacher, Matija Hedl, Clara Abraham, Jessica K. Bernard, (unknown), (unknown), Dana Almohazey, (unknown), Shivesh Punit, Peter J. Dempsey, Mark R. Frey	77
9	Human LACC1 increases innate receptor-induced responses and a LACC1 disease-risk variant modulates these outcomes 2017 ·Nature Communications ·Amit Lahiri, Matija Hedl, Jie Yan, Clara Abraham	56
10	IRF5 and IRF5 Disease-Risk Variants Increase Glycolysis and Human M1 Macrophage Polarization by Regulating Proximal Signaling and Akt2 Activation 2016 ·Cell Reports ·Matija Hedl, Jie Yan, Clara Abraham	86
11	Pattern Recognition Receptor Signaling in Human Dendritic Cells is Enhanced by ICOS Ligand and Modulated by the Crohn’s Disease ICOSLG Risk Allele 2014 ·Immunity ·Matija Hedl, Amit Lahiri, Kaida Ning, Judy H. Cho, Clara Abraham	59
12	Negative regulation of human mononuclear phagocyte function 2013 ·Mucosal Immunology ·Matija Hedl, Clara Abraham	13
13	NLRP1 and NLRP3 inflammasomes are essential for distinct outcomes of decreased cytokines but enhanced bacterial killing upon chronic Nod2 stimulation 2013 ·American Journal of Physiology-Gastrointestinal and Liver Physiology ·Matija Hedl, Clara Abraham	27
14	IL-22BP is regulated by the inflammasome and modulates tumorigenesis in the intestine breakdown → 2012 ·Nature ·Samuel Huber, Nicola Gagliani, Lauren A. Zenewicz, Francis J. Huber, Lidia Bosurgi, Bo Hu, Matija Hedl, Wei Zhang, William O’Connor, Andrew Murphy, David M. Valenzuela, George D. Yancopoulos, Carmen J. Booth, Judy H. Cho, Wenjun Ouyang, Clara Abraham, Richard A. Flavell	583
15	Distinct Roles for Nod2 Protein and Autocrine Interleukin-1β in Muramyl Dipeptide-induced Mitogen-activated Protein Kinase Activation and Cytokine Secretion in Human Macrophages 2011 ·Journal of Biological Chemistry ·Matija Hedl, Clara Abraham	54
16	Secretory Mediators Regulate Nod2-Induced Tolerance in Human Macrophages 2010 ·Gastroenterology ·Matija Hedl, Clara Abraham	58
17	Chronic stimulation of Nod2 mediates tolerance to bacterial products 2007 ·Proceedings of the National Academy of Sciences ·Matija Hedl, Jing Li, Judy H. Cho, Clara Abraham	214
18	Inhibition of the Class II HMG–CoA reductase of Pseudomonas mevalonii 2004 ·Protein Science ·Matija Hedl, Victor W. Rodwell	16
19	Enterococcus faecalis mevalonate kinase 2004 ·Protein Science ·Matija Hedl, Victor W. Rodwell	11
20	3-Hydroxy-3-methylglutaryl-CoA Reductase 2000 ·Methods in enzymology on CD-ROM/Methods in enzymology ·Victor W. Rodwell, Michael J. Beach, Kenneth M. Bischoff, Daniel A. Bochar, Bryant G. Darnay, Jon A. Friesen, J F Gill, Matija Hedl, (unknown), Peter J. Kennelly, (unknown), Yuli Wang	29

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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