Barbara Stiller

2.3k total citations · 1 hit paper
12 papers, 1.5k citations indexed

About

Barbara Stiller is a scholar working on Cell Biology, Neurology and Physiology. According to data from OpenAlex, Barbara Stiller has authored 12 papers receiving a total of 1.5k indexed citations (citations by other indexed papers that have themselves been cited), including 6 papers in Cell Biology, 5 papers in Neurology and 5 papers in Physiology. Recurrent topics in Barbara Stiller's work include Parkinson's Disease Mechanisms and Treatments (5 papers), Autophagy in Disease and Therapy (4 papers) and Endoplasmic Reticulum Stress and Disease (3 papers). Barbara Stiller is often cited by papers focused on Parkinson's Disease Mechanisms and Treatments (5 papers), Autophagy in Disease and Therapy (4 papers) and Endoplasmic Reticulum Stress and Disease (3 papers). Barbara Stiller collaborates with scholars based in United States, Germany and France. Barbara Stiller's co-authors include Christian Kubisch, André Heimbach, Jan Gründemann, Alfredo Ramı́rez, L. Pablo Cid, Birgit Liss, Meliha Karsak, A. S. Najim Al-Din, Ammar F. Mubaidin and Axel M. Hillmer and has published in prestigious journals such as Journal of Biological Chemistry, Nature Genetics and Journal of Neuroscience.

In The Last Decade

Barbara Stiller

11 papers receiving 1.4k 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.

Hereditary parkinsonism with dementia is caused by mutations in ATP13A2, encoding a lysosomal type 5 P-type ATPase

2006 881 citations Alfredo Ramı́rez, André Heimbach et al. Nature Genetics profile →

Peers — A (Enhanced Table)

Peers by citation overlap · career bar shows stage (early→late) cites · hero ref

Name	h						Papers	Cites
Barbara Stiller United States	11	810	511	483	376	346	12	1.5k
Adamantios Mamais United States	22	1.0k 1.3×	552 1.1×	610 1.3×	284 0.8×	300 0.9×	33	1.6k
A. Kathrin Lutz Germany	6	821 1.0×	878 1.7×	390 0.8×	481 1.3×	452 1.3×	6	1.6k
Ammar F. Mubaidin Jordan	4	605 0.7×	395 0.8×	275 0.6×	198 0.5×	293 0.8×	7	1.1k
Sara Sáez-Atiénzar United States	16	503 0.6×	482 0.9×	356 0.7×	206 0.5×	174 0.5×	24	1.2k
Emilie Giaime United States	12	797 1.0×	539 1.1×	375 0.8×	342 0.9×	345 1.0×	15	1.3k
Álvaro Sánchez-Martínez United Kingdom	17	529 0.7×	765 1.5×	398 0.8×	579 1.5×	228 0.7×	26	1.5k
Hervé Rhinn United States	15	485 0.6×	512 1.0×	527 1.1×	115 0.3×	197 0.6×	25	1.5k
Insup Choi United States	18	515 0.6×	409 0.8×	325 0.7×	269 0.7×	301 0.9×	21	1.2k
Amanda M. Gysbers Australia	11	818 1.0×	260 0.5×	520 1.1×	218 0.6×	282 0.8×	11	1.2k
Evy Lobbestael Belgium	22	1.1k 1.3×	892 1.7×	403 0.8×	118 0.3×	320 0.9×	33	1.7k

Countries citing papers authored by Barbara Stiller

Since Specialization

Citations

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

Fields of papers citing papers by Barbara Stiller

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Barbara Stiller

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

All Works

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12 of 12 papers shown

Cai, Zhengnan, Martin Brenner, Christian Winter, et al.. (2025). Hesperetin Protects from Palmitic-Acid-Induced Lipotoxicity through the Inhibition of Glutaminolysis, mTORC1 Signaling, and Limited Apoptosis. Journal of Agricultural and Food Chemistry. 73(35). 21932–21946.

Krause, Gregory J., Philipp Kirchner, Barbara Stiller, et al.. (2023). Molecular determinants of the crosstalk between endosomal microautophagy and chaperone-mediated autophagy. Cell Reports. 42(12). 113529–113529. 17 indexed citations

Schunkert, Heribert, Moritz von Scheidt, Thorsten Kessler, et al.. (2018). Genetics of coronary artery disease in the light of genome-wide association studies. Clinical Research in Cardiology. 107(S2). 2–9. 37 indexed citations

Fazeli, Walid, Peter Herkenrath, Barbara Stiller, et al.. (2017). A TUBB6 mutation is associated with autosomal dominant non-progressive congenital facial palsy, bilateral ptosis and velopharyngeal dysfunction. Human Molecular Genetics. 26(20). 4055–4066. 15 indexed citations

Caballero, Benjamı́n, Yipeng Wang, Antonio Díaz, et al.. (2017). Interplay of pathogenic forms of human tau with different autophagic pathways. Aging Cell. 17(1). 150 indexed citations

Morozova, Kateryna, Cristina C. Clement, Susmita Kaushik, et al.. (2016). Structural and Biological Interaction of hsc-70 Protein with Phosphatidylserine in Endosomal Microautophagy. Journal of Biological Chemistry. 291(35). 18096–18106. 55 indexed citations

Stiller, Barbara, et al.. (2016). Increased copper toxicity in Saccharomyces cerevisiae lacking VPS35, a component of the retromer and monogenic Parkinson disease gene in humans. Biochemical and Biophysical Research Communications. 476(4). 528–533. 10 indexed citations

Kett, Lauren R., Barbara Stiller, Inmaculada Tasset, et al.. (2015). α-Synuclein-Independent Histopathological and Motor Deficits in Mice Lacking the Endolysosomal Parkinsonism Protein Atp13a2. Journal of Neuroscience. 35(14). 5724–5742. 79 indexed citations

Park, Jin‐Sung, Prachi Mehta, Antony A. Cooper, et al.. (2011). Pathogenic effects of novel mutations in the P‐type ATPase ATP13A2 ( PARK9 ) causing Kufor‐Rakeb syndrome, a form of early‐onset parkinsonism. Human Mutation. 32(8). 956–964. 97 indexed citations

10.

Schmidt, Karyn, Devin M. Wolfe, Barbara Stiller, & David A. Pearce. (2009). Cd2+, Mn2+, Ni2+ and Se2+ toxicity to Saccharomyces cerevisiae lacking YPK9p the orthologue of human ATP13A2. Biochemical and Biophysical Research Communications. 383(2). 198–202. 100 indexed citations

11.

Raković, Aleksandar, Barbara Stiller, Ana Djarmati, et al.. (2008). Genetic association study of the P‐type ATPase ATP13A2 in late‐onset Parkinson's disease. Movement Disorders. 24(3). 429–433. 10 indexed citations

12.

Ramı́rez, Alfredo, André Heimbach, Jan Gründemann, et al.. (2006). Hereditary parkinsonism with dementia is caused by mutations in ATP13A2, encoding a lysosomal type 5 P-type ATPase. Nature Genetics. 38(10). 1184–1191. 881 indexed citations breakdown →

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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