Julius A. Steinbeck

2.4k total citations
15 papers, 1.8k citations indexed

About

Julius A. Steinbeck is a scholar working on Molecular Biology, Developmental Neuroscience and Cellular and Molecular Neuroscience. According to data from OpenAlex, Julius A. Steinbeck has authored 15 papers receiving a total of 1.8k indexed citations (citations by other indexed papers that have themselves been cited), including 11 papers in Molecular Biology, 6 papers in Developmental Neuroscience and 5 papers in Cellular and Molecular Neuroscience. Recurrent topics in Julius A. Steinbeck's work include Pluripotent Stem Cells Research (9 papers), Neurogenesis and neuroplasticity mechanisms (6 papers) and CRISPR and Genetic Engineering (5 papers). Julius A. Steinbeck is often cited by papers focused on Pluripotent Stem Cells Research (9 papers), Neurogenesis and neuroplasticity mechanisms (6 papers) and CRISPR and Genetic Engineering (5 papers). Julius A. Steinbeck collaborates with scholars based in United States, Germany and Italy. Julius A. Steinbeck's co-authors include Lorenz Studer, Philipp Koch, Oliver Brüstle, Julia Ladewig, Thoralf Opitz, David Sulzer, Jason Tchieu, Elizabeth L. Calder, Peter A. Goldstein and Ana Mrejeru and has published in prestigious journals such as Nature, Proceedings of the National Academy of Sciences and Nature Communications.

In The Last Decade

Julius A. Steinbeck

15 papers receiving 1.8k citations

Author Peers

Peers are selected by citation overlap in the author's most active subfields. citations · hero ref

Author Last Decade Papers Cites
Julius A. Steinbeck 1.1k 726 392 249 245 15 1.8k
Barbara S. Mallon 1.3k 1.2× 561 0.8× 471 1.2× 252 1.0× 262 1.1× 38 2.3k
Lixiang Ma 1.7k 1.6× 694 1.0× 459 1.2× 171 0.7× 144 0.6× 61 2.3k
Tong Zang 1.3k 1.3× 605 0.8× 621 1.6× 154 0.6× 98 0.4× 30 1.9k
Dustin R. Wakeman 1.5k 1.4× 946 1.3× 524 1.3× 90 0.4× 332 1.4× 19 2.0k
Dong‐Youn Hwang 1.4k 1.3× 868 1.2× 241 0.6× 85 0.3× 230 0.9× 58 2.1k
Lachlan H. Thompson 1.5k 1.4× 1.5k 2.0× 636 1.6× 143 0.6× 465 1.9× 81 2.5k
Kathrin Hemmer 1.1k 1.0× 487 0.7× 358 0.9× 93 0.4× 201 0.8× 18 1.5k
Marcel M. Daadi 794 0.7× 673 0.9× 715 1.8× 267 1.1× 185 0.8× 52 1.6k
Sara Patel 805 0.8× 579 0.8× 495 1.3× 218 0.9× 108 0.4× 24 1.7k
Afsaneh Gaillard 1.4k 1.3× 1.2k 1.7× 1.0k 2.7× 206 0.8× 216 0.9× 61 2.5k

Countries citing papers authored by Julius A. Steinbeck

Since Specialization
Citations

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

Fields of papers citing papers by Julius A. Steinbeck

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Julius A. Steinbeck. 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 Julius A. Steinbeck. The network helps show where Julius A. Steinbeck may publish in the future.

Co-authorship network of co-authors of Julius A. Steinbeck

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

All Works

15 of 15 papers shown
1.
Tchieu, Jason, Elizabeth L. Calder, Eveline Gutzwiller, et al.. (2019). NFIA is a gliogenic switch enabling rapid derivation of functional human astrocytes from pluripotent stem cells. Nature Biotechnology. 37(3). 267–275. 150 indexed citations
2.
Zimmer, Bastian, Oliver Harschnitz, Yoon Seung Lee, et al.. (2018). Human iPSC-derived trigeminal neurons lack constitutive TLR3-dependent immunity that protects cortical neurons from HSV-1 infection. Proceedings of the National Academy of Sciences. 115(37). E8775–E8782. 56 indexed citations
3.
Poppe, Daniel, Jonas Doerr, Marion Schneider, et al.. (2018). Genome Editing in Neuroepithelial Stem Cells to Generate Human Neurons with High Adenosine-Releasing Capacity. Stem Cells Translational Medicine. 7(6). 477–486. 10 indexed citations
4.
Fattahi, Faranak, Julius A. Steinbeck, Sonja Kriks, et al.. (2016). Deriving human ENS lineages for cell therapy and drug discovery in Hirschsprung disease. Nature. 531(7592). 105–109. 218 indexed citations
5.
Steinbeck, Julius A., Manoj Kumar Jaiswal, Elizabeth L. Calder, et al.. (2015). Functional Connectivity under Optogenetic Control Allows Modeling of Human Neuromuscular Disease. Cell stem cell. 18(1). 134–143. 89 indexed citations
6.
Calder, Elizabeth L., Jason Tchieu, Julius A. Steinbeck, et al.. (2015). Retinoic Acid-Mediated Regulation of GLI3 Enables Efficient Motoneuron Derivation from Human ESCs in the Absence of Extrinsic SHH Activation. Journal of Neuroscience. 35(33). 11462–11481. 23 indexed citations
7.
Steinbeck, Julius A., Se Joon Choi, Ana Mrejeru, et al.. (2015). Optogenetics enables functional analysis of human embryonic stem cell–derived grafts in a Parkinson's disease model. Nature Biotechnology. 33(2). 204–209. 233 indexed citations
8.
Steinbeck, Julius A. & Lorenz Studer. (2015). Moving Stem Cells to the Clinic: Potential and Limitations for Brain Repair. Neuron. 86(1). 187–206. 110 indexed citations
9.
Cebrián, Carolina, Fabio A. Zucca, Pierluigi Mauri, et al.. (2014). MHC-I expression renders catecholaminergic neurons susceptible to T-cell-mediated degeneration. Nature Communications. 5(1). 3633–3633. 262 indexed citations
10.
Steinbeck, Julius A., Nadine Henke, Joanna Gruszczynska‐Biegala, et al.. (2011). Store-operated calcium entry modulates neuronal network activity in a model of chronic epilepsy. Experimental Neurology. 232(2). 185–194. 64 indexed citations
11.
Steinbeck, Julius A., Philipp Koch, Amin Derouiche, & Oliver Brüstle. (2011). Human embryonic stem cell-derived neurons establish region-specific, long-range projections in the adult brain. Cellular and Molecular Life Sciences. 69(3). 461–470. 46 indexed citations
12.
Koch, Philipp, Thoralf Opitz, Julius A. Steinbeck, Julia Ladewig, & Oliver Brüstle. (2009). A rosette-type, self-renewing human ES cell-derived neural stem cell with potential for in vitro instruction and synaptic integration. Proceedings of the National Academy of Sciences. 106(9). 3225–3230. 381 indexed citations
13.
Testa, Giuseppe, Lodovica Borghese, Julius A. Steinbeck, & Oliver Brüstle. (2007). Breakdown of the Potentiality Principle and Its Impact on Global Stem Cell Research. Cell stem cell. 1(2). 153–156. 18 indexed citations
14.
Steinbeck, Julius A., Theresa A. Lusardi, Philipp Koch, et al.. (2007). Suppression of kindling epileptogenesis by adenosine releasing stem cell-derived brain implants. Brain. 130(5). 1276–1288. 129 indexed citations
15.
Steinbeck, Julius A. & Axel Methner. (2005). Translational Downregulation of the Noncatalytic Growth Factor Receptor TrkB.T1 by Ischemic Preconditioning of Primary Neurons. Gene Expression. 12(2). 99–106. 9 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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