Matthias Stanke

718 total citations
9 papers, 605 citations indexed

About

Matthias Stanke is a scholar working on Cellular and Molecular Neuroscience, Molecular Biology and Genetics. According to data from OpenAlex, Matthias Stanke has authored 9 papers receiving a total of 605 indexed citations (citations by other indexed papers that have themselves been cited), including 5 papers in Cellular and Molecular Neuroscience, 4 papers in Molecular Biology and 3 papers in Genetics. Recurrent topics in Matthias Stanke's work include Nuclear Receptors and Signaling (2 papers), Neuropeptides and Animal Physiology (2 papers) and Congenital heart defects research (2 papers). Matthias Stanke is often cited by papers focused on Nuclear Receptors and Signaling (2 papers), Neuropeptides and Animal Physiology (2 papers) and Congenital heart defects research (2 papers). Matthias Stanke collaborates with scholars based in Germany, France and United States. Matthias Stanke's co-authors include Hermann Rohrer, Uwe Ernsberger, Markus Geißen, Marthe J. Howard, Xiaodong Wu, Carolin Schneider, Christo Goridis, Dirk Junghans, Herbert Zimmermann and Christian Gachet and has published in prestigious journals such as Development, Journal of Cell Science and Developmental Biology.

In The Last Decade

Matthias Stanke

9 papers receiving 601 citations

Peers

Matthias Stanke

MB

CMN

GENET

DN

NEURO

Emmanuelle Buhler France

K S Simburger United States

Perrine Gaub Canada

Mei-Ying Liang China

Fabrice Lisovoski France

Felicia Yu Hsuan Teng Singapore

Ming Sum Ruby Chiang United States

Javier Villadiego Spain

Francesca Viganò Germany

Erica Butti Italy

Emmanuelle Buhler France

Matthias Stanke

367 ×0.9

MB

298 ×1.4

CMN

117 ×0.9

GENET

77 ×0.9

DN

126 ×2.2

NEURO

Citations per year, relative to Matthias Stanke Matthias Stanke (= 1×) peers Emmanuelle Buhler

Countries citing papers authored by Matthias Stanke

Since Specialization

Citations

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

Fields of papers citing papers by Matthias Stanke

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Matthias Stanke

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

All Works

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9 of 9 papers shown

1.

Leib, Christoph, et al.. (2010). Knockdown of tissue nonspecific alkaline phosphatase impairs neural stem cell proliferation and differentiation. Neuroscience Letters. 485(3). 208–211. 53 indexed citations

2.

Ernsberger, Uwe, et al.. (2009). The bHLH transcription factor Hand2 is essential for the maintenance of noradrenergic properties in differentiated sympathetic neurons. Developmental Biology. 329(2). 191–200. 52 indexed citations

3.

Stanke, Matthias, et al.. (2009). Coordinate pathways for nucleotide and EGF signaling in cultured adult neural progenitor cells. Journal of Cell Science. 122(14). 2524–2533. 61 indexed citations

4.

Stanke, Matthias, Markus Geißen, Guido J. Burbach, et al.. (2005). Target-dependent specification of the neurotransmitter phenotype:cholinergic differentiation of sympathetic neurons is mediated in vivo by gp130 signaling. Development. 133(1). 141–150. 95 indexed citations

5.

Stanke, Matthias, Jutta Stubbusch, & Hermann Rohrer. (2004). Interaction of Mash1 and Phox2b in sympathetic neuron development. Molecular and Cellular Neuroscience. 25(3). 374–382. 32 indexed citations

6.

Patzke, Holger, Eva Reissmann, Matthias Stanke, John L. Bixby, & Uwe Ernsberger. (2001). BMP growth factors and Phox2 transcription factors can induce synaptotagmin I and neurexin I during sympathetic neuron development. Mechanisms of Development. 108(1-2). 149–159. 26 indexed citations

7.

Stanke, Matthias, Markus Geißen, Rudolf Götz, Uwe Ernsberger, & Hermann Rohrer. (2000). The early expression of VAChT and VIP in mouse sympathetic ganglia is not induced by cytokines acting through LIFRβ or CNTFRα. Mechanisms of Development. 91(1-2). 91–96. 21 indexed citations

8.

Howard, Marthe J., Matthias Stanke, Carolin Schneider, Xiaodong Wu, & Hermann Rohrer. (2000). The transcription factor dHAND is a downstream effector of BMPs in sympathetic neuron specification. Development. 127(18). 4073–4081. 129 indexed citations

9.

Stanke, Matthias, Dirk Junghans, Markus Geißen, et al.. (1999). The Phox2 homeodomain proteins are sufficient to promote the development of sympathetic neurons. Development. 126(18). 4087–4094. 136 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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