Silke E. Lindner

458 total citations
9 papers, 341 citations indexed

About

Silke E. Lindner is a scholar working on Molecular Biology, Oncology and Cancer Research. According to data from OpenAlex, Silke E. Lindner has authored 9 papers receiving a total of 341 indexed citations (citations by other indexed papers that have themselves been cited), including 9 papers in Molecular Biology, 4 papers in Oncology and 3 papers in Cancer Research. Recurrent topics in Silke E. Lindner's work include Cell death mechanisms and regulation (3 papers), Cancer-related Molecular Pathways (3 papers) and MicroRNA in disease regulation (3 papers). Silke E. Lindner is often cited by papers focused on Cell death mechanisms and regulation (3 papers), Cancer-related Molecular Pathways (3 papers) and MicroRNA in disease regulation (3 papers). Silke E. Lindner collaborates with scholars based in Austria, Germany and United States. Silke E. Lindner's co-authors include Leo D. Wang, Shereé M. Johnson, Christine E. Brown, Andreas Villunger, Sebastian Herzog, Moshe Oren, Eyal Gottlieb, Wei Gu, Christoph Borner and Fabian Schuler and has published in prestigious journals such as Nature Communications, Molecular Cell and Oncogene.

In The Last Decade

Silke E. Lindner

9 papers receiving 336 citations

Peers — A (Enhanced Table)

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

Name	h						Papers	Cites
Silke E. Lindner Austria	7	213	179	80	60	36	9	341
Shaochang Jia China	8	232 1.1×	137 0.8×	106 1.3×	86 1.4×	33 0.9×	18	400
Hubert Fleury Canada	11	224 1.1×	179 1.0×	69 0.9×	48 0.8×	44 1.2×	13	390
Mala K. Talekar United States	11	197 0.9×	203 1.1×	63 0.8×	25 0.4×	21 0.6×	17	372
Size Chen China	11	310 1.5×	178 1.0×	82 1.0×	169 2.8×	37 1.0×	29	483
Gunjan Dagar India	8	129 0.6×	156 0.9×	64 0.8×	25 0.4×	45 1.3×	16	283
Renske de Korte‐Grimmerink Netherlands	6	294 1.4×	294 1.6×	166 2.1×	101 1.7×	19 0.5×	6	537
Andrew A. Guirguis Australia	8	259 1.2×	207 1.2×	69 0.9×	51 0.8×	67 1.9×	12	410
Jing‐Ru Pang China	7	325 1.5×	118 0.7×	70 0.9×	94 1.6×	11 0.3×	11	387
Regina Lin United States	9	141 0.7×	119 0.7×	118 1.5×	88 1.5×	28 0.8×	13	314

Countries citing papers authored by Silke E. Lindner

Since Specialization

Citations

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

Fields of papers citing papers by Silke E. Lindner

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Silke E. Lindner. 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 Silke E. Lindner. The network helps show where Silke E. Lindner may publish in the future.

Co-authorship network of co-authors of Silke E. Lindner

This figure shows the co-authorship network connecting the top 25 collaborators of Silke E. Lindner. A scholar is included among the top collaborators of Silke E. Lindner 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 Silke E. Lindner. Silke E. Lindner 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

Lindner, Silke E., et al.. (2022). The miR-26 family regulates early B cell development and transformation. Life Science Alliance. 5(8). e202101303–e202101303. 9 indexed citations

Lindner, Silke E., et al.. (2020). Arhgap25 Deficiency Leads to Decreased Numbers of Peripheral Blood B Cells and Defective Germinal Center Reactions. ImmunoHorizons. 4(5). 274–281. 4 indexed citations

Lindner, Silke E., Shereé M. Johnson, Christine E. Brown, & Leo D. Wang. (2020). Chimeric antigen receptor signaling: Functional consequences and design implications. Science Advances. 6(21). eaaz3223–eaaz3223. 109 indexed citations

Lindner, Silke E., et al.. (2017). The miR‐15 family reinforces the transition from proliferation to differentiation in pre‐B cells. EMBO Reports. 18(9). 1604–1617. 31 indexed citations

Schuler, Fabian, Silke E. Lindner, Sebastian Herzog, et al.. (2017). Checkpoint kinase 1 is essential for normal B cell development and lymphomagenesis. Nature Communications. 8(1). 1697–1697. 27 indexed citations

Lindner, Silke E., et al.. (2015). MAP3K11 is a tumor suppressor targeted by the oncomiR miR-125b in early B cells. Cell Death and Differentiation. 23(2). 242–252. 25 indexed citations

Lindner, Silke E., Manuela Wissler, Albert Gründer, et al.. (2013). Increased leukocyte survival and accelerated onset of lymphoma in the absence of MCL-1 S159-phosphorylation. Oncogene. 33(44). 5221–5224. 6 indexed citations

Charvet, Céline, Manuela Wissler, Prisca Brauns‐Schubert, et al.. (2011). Phosphorylation of Tip60 by GSK-3 Determines the Induction of PUMA and Apoptosis by p53. Molecular Cell. 42(5). 584–596. 104 indexed citations

Gottlieb, Eyal, Silke E. Lindner, & Moshe Oren. (1996). Relationship of sequence-specific transactivation and p53-regulated apoptosis in interleukin 3-dependent hematopoietic cells.. PubMed. 7(3). 301–10. 26 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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