Martin Böttcher

3.5k total citations · 1 hit paper
46 papers, 1.7k citations indexed

About

Martin Böttcher is a scholar working on Immunology, Molecular Biology and Genetics. According to data from OpenAlex, Martin Böttcher has authored 46 papers receiving a total of 1.7k indexed citations (citations by other indexed papers that have themselves been cited), including 23 papers in Immunology, 21 papers in Molecular Biology and 14 papers in Genetics. Recurrent topics in Martin Böttcher's work include Immune Cell Function and Interaction (14 papers), Immune cells in cancer (9 papers) and Chronic Lymphocytic Leukemia Research (8 papers). Martin Böttcher is often cited by papers focused on Immune Cell Function and Interaction (14 papers), Immune cells in cancer (9 papers) and Chronic Lymphocytic Leukemia Research (8 papers). Martin Böttcher collaborates with scholars based in Germany, United States and Switzerland. Martin Böttcher's co-authors include Dimitrios Mougiakakos, Andréas Mackensen, Regina Jitschin, Heiko Bruns, Georg Schett, Gerhard Krönke, Brenda Krishnacoumar, Jörg Hofmann, Sébastien Lucas and Olivia Albrecht and has published in prestigious journals such as Nature Communications, Blood and Cancer Research.

In The Last Decade

Martin Böttcher

42 papers receiving 1.7k 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.

Short-chain fatty acids regulate systemic bone mass and protect from pathological bone loss

2017 527 citations Sébastien Lucas, Yasunori Omata et al. Nature Communications profile →

Peers

Countries citing papers authored by Martin Böttcher

Since Specialization

Citations

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

Fields of papers citing papers by Martin Böttcher

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Martin Böttcher

This figure shows the co-authorship network connecting the top 25 collaborators of Martin Böttcher. A scholar is included among the top collaborators of Martin Böttcher 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 Martin Böttcher. Martin Böttcher 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

#	Title	Journal	Authors	Indexed citations
1	CAR T-cell therapy induces remission in multiorgan IgG4-related disease with hepatobiliary involvement	Journal of Hepatology	Verena Keitel, Michael C. Kreißl et al.	0
2	Metabolic T-cell phenotypes: from bioenergetics to function	American Journal of Physiology-Cell Physiology	Romy Loschinski, Martin Böttcher et al.	3
3	A network-based approach to overcome BCR::ABL1-independent resistance in chronic myeloid leukemia	Cell Communication and Signaling	Silvio Gualdi, Patrizia Chiusolo et al.	0
4	Increased PD-1 Expression on Circulating T Cells Correlates with Inferior Outcome after Autologous Stem Cell Transplantation	Transplantation and Cellular Therapy	Martin Böttcher, Andrej Stoll et al.	1
5	Activating mutations in JAK2 and CALR differentially affect intracellular calcium flux in store operated calcium entry	Cell Communication and Signaling	Tobias Franz, Martin Böttcher et al.	4
6	Oxidative DNA damage in reconstituting T cells is associated with relapse and inferior survival after allo-SCT	Blood	Chunguang Liang, Romy Loschinski et al.	8
7	Unveiling the signaling network of FLT3-ITD AML improves drug sensitivity prediction	eLife	Marta Iannuccelli, Patrizia Chiusolo et al.	5
8	Synergistic lethality in chronic myeloid leukemia – targeting oxidative phosphorylation and unfolded protein response effectively complements tyrosine kinase inhibitor treatment	BMC Cancer	Domenica Saul, Manuela Krumbholz et al.	2
9	Accumulation of T-cell-suppressive PD-L1^high extracellular vesicles is associated with GvHD and might impact GvL efficacy	Journal for ImmunoTherapy of Cancer	Franziska Karl, Romy Loschinski et al.	10
10	Effects of the STAMP-inhibitor asciminib on T cell activation and metabolic fitness compared to tyrosine kinase inhibition by imatinib, dasatinib, and nilotinib	Cancer Immunology Immunotherapy	Axel Karow, Kristin Mentz et al.	2
11	Pleiotropic effects of antibiotics on T cell metabolism and T cell-mediated immunity	Frontiers in Microbiology	Tobias Franz, Martin Böttcher et al.	11
12	The metabolic profile of reconstituting T-cells, NK-cells, and monocytes following autologous stem cell transplantation and its impact on outcome	Scientific Reports	Martin Böttcher, Simon Völkl et al.	5
13	Palmitoylated Proteins on AML-Derived Extracellular Vesicles Promote Myeloid-Derived Suppressor Cell Differentiation via TLR2/Akt/mTOR Signaling	Cancer Research	Martin Böttcher, Andrej Stoll et al.	49
14	Linking Immunoevasion and Metabolic Reprogramming in B-Cell–Derived Lymphomas	Frontiers in Oncology	Martin Böttcher, Andrej Stoll et al.	22
15	PPARδ-mediated mitochondrial rewiring of osteoblasts determines bone mass	Scientific Reports	Cornelia Stoll, Katrin Palumbo‐Zerr et al.	19
16	Selective PRMT5 Inhibitors Suppress Human CD8+ T Cells by Upregulation of p53 and Impairment of the AKT Pathway Similar to the Tumor Metabolite MTA	Molecular Cancer Therapeutics	Stefanie Schaffer, Simon Völkl et al.	25
17	Energy metabolism is co-determined by genetic variants in chronic lymphocytic leukemia and influences drug sensitivity	Haematologica	Junyan Lu, Martin Böttcher et al.	21
18	Inflammation-induced glycolytic switch controls suppressivity of mesenchymal stem cells via STAT1 glycosylation	Leukemia	Regina Jitschin, Martin Böttcher et al.	63
19	Short-chain fatty acids regulate systemic bone mass and protect from pathological bone loss breakdown →	Nature Communications	Sébastien Lucas, Yasunori Omata et al.	527
20	Reversibility of symptoms in a conditional mouse model of spinocerebellar ataxia type 3	Human Molecular Genetics	Jana Boy, Thorsten Schmidt et al.	83

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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