Michael D. Bern

1.4k total citations · 1 hit paper
14 papers, 1.0k citations indexed

About

Michael D. Bern is a scholar working on Immunology, Epidemiology and Molecular Biology. According to data from OpenAlex, Michael D. Bern has authored 14 papers receiving a total of 1.0k indexed citations (citations by other indexed papers that have themselves been cited), including 11 papers in Immunology, 4 papers in Epidemiology and 2 papers in Molecular Biology. Recurrent topics in Michael D. Bern's work include Immune Cell Function and Interaction (10 papers), T-cell and B-cell Immunology (6 papers) and IL-33, ST2, and ILC Pathways (3 papers). Michael D. Bern is often cited by papers focused on Immune Cell Function and Interaction (10 papers), T-cell and B-cell Immunology (6 papers) and IL-33, ST2, and ILC Pathways (3 papers). Michael D. Bern collaborates with scholars based in United States, Russia and Israel. Michael D. Bern's co-authors include Wayne M. Yokoyama, Kenneth M. Murphy, Liping Yang, David C. Fargo, Karen Adelman, Telmo Henriques, Daniel A. Gilchrist, Ginger W. Muse, Sergei Nechaev and Adam Burkholder and has published in prestigious journals such as Nature, Proceedings of the National Academy of Sciences and The Journal of Experimental Medicine.

In The Last Decade

Michael D. Bern

12 papers receiving 986 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.

cDC1 prime and are licensed by CD4+ T cells to induce anti-tumour immunity

2020 356 citations Stephen T. Ferris, Vivek Durai et al. Nature profile →

Peers

Countries citing papers authored by Michael D. Bern

Since Specialization

Citations

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

Fields of papers citing papers by Michael D. Bern

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Michael D. Bern. 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 Michael D. Bern. The network helps show where Michael D. Bern may publish in the future.

Co-authorship network of co-authors of Michael D. Bern

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

All Works

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14 of 14 papers shown

#	Work	Indexed citations
1	Expression of a single inhibitory member of the Ly49 receptor family is sufficient to license NK cells for effector functions 2025 ·eLife ·Sytse J. Piersma, (unknown), Pamela Wong, Michael D. Bern, Jennifer Poursine‐Laurent, Liping Yang, Diana L. Beckman, Bijal A. Parikh, Wayne M. Yokoyama	0
2	Expression of a single inhibitory member of the Ly49 receptor family is sufficient to license NK cells for effector functions 2024 ·eLife ·Sytse J. Piersma, (unknown), Pamela Wong, Michael D. Bern, Jennifer Poursine‐Laurent, Liping Yang, Diana L. Beckman, Bijal A. Parikh, Wayne M. Yokoyama	1
3	VISTA As a Mediator of Immune Suppression in AML Initiated By DNMT3A and NPM1 mutations 2024 ·Blood ·(unknown), Michael H. Kramer, Michael D. Bern, Nichole Helton, Daniel R. George, (unknown), Sai Mukund Ramakrishnan, Christopher A. Miller, Timothy J. Ley	0
4	Immune Adjuvant Therapy With Interleukin-7 in a Lymphopenic Patient With Aplastic Anemia and Mucormycosis 2023 ·Critical Care Explorations ·Zachary Crees, (unknown), (unknown), Miriam Kim, Michael D. Bern, Allison R. Eberly, Kristan Augustin, Richard S. Hotchkiss, John F. DiPersio	1
5	The transcription factor Bach2 negatively regulates murine natural killer cell maturation and function 2022 ·eLife ·(unknown), Michael D. Bern, Benpeng Miao, Changxu Fan, Xiaoyun Xing, Takeshi Inoue, Sytse J. Piersma, Ting Wang, Marco Colonna, Tomohiro Kurosaki, Wayne M. Yokoyama	13
6	Control of Viral Infection by Natural Killer Cell Inhibitory Receptors 2020 ·Cell Reports ·Bijal A. Parikh, Michael D. Bern, Sytse J. Piersma, Liping Yang, Diana L. Beckman, Jennifer Poursine‐Laurent, Béatrice Plougastel-Douglas, Wayne M. Yokoyama	22
7	cDC1 prime and are licensed by CD4+ T cells to induce anti-tumour immunity breakdown → 2020 ·Nature ·Stephen T. Ferris, Vivek Durai, Renee Wu, Derek J. Theisen, Jeffrey P. Ward, Michael D. Bern, Jesse T. Davidson, Prachi Bagadia, Tiantian Liu, Carlos G. Briseño, Lijin Li, William E. Gillanders, Gregory F. Wu, Wayne M. Yokoyama, Theresa L. Murphy, Robert D. Schreiber, Kenneth M. Murphy	356
8	Toxoplasma gondii infection drives conversion of NK cells into ILC1-like cells 2019 ·eLife ·Eugene Park, Swapneel J. Patel, Qiuling Wang, Prabhakar S. Andhey, Konstantin Zaitsev, (unknown), (unknown), Michael D. Bern, Béatrice Plougastel-Douglas, Patrick L. Collins, Marco Colonna, Kenneth M. Murphy, Eugene M. Oltz, Maxim N. Artyomov, L. David Sibley, Wayne M. Yokoyama	90
9	Viral MHCI inhibition evades tissue-resident memory T cell formation and responses 2018 ·The Journal of Experimental Medicine ·Elvin J. Lauron, Liping Yang, Ian B. Harvey, Dorothy K. Sojka, Graham D. Williams, Michael Paley, Michael D. Bern, Eugene Park, Francisco Victorino, Adrianus C. M. Boon, Wayne M. Yokoyama	13
10	Inducible down-regulation of MHC class I results in natural killer cell tolerance 2018 ·The Journal of Experimental Medicine ·Michael D. Bern, Bijal A. Parikh, Liping Yang, Diana L. Beckman, Jennifer Poursine‐Laurent, Wayne M. Yokoyama	54
11	Immunoreceptor tyrosine-based inhibitory motif–dependent functions of an MHC class I-specific NK cell receptor 2017 ·Proceedings of the National Academy of Sciences ·Michael D. Bern, Diana L. Beckman, Takashi Ebihara, Samantha Taffner, Jennifer Poursine‐Laurent, J. Michael White, Wayne M. Yokoyama	16
12	Runx3 specifies lineage commitment of innate lymphoid cells 2015 ·Nature Immunology ·Takashi Ebihara, Christina Song, Hyunji Ryu, Béatrice Plougastel-Douglas, Liping Yang, Ditsa Levanon, Yoram Groner, Michael D. Bern, Thaddeus S. Stappenbeck, Marco Colonna, Takeshi Egawa, Wayne M. Yokoyama	144
13	Stable Pausing by RNA Polymerase II Provides an Opportunity to Target and Integrate Regulatory Signals 2013 ·Molecular Cell ·Telmo Henriques, Daniel A. Gilchrist, Sergei Nechaev, Michael D. Bern, Ginger W. Muse, Adam Burkholder, David C. Fargo, Karen Adelman	174
14	IKKβ phosphorylation regulates RPS3 nuclear translocation and NF-κB function during infection with Escherichia coli strain O157:H7 2011 ·Nature Immunology ·Fengyi Wan, (unknown), Xiaofei Gao, Michael D. Bern, Philip R. Hardwidge, Michael J. Lenardo	117

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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