R. Michael Henke

1.3k total citations
18 papers, 999 citations indexed

About

R. Michael Henke is a scholar working on Molecular Biology, Cell Biology and Genetics. According to data from OpenAlex, R. Michael Henke has authored 18 papers receiving a total of 999 indexed citations (citations by other indexed papers that have themselves been cited), including 17 papers in Molecular Biology, 5 papers in Cell Biology and 4 papers in Genetics. Recurrent topics in R. Michael Henke's work include Developmental Biology and Gene Regulation (5 papers), RNA and protein synthesis mechanisms (4 papers) and Mitochondrial Function and Pathology (3 papers). R. Michael Henke is often cited by papers focused on Developmental Biology and Gene Regulation (5 papers), RNA and protein synthesis mechanisms (4 papers) and Mitochondrial Function and Pathology (3 papers). R. Michael Henke collaborates with scholars based in United States, Germany and Australia. R. Michael Henke's co-authors include Jane E. Johnson, Raymond J. MacDonald, Stacey M. Glasgow, Yuji Nakada, Christopher V.E. Wright, Toshihiko Masui, Thomas M. Beres, Galvin H. Swift, Ling Shi and Philip S. Perlman and has published in prestigious journals such as Journal of Biological Chemistry, Genes & Development and SHILAP Revista de lepidopterología.

In The Last Decade

R. Michael Henke

18 papers receiving 988 citations

Peers

R. Michael Henke
A. Stoykova Germany
Kevin J. Kim United States
Roger Pedersen United Kingdom
Gerald D. Maxwell United States
Grace M. Hobson United States
Moritz Mall United States
A. Stoykova Germany
R. Michael Henke
Citations per year, relative to R. Michael Henke R. Michael Henke (= 1×) peers A. Stoykova

Countries citing papers authored by R. Michael Henke

Since Specialization
Citations

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

Fields of papers citing papers by R. Michael Henke

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of R. Michael Henke

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

All Works

18 of 18 papers shown
1.
Cadinu, Daniela, et al.. (2014). Comparative proteomic analysis reveals characteristic molecular changes accompanying the transformation of nonmalignant to cancer lung cells. SHILAP Revista de lepidopterología. 3. 1–12. 7 indexed citations
2.
Alam, Md Maksudul, Jagmohan Hooda, Daniela Cadinu, et al.. (2013). Comparative proteomic analysis of an isogenic pair of lung normal and lung cancer cell line. The FASEB Journal. 27(S1). 1 indexed citations
3.
Hooda, Jagmohan, et al.. (2012). The nuclear localization of SWI/SNF proteins is subjected to oxygen regulation. Cell & Bioscience. 2(1). 30–30. 45 indexed citations
4.
Shah, Ajit, et al.. (2011). Deletion of a subgroup of ribosome-related genes minimizes hypoxia-induced changes and confers hypoxia tolerance. Physiological Genomics. 43(14). 855–872. 11 indexed citations
5.
Henke, R. Michael, Ajit Shah, Daniela Cadinu, et al.. (2011). Hypoxia elicits broad and systematic changes in protein subcellular localization. American Journal of Physiology-Cell Physiology. 301(4). C913–C928. 23 indexed citations
6.
Henke, R. Michael, David M. Meredith, Mark D. Borromeo, Trisha K. Savage, & Jane E. Johnson. (2009). Ascl1 and Neurog2 form novel complexes and regulate Delta-like3 (Dll3) expression in the neural tube. Developmental Biology. 328(2). 529–540. 78 indexed citations
7.
Henke, R. Michael, Trisha K. Savage, David M. Meredith, et al.. (2009). Neurog2 is a direct downstream target of the Ptf1a-Rbpj transcription complex in dorsal spinal cord. Development. 136(17). 2945–2954. 47 indexed citations
8.
Hori, Kei, Justyna Cholewa-Waclaw, Yuji Nakada, et al.. (2008). A nonclassical bHLH–Rbpj transcription factor complex is required for specification of GABAergic neurons independent of Notch signaling. Genes & Development. 22(2). 166–178. 102 indexed citations
9.
Helms, Amy W., James Battiste, R. Michael Henke, et al.. (2005). Sequential roles for Mash1 and Ngn2 in the generation of dorsal spinal cord interneurons. Development. 132(12). 2709–2719. 101 indexed citations
10.
Beres, Thomas M., Toshihiko Masui, Galvin H. Swift, et al.. (2005). PTF1 Is an Organ-Specific and Notch-Independent Basic Helix-Loop-Helix Complex Containing the Mammalian Suppressor of Hairless (RBP-J) or Its Paralogue, RBP-L. Molecular and Cellular Biology. 26(1). 117–130. 170 indexed citations
11.
Glasgow, Stacey M., R. Michael Henke, Raymond J. MacDonald, Christopher V.E. Wright, & Jane E. Johnson. (2005). Ptf1a determines GABAergic over glutamatergic neuronal cell fate in the spinal cord dorsal horn. Development. 132(24). 5461–5469. 183 indexed citations
12.
Biggin, Andrew, R. Michael Henke, Bruce Bennetts, David R. Thorburn, & John Christodoulou. (2004). Mutation screening of the mitochondrial genome using denaturing high-performance liquid chromatography. Molecular Genetics and Metabolism. 84(1). 61–74. 45 indexed citations
13.
Dickson, Lorna M., Stuart Connell, Hon-Ren Huang, et al.. (2004). Abortive Transposition by a Group II Intron in Yeast Mitochondria. Genetics. 168(1). 77–87. 3 indexed citations
14.
Nakada, Yuji, Thomas Hunsaker, R. Michael Henke, & Jane E. Johnson. (2004). Distinct domains within Mash1 and Math1 are required for function in neuronal differentiation versus neuronal cell-type specification. Development. 131(6). 1319–1330. 87 indexed citations
15.
Butow, Ronald A., R. Michael Henke, John V. Moran, Scott M. Belcher, & Philip S. Perlman. (1996). [24] Transformation of Saccharomyces cerevisiae mitochondria using the biolistic gun. Methods in enzymology on CD-ROM/Methods in enzymology. 264. 265–278. 36 indexed citations
16.
Moran, John V., et al.. (1995). The Mobile Group I Intron 3α of the Yeast Mitochondrial COXI Gene Encodes a 35-kDa Processed Protein That Is an Endonuclease but Not a Maturase. Journal of Biological Chemistry. 270(26). 15563–15570. 14 indexed citations
17.
Henke, R. Michael, Ronald A. Butow, & Philip S. Perlman. (1995). Maturase and endonuclease functions depend on separate conserved domains of the bifunctional protein encoded by the group I intron aI4 alpha of yeast mitochondrial DNA.. The EMBO Journal. 14(20). 5094–5099. 45 indexed citations
18.
Nelson, Gregory A., et al.. (1994). Nematode radiobiology and development in space. Results from IML-1. NASA Technical Reports Server (NASA). 366. 187. 1 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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