Robert E. Gerl

839 total citations
8 papers, 701 citations indexed

About

Robert E. Gerl is a scholar working on Molecular Biology, Oncology and Pathology and Forensic Medicine. According to data from OpenAlex, Robert E. Gerl has authored 8 papers receiving a total of 701 indexed citations (citations by other indexed papers that have themselves been cited), including 6 papers in Molecular Biology, 3 papers in Oncology and 2 papers in Pathology and Forensic Medicine. Recurrent topics in Robert E. Gerl's work include Cell death mechanisms and regulation (4 papers), Cancer-related Molecular Pathways (2 papers) and Phagocytosis and Immune Regulation (2 papers). Robert E. Gerl is often cited by papers focused on Cell death mechanisms and regulation (4 papers), Cancer-related Molecular Pathways (2 papers) and Phagocytosis and Immune Regulation (2 papers). Robert E. Gerl collaborates with scholars based in Australia and Canada. Robert E. Gerl's co-authors include John W. Schrader, Xuecui Guo, David L. Vaux, John Silke, Paul G. Ekert, Hitto Kaufmann, Vanessa S. Marsden, Sharad Kumar, Stuart H. Read and Christine J. Hawkins and has published in prestigious journals such as Journal of Biological Chemistry, The Journal of Cell Biology and Journal of Molecular Biology.

In The Last Decade

Robert E. Gerl

7 papers receiving 689 citations

Peers — A (Enhanced Table)

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

Name	h						Papers	Cites
Robert E. Gerl Australia	6	447	134	114	76	70	8	701
Evdokia Pasheva Bulgaria	18	474 1.1×	139 1.0×	189 1.7×	80 1.1×	34 0.5×	33	886
J Sedlák Slovakia	16	450 1.0×	175 1.3×	139 1.2×	87 1.1×	54 0.8×	77	837
Pei Yen Yeh Taiwan	8	351 0.8×	137 1.0×	73 0.6×	148 1.9×	88 1.3×	9	540
Changping Zou United States	17	396 0.9×	88 0.7×	55 0.5×	67 0.9×	55 0.8×	31	857
Hwa Young Lee South Korea	16	351 0.8×	108 0.8×	94 0.8×	82 1.1×	41 0.6×	33	685
A Haeffner France	6	636 1.4×	109 0.8×	203 1.8×	99 1.3×	74 1.1×	7	930
Anna Stępczyńska Germany	7	769 1.7×	222 1.7×	156 1.4×	140 1.8×	116 1.7×	9	1.2k
Milena Pervan United States	6	317 0.7×	204 1.5×	139 1.2×	75 1.0×	44 0.6×	8	768
Chul-Koo Cho South Korea	18	771 1.7×	194 1.4×	108 0.9×	147 1.9×	83 1.2×	20	1.1k
Kwang-Rok Kim South Korea	12	382 0.9×	199 1.5×	82 0.7×	173 2.3×	39 0.6×	14	692

Countries citing papers authored by Robert E. Gerl

Since Specialization

Citations

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

Fields of papers citing papers by Robert E. Gerl

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Robert E. Gerl

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

All Works

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8 of 8 papers shown

1.

Callus, Bernard A., John Silke, Robert E. Gerl, et al.. (2008). Triggering of Apoptosis by Puma Is Determined by the Threshold Set by Prosurvival Bcl-2 Family Proteins. Journal of Molecular Biology. 384(2). 313–323. 24 indexed citations

2.

Gerl, Robert E. & Anne M. Verhagen. (2005). IAPs, their Antagonists and their Role in Neurological Disease and Cancer. 4(4). 393–406. 1 indexed citations

3.

Read, Stuart H., John Silke, Hitto Kaufmann, et al.. (2004). Apaf-1, Caspase-2 and Caspase-9 accelerate apoptosis, but do not determine whether factor-deprived cells die. Pediatric Research. 55(4).

4.

Ekert, Paul G., Stuart H. Read, John Silke, et al.. (2004). Apaf-1 and caspase-9 accelerate apoptosis, but do not determine whether factor-deprived or drug-treated cells die. The Journal of Cell Biology. 165(6). 835–842. 146 indexed citations

5.

Gerl, Robert E.. (2004). Apoptosis in the development and treatment of cancer. Carcinogenesis. 26(2). 263–270. 329 indexed citations

6.

Guo, Xuecui, Robert E. Gerl, & John W. Schrader. (2003). Defining the Involvement of p38α MAPK in the Production of Anti- and Proinflammatory Cytokines Using an SB 203580-resistant Form of the Kinase. Journal of Biological Chemistry. 278(25). 22237–22242. 67 indexed citations

7.

Gerl, Robert E.. (2000). Urinary Excretion of Platinum in Chemotherapy-treated Long-term Survivors of Testicular Cancer. Acta Oncologica. 39(4). 519–522. 49 indexed citations

8.

Foltz, Ian N., et al.. (1998). Human Mitogen-activated Protein Kinase Kinase 7 (MKK7) Is a Highly Conserved c-Jun N-terminal Kinase/Stress-activated Protein Kinase (JNK/SAPK) Activated by Environmental Stresses and Physiological Stimuli. Journal of Biological Chemistry. 273(15). 9344–9351. 85 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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