Eva M. Goellner

1.5k total citations
17 papers, 1.2k citations indexed

About

Eva M. Goellner is a scholar working on Molecular Biology, Pathology and Forensic Medicine and Oncology. According to data from OpenAlex, Eva M. Goellner has authored 17 papers receiving a total of 1.2k indexed citations (citations by other indexed papers that have themselves been cited), including 17 papers in Molecular Biology, 7 papers in Pathology and Forensic Medicine and 5 papers in Oncology. Recurrent topics in Eva M. Goellner's work include DNA Repair Mechanisms (13 papers), Genetic factors in colorectal cancer (7 papers) and PARP inhibition in cancer therapy (5 papers). Eva M. Goellner is often cited by papers focused on DNA Repair Mechanisms (13 papers), Genetic factors in colorectal cancer (7 papers) and PARP inhibition in cancer therapy (5 papers). Eva M. Goellner collaborates with scholars based in United States, Netherlands and Canada. Eva M. Goellner's co-authors include Robert W. Sobol, David Svilar, Karen H. Almeida, Richard D. Kolodner, Christopher D. Putnam, Ram N. Trivedi, Jiang-bo Tang, Ashley R. Brown, Xiaohong Wang and Elena Jelezcova and has published in prestigious journals such as Journal of Biological Chemistry, Nature Communications and Molecular Cell.

In The Last Decade

Eva M. Goellner

17 papers receiving 1.1k citations

Peers

Countries citing papers authored by Eva M. Goellner

Since Specialization

Citations

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

Fields of papers citing papers by Eva M. Goellner

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Eva M. Goellner. 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 Eva M. Goellner. The network helps show where Eva M. Goellner may publish in the future.

Co-authorship network of co-authors of Eva M. Goellner

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

All Works

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17 of 17 papers shown

#	Title	Journal	Authors	Indexed citations
1	Inhibition of ABL1 by tyrosine kinase inhibitors leads to a downregulation of MLH1 by Hsp70-mediated lysosomal protein degradation	Frontiers in Genetics	Rina Plattner, Eva M. Goellner et al.	1
2	Rad5 and Its Human Homologs, HLTF and SHPRH, Are Novel Interactors of Mismatch Repair	Frontiers in Cell and Developmental Biology	Guogen Mao, Christopher D. Putnam et al.	7
3	Chromatin remodeling and mismatch repair: Access and excision	DNA repair	Eva M. Goellner	13
4	Identification of Exo1-Msh2 interaction motifs in DNA mismatch repair and new Msh2-binding partners	Nature Structural & Molecular Biology	Eva M. Goellner, Christopher D. Putnam et al.	35
5	Exonuclease 1-dependent and independent mismatch repair	DNA repair	Eva M. Goellner, Christopher D. Putnam et al.	106
6	Activation of Saccharomyces cerevisiae Mlh1-Pms1 Endonuclease in a Reconstituted Mismatch Repair System	Journal of Biological Chemistry	Catherine E. Smith, Eva M. Goellner et al.	27
7	ARTD1/PARP1 Negatively Regulates Glycolysis by Inhibiting Hexokinase 1 Independent of NAD+ Depletion	Cell Reports	Elise Fouquerel, Eva M. Goellner et al.	176
8	HSP90 regulates DNA repair via the interaction between XRCC1 and DNA polymerase β	Nature Communications	Qingming Fang, Xiaohong Wang et al.	98
9	PCNA and Msh2-Msh6 Activate an Mlh1-Pms1 Endonuclease Pathway Required for Exo1-Independent Mismatch Repair	Molecular Cell	Eva M. Goellner, Catherine E. Smith et al.	79
10	Targeting DNA Polymerase ß for Therapeutic Intervention	Current Molecular Pharmacology	Eva M. Goellner, David Svilar et al.	16
11	Overcoming Temozolomide Resistance in Glioblastoma via Dual Inhibition of NAD+ Biosynthesis and Base Excision Repair	Cancer Research	Eva M. Goellner, Ashley R. Brown et al.	122
12	N-methylpurine DNA glycosylase and DNA polymerase β modulate BER inhibitor potentiation of glioma cells to temozolomide	Neuro-Oncology	Jiang-bo Tang, David Svilar et al.	92
13	Targeting DNA Polymerase ß for Therapeutic Intervention	Current Molecular Pharmacology	Eva M. Goellner, David Svilar et al.	21
14	Bioenergetic Metabolites Regulate Base Excision Repair–Dependent Cell Death in Response to DNA Damage	Molecular Cancer Research	Jiang-bo Tang, Eva M. Goellner et al.	57
15	Base Excision Repair and Lesion-Dependent Subpathways for Repair of Oxidative DNA Damage	Antioxidants and Redox Signaling	David Svilar, Eva M. Goellner et al.	211
16	Parp1 activation in mouse embryonic fibroblasts promotes Pol β-dependent cellular hypersensitivity to alkylation damage	Mutation research. Fundamental and molecular mechanisms of mutagenesis	Elena Jelezcova, Ram N. Trivedi et al.	25
17	Human Methyl Purine DNA Glycosylase and DNA Polymerase β Expression Collectively Predict Sensitivity to Temozolomide	Molecular Pharmacology	Ram N. Trivedi, Xiaohong Wang et al.	74

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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