James E. Sligh

3.3k total citations · 1 hit paper
34 papers, 2.6k citations indexed

About

James E. Sligh is a scholar working on Molecular Biology, Oncology and Epidemiology. According to data from OpenAlex, James E. Sligh has authored 34 papers receiving a total of 2.6k indexed citations (citations by other indexed papers that have themselves been cited), including 18 papers in Molecular Biology, 10 papers in Oncology and 8 papers in Epidemiology. Recurrent topics in James E. Sligh's work include Nonmelanoma Skin Cancer Studies (6 papers), Mitochondrial Function and Pathology (5 papers) and Cutaneous Melanoma Detection and Management (5 papers). James E. Sligh is often cited by papers focused on Nonmelanoma Skin Cancer Studies (6 papers), Mitochondrial Function and Pathology (5 papers) and Cutaneous Melanoma Detection and Management (5 papers). James E. Sligh collaborates with scholars based in United States, Spain and France. James E. Sligh's co-authors include Shawn Levy, Grant R. MacGregor, Douglas C. Wallace, Katrina G. Waymire, Dean P. Jones, Jason E. Kokoszka, Jiyang Cai, Arthur L. Beaudet, Christie M. Ballantyne and Allan Bradley and has published in prestigious journals such as Nature, Proceedings of the National Academy of Sciences and Journal of Biological Chemistry.

In The Last Decade

James E. Sligh

31 papers receiving 2.6k 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.

The ADP/ATP translocator is not essential for the mitochondrial permeability transition pore

2004 849 citations James E. Sligh et al. profile →

Peers — A (Enhanced Table)

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

Name	h						Papers	Cites
James E. Sligh United States	18	1.5k	565	437	381	274	34	2.6k
Kazuko Saeki Japan	27	978 0.7×	911 1.6×	157 0.4×	142 0.4×	401 1.5×	53	2.3k
Igor Buchwalow Germany	27	1.1k 0.8×	530 0.9×	110 0.3×	182 0.5×	331 1.2×	126	2.7k
Manfred Kunz Germany	34	2.3k 1.5×	970 1.7×	133 0.3×	327 0.9×	806 2.9×	114	3.8k
Florian C. Kurschus Germany	26	831 0.6×	1.7k 3.0×	80 0.2×	250 0.7×	374 1.4×	47	3.1k
Fredrik Ivars Sweden	27	1.2k 0.8×	2.1k 3.7×	243 0.6×	200 0.5×	407 1.5×	68	3.5k
Julián Gómez-Cambronero United States	35	2.1k 1.4×	1.0k 1.8×	297 0.7×	224 0.6×	546 2.0×	113	3.6k
Eleni Douni Greece	27	1.2k 0.8×	1.4k 2.4×	143 0.3×	323 0.8×	635 2.3×	58	3.2k
Jennifer L. Johnson United States	28	1.3k 0.9×	1.1k 2.0×	212 0.5×	241 0.6×	117 0.4×	52	2.6k
David Chang United States	17	729 0.5×	803 1.4×	82 0.2×	164 0.4×	315 1.1×	32	2.2k
David W. Powell United States	25	1.7k 1.1×	838 1.5×	160 0.4×	186 0.5×	158 0.6×	58	2.8k

Countries citing papers authored by James E. Sligh

Since Specialization

Citations

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

Fields of papers citing papers by James E. Sligh

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of James E. Sligh

This figure shows the co-authorship network connecting the top 25 collaborators of James E. Sligh. A scholar is included among the top collaborators of James E. Sligh 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 James E. Sligh. James E. Sligh 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

Sligh, James E., et al.. (2022). Annular scaly plaques with peripheral pustules. JAAD Case Reports. 21. 185–188.

Eisen, Daniel B., Maryam M. Asgari, Daniel Bennett, et al.. (2021). Guidelines of care for the management of actinic keratosis: Executive summary. Journal of the American Academy of Dermatology. 85(4). 945–955. 15 indexed citations

Eisen, Daniel B., Maryam M. Asgari, Daniel Bennett, et al.. (2021). Guidelines of care for the management of actinic keratosis. Journal of the American Academy of Dermatology. 85(4). e209–e233. 90 indexed citations

Ferris, Laura K., Pedram Gerami, James E. Sligh, et al.. (2018). LB1593 Real-world experience and clinical utility of a non-invasive gene expression test for primary cutaneous melanoma and validation against high risk driver mutations in BRAF, NRAS and the TERT promoter. Journal of Investigative Dermatology. 138(9). B21–B21.

Ferris, Laura K., Ronald L. Moy, Pedram Gerami, et al.. (2018). Noninvasive Analysis of High-Risk Driver Mutations and Gene Expression Profiles in Primary Cutaneous Melanoma. Journal of Investigative Dermatology. 139(5). 1127–1134. 19 indexed citations

Wondrak, Georg T., Annadurai Anandhan, Zain Khalpey, et al.. (2018). Parkinson's Disease Skin Fibroblasts Display Signature Alterations in Growth, Redox Homeostasis, Mitochondrial Function, and Autophagy. Frontiers in Neuroscience. 11. 737–737. 53 indexed citations

Nfonsam, Valentine, et al.. (2016). Modulation of ROS levels in fibroblasts by altering mitochondria regulates the process of wound healing. Archives of Dermatological Research. 308(4). 239–248. 43 indexed citations

Sligh, James E., et al.. (2014). Mutations in BALB mitochondrial DNA induce CCL20 up-regulation promoting tumorigenic phenotypes. Mutation research. Fundamental and molecular mechanisms of mutagenesis. 769. 49–58. 3 indexed citations

Sligh, James E.. (2014). New Therapeutic Options for Actinic Keratosis and Basal Cell Carcinoma. Seminars in Cutaneous Medicine and Surgery. 33(4S). S76–S80. 6 indexed citations

10.

Loescher, Lois J., et al.. (2013). A Preliminary Study of a Video Intervention to Inform Solid Organ Transplant Recipients About Skin Cancer. Transplantation Proceedings. 45(9). 3187–3189. 8 indexed citations

11.

Jandová, Jana, et al.. (2012). Cyclophilin 40 alters UVA-induced apoptosis and mitochondrial ROS generation in keratinocytes. Experimental Cell Research. 319(5). 750–760. 18 indexed citations

12.

Jandová, Jana, et al.. (2011). Identification of an mtDNA Mutation Hot Spot in UV-Induced Mouse Skin Tumors Producing Altered Cellular Biochemistry. Journal of Investigative Dermatology. 132(2). 421–428. 9 indexed citations

13.

Jandová, Jana, Mingjian Shi, Kimberly G. Norman, George P. Stricklin, & James E. Sligh. (2011). Somatic alterations in mitochondrial DNA produce changes in cell growth and metabolism supporting a tumorigenic phenotype. Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease. 1822(2). 293–300. 11 indexed citations

14.

Vleugels, Ruth Ann, et al.. (2005). Mitochondrial DNA Deletions Serve as Biomarkers of Aging in the Skin, but Are Typically Absent in Nonmelanoma Skin Cancers. Journal of Investigative Dermatology. 126(2). 336–344. 70 indexed citations

15.

Canter, Jeffrey A., Joshua P. Fessel, Marshall Summar, et al.. (2004). Degree of heteroplasmy reflects oxidant damage in a large family with the mitochondrial DNA A8344G mutation. Free Radical Biology and Medicine. 38(5). 678–683. 14 indexed citations

16.

Kumasaka, Takashi, W M Quinlan, N A Doyle, et al.. (1996). Role of the intercellular adhesion molecule-1(ICAM-1) in endotoxin-induced pneumonia evaluated using ICAM-1 antisense oligonucleotides, anti-ICAM-1 monoclonal antibodies, and ICAM-1 mutant mice.. Journal of Clinical Investigation. 97(10). 2362–2369. 173 indexed citations

17.

Qin, Li, W M Quinlan, N A Doyle, et al.. (1996). The roles of CD11/CD18 and ICAM-1 in acute Pseudomonas aeruginosa-induced pneumonia in mice. The Journal of Immunology. 157(11). 5016–5021. 108 indexed citations

18.

Quinlan, W M, et al.. (1995). Lymphocyte Accumulation During Pseudomonas aeruginosa-Induced Pneumonia in Rodents Does Not Require CD11a and Intercellular Adhesion Molecule-1. American Journal of Respiratory Cell and Molecular Biology. 12(5). 513–519. 2 indexed citations

19.

Ballantyne, Christie M., et al.. (1992). Characterization of the murine Icam-1 gene. Genomics. 14(4). 1076–1080. 35 indexed citations

20.

Sokol-Anderson, Marcia L., James E. Sligh, S Elberg, et al.. (1988). Role of cell defense against oxidative damage in the resistance of Candida albicans to the killing effect of amphotericin B. Antimicrobial Agents and Chemotherapy. 32(5). 702–705. 89 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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