David E. Sleat

6.6k total citations · 1 hit paper
79 papers, 5.2k citations indexed

About

David E. Sleat is a scholar working on Physiology, Molecular Biology and Cell Biology. According to data from OpenAlex, David E. Sleat has authored 79 papers receiving a total of 5.2k indexed citations (citations by other indexed papers that have themselves been cited), including 53 papers in Physiology, 41 papers in Molecular Biology and 41 papers in Cell Biology. Recurrent topics in David E. Sleat's work include Lysosomal Storage Disorders Research (50 papers), Cellular transport and secretion (41 papers) and Glycosylation and Glycoproteins Research (17 papers). David E. Sleat is often cited by papers focused on Lysosomal Storage Disorders Research (50 papers), Cellular transport and secretion (41 papers) and Glycosylation and Glycoproteins Research (17 papers). David E. Sleat collaborates with scholars based in United States, United Kingdom and Belgium. David E. Sleat's co-authors include Peter Lobel, István Sohár, Henry Lackland, T. M. A. Wilson, Philip Turner, Michel Jadot, Daniel Gallie, John W. Watts, Marie T. Vanier and Peter Palukaitis and has published in prestigious journals such as Science, Proceedings of the National Academy of Sciences and Nucleic Acids Research.

In The Last Decade

David E. Sleat

79 papers receiving 5.1k 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.

Identification of HE1 as the Second Gene of Niemann-Pick C Disease

2000 666 citations Saule Naureckiene, David E. Sleat et al. Science profile →

Peers — A (Enhanced Table)

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

Name	h						Papers	Cites
David E. Sleat United States	40	2.7k	2.3k	1.6k	936	685	79	5.2k
Rolf G. Boot Netherlands	52	4.2k 1.6×	5.9k 2.6×	1.7k 1.0×	460 0.5×	1.6k 2.3×	120	9.2k
E H Birkenmeier United States	40	1.7k 0.6×	3.6k 1.6×	721 0.5×	265 0.3×	790 1.2×	79	6.6k
Eric Spooner United States	43	654 0.2×	5.6k 2.4×	1.1k 0.7×	208 0.2×	1.6k 2.4×	58	8.4k
Hans‐Peter Hauri Switzerland	42	695 0.3×	3.6k 1.6×	3.3k 2.1×	231 0.2×	452 0.7×	73	6.1k
Yusuke Maeda Japan	49	1.1k 0.4×	4.1k 1.8×	2.0k 1.2×	274 0.3×	1.8k 2.6×	154	6.8k
David L. Marks United States	37	1.4k 0.5×	2.7k 1.2×	2.0k 1.2×	100 0.1×	254 0.4×	69	4.4k
Ineke Braakman Netherlands	45	619 0.2×	5.2k 2.2×	3.7k 2.3×	350 0.4×	1.4k 2.0×	100	8.3k
Peter van der Sluijs Netherlands	43	1.2k 0.4×	4.6k 2.0×	3.2k 2.0×	173 0.2×	373 0.5×	90	6.9k
Mitsuo Tagaya Japan	40	544 0.2×	3.3k 1.4×	2.2k 1.4×	239 0.3×	485 0.7×	123	4.8k
Sven R. Carlsson Sweden	36	702 0.3×	2.3k 1.0×	1.5k 0.9×	93 0.1×	1.0k 1.5×	65	4.1k

Countries citing papers authored by David E. Sleat

Since Specialization

Citations

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

Fields of papers citing papers by David E. Sleat

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of David E. Sleat

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

Sleat, David E., Whitney Banach‐Petrosky, Katherine E. Larrimore, et al.. (2022). Elevated levels of tripeptidyl peptidase 1 do not ameliorate pathogenesis in a mouse model of Alzheimer disease. Neurobiology of Aging. 118. 106–107. 2 indexed citations

Wiseman, Jennifer A., et al.. (2018). Inducible transgenic expression of tripeptidyl peptidase 1 in a mouse model of late-infantile neuronal ceroid lipofuscinosis. PLoS ONE. 13(2). e0192286–e0192286. 3 indexed citations

Wiseman, Jennifer A., Yu Meng, Paul G. Matteson, et al.. (2017). Chronic Enzyme Replacement to the Brain of a Late Infantile Neuronal Ceroid Lipofuscinosis Mouse Has Differential Effects on Phenotypes of Disease. Molecular Therapy — Methods & Clinical Development. 4. 204–212. 13 indexed citations

Huang, Ling, Douglas H. Pike, David E. Sleat, Vikas Nanda, & Peter Lobel. (2014). Potential Pitfalls and Solutions for Use of Fluorescent Fusion Proteins to Study the Lysosome. PLoS ONE. 9(2). e88893–e88893. 47 indexed citations

Meng, Yu, István Sohár, David E. Sleat, et al.. (2013). Effective Intravenous Therapy for Neurodegenerative Disease With a Therapeutic Enzyme and a Peptide That Mediates Delivery to the Brain. Molecular Therapy. 22(3). 547–553. 40 indexed citations

Sleat, David E., Pengling Sun, Jennifer A. Wiseman, et al.. (2013). Extending the Mannose 6-Phosphate Glycoproteome by High Resolution/Accuracy Mass Spectrometry Analysis of Control and Acid Phosphatase 5-Deficient Mice. Molecular & Cellular Proteomics. 12(7). 1806–1817. 41 indexed citations

Lübke, Torben, Peter Lobel, & David E. Sleat. (2008). Proteomics of the lysosome. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research. 1793(4). 625–635. 215 indexed citations

Sleat, David E., Mukarram El-Banna, István Sohár, et al.. (2008). Residual levels of tripeptidyl-peptidase I activity dramatically ameliorate disease in late-infantile neuronal ceroid lipofuscinosis. Molecular Genetics and Metabolism. 94(2). 222–233. 42 indexed citations

Sun, Pengling, David E. Sleat, Michèle Lecocq, et al.. (2008). Acid phosphatase 5 is responsible for removing the mannose 6-phosphate recognition marker from lysosomal proteins. Proceedings of the National Academy of Sciences. 105(43). 16590–16595. 46 indexed citations

10.

Cabrera-Salazar, Mario A., Eric M. Roskelley, Jie Bu, et al.. (2007). Timing of Therapeutic Intervention Determines Functional and Survival Outcomes in a Mouse Model of Late Infantile Batten Disease. Molecular Therapy. 15(10). 1782–1788. 65 indexed citations

11.

Sleat, David E., Haiyan Zheng, & Peter Lobel. (2006). The human urine mannose 6-phosphate glycoproteome. Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics. 1774(3). 368–372. 29 indexed citations

12.

Millat, Gilles, Karim Chikh, Saule Naureckiene, et al.. (2001). Niemann-Pick Disease Type C: Spectrum of HE1 Mutations and Genotype/Phenotype Correlations in the NPC2 Group. The American Journal of Human Genetics. 69(5). 1013–1021. 119 indexed citations

13.

Naureckiene, Saule, David E. Sleat, Henry Lackland, et al.. (2000). Identification of HE1 as the Second Gene of Niemann-Pick C Disease. Science. 290(5500). 2298–2301. 666 indexed citations breakdown →

14.

Sleat, David E., István Sohár, Krystyna E. Wisniewski, et al.. (1999). Mutational Analysis of the Defective Protease in Classic Late-Infantile Neuronal Ceroid Lipofuscinosis, a Neurodegenerative Lysosomal Storage Disorder. The American Journal of Human Genetics. 64(6). 1511–1523. 132 indexed citations

15.

Liu, Chang‐Gong, David E. Sleat, Robert Donnelly, & Peter Lobel. (1998). Structural Organization and Sequence ofCLN2,the Defective Gene in Classical Late Infantile Neuronal Ceroid Lipofuscinosis. Genomics. 50(2). 206–212. 51 indexed citations

16.

Sleat, David E., István Sohár, Henry Lackland, John Majercak, & Peter Lobel. (1996). Rat Brain Contains High Levels of Mannose-6-phosphorylated Glycoproteins Including Lysosomal Enzymes and Palmitoyl-Protein Thioesterase, an Enzyme Implicated in Infantile Neuronal Lipofuscinosis. Journal of Biological Chemistry. 271(32). 19191–19198. 100 indexed citations

17.

Roossinck, Marilyn J., David E. Sleat, & Peter Palukaitis. (1992). Satellite RNAs of plant viruses: structures and biological effects.. Microbiological Reviews. 56(2). 265–279. 168 indexed citations

18.

Jupin, Isabelle, David E. Sleat, Paul A. Watkins, & T. M. A. Wilson. (1989). Direct recovery ofin vitrotranscripts in a protected form suitable for prolonged storage and shipment at ambient temperatures. Nucleic Acids Research. 17(2). 815–815. 8 indexed citations

19.

Sleat, David E., Daniel Gallie, John W. Watts, et al.. (1988). Selective recovery of foreign gene transcripts as virus-like particles in TMV-infected transgenic tobaccos. Nucleic Acids Research. 16(8). 3127–3140. 25 indexed citations

20.

Gallie, Daniel, David E. Sleat, John W. Watts, Philip Turner, & T. M. A. Wilson. (1988). Mutational analysis of the tobacco mosaic virus 5′-leader for altered ability to enhance translation. Nucleic Acids Research. 16(3). 883–893. 67 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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