S. W. Knight

2.6k total citations · 1 hit paper
20 papers, 1.9k citations indexed

About

S. W. Knight is a scholar working on Molecular Biology, Physiology and Cell Biology. According to data from OpenAlex, S. W. Knight has authored 20 papers receiving a total of 1.9k indexed citations (citations by other indexed papers that have themselves been cited), including 16 papers in Molecular Biology, 8 papers in Physiology and 3 papers in Cell Biology. Recurrent topics in S. W. Knight's work include RNA regulation and disease (9 papers), Telomeres, Telomerase, and Senescence (8 papers) and RNA modifications and cancer (5 papers). S. W. Knight is often cited by papers focused on RNA regulation and disease (9 papers), Telomeres, Telomerase, and Senescence (8 papers) and RNA modifications and cancer (5 papers). S. W. Knight collaborates with scholars based in United Kingdom, Germany and United States. S. W. Knight's co-authors include Philip J. Mason, Inderjeet Dokal, Tom Vulliamy, Annemarie Poustka, Nina S. Heiss, Stefan Wiemann, Sabine M. Klauck, Amanda J. Walne, Anna Marrone and T. Vulliamy and has published in prestigious journals such as Nature Genetics, The EMBO Journal and Blood.

In The Last Decade

S. W. Knight

20 papers receiving 1.9k citations

Hit Papers

X-linked dyskeratosis congenita is caused by mutations in... 1998 2026 2007 2016 1998 200 400 600

Peers

S. W. Knight
Robert R. Adams United States
Miranda R.M. Baert Netherlands
S Kyo Japan
William T. Yewdell United States
R L Stevens United States
J. Paul Schofield United Kingdom
Reena Rani United States
David L. Waning United States
S. W. Knight
Citations per year, relative to S. W. Knight S. W. Knight (= 1×) peers Natalie Erdmann

Countries citing papers authored by S. W. Knight

Since Specialization
Citations

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

Fields of papers citing papers by S. W. Knight

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by S. W. Knight. 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 S. W. Knight. The network helps show where S. W. Knight may publish in the future.

Co-authorship network of co-authors of S. W. Knight

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

All Works

20 of 20 papers shown
1.
Vulliamy, Tom, Anna Marrone, S. W. Knight, et al.. (2005). Mutations in dyskeratosis congenita: their impact on telomere length and the diversity of clinical presentation. Blood. 107(7). 2680–2685. 236 indexed citations
2.
Knight, S. W., et al.. (2001). Identification of novel DKC1 mutations in patients with dyskeratosis congenita: implications for pathophysiology and diagnosis. Human Genetics. 108(4). 299–303. 66 indexed citations
3.
Vulliamy, Tom, S. W. Knight, Philip J. Mason, & Inderjeet Dokal. (2001). Very Short Telomeres in the Peripheral Blood of Patients with X-Linked and Autosomal Dyskeratosis Congenita. Blood Cells Molecules and Diseases. 27(2). 353–357. 174 indexed citations
4.
Mason, Philip J., et al.. (1999). Human Hexose-6-phosphate Dehydrogenase (Glucose 1-Dehydrogenase) Encoded at 1p36: Coding Sequence and Expression. Blood Cells Molecules and Diseases. 25(1). 30–37. 45 indexed citations
5.
Knight, S. W.. (1999). Natural synthesis of a DNA-binding protein from the C-terminal domain of DNA gyrase A in Borrelia burgdorferi. The EMBO Journal. 18(17). 4875–4881. 46 indexed citations
6.
Knight, S. W., Nina S. Heiss, T. Vulliamy, et al.. (1999). X-Linked Dyskeratosis Congenita Is Predominantly Caused by Missense Mutations in the DKC1 Gene. The American Journal of Human Genetics. 65(1). 50–58. 187 indexed citations
7.
Knight, S. W., Nina S. Heiss, Tom Vulliamy, et al.. (1999). Unexplained aplastic anaemia, immunodeficiency, and cerebellar hypoplasia (Hoyeraal‐Hreidarsson syndrome) due to mutations in the dyskeratosis congenita gene, DKC1. British Journal of Haematology. 107(2). 335–339. 163 indexed citations
8.
Vulliamy, Tom, S. W. Knight, Nina S. Heiss, et al.. (1999). Dyskeratosis Congenita Caused by a 3′ Deletion: Germline and Somatic Mosaicism in a Female Carrier. Blood. 94(4). 1254–1260. 3 indexed citations
9.
Vulliamy, Tom, S. W. Knight, Nina S. Heiss, et al.. (1999). Dyskeratosis Congenita Caused by a 3′ Deletion: Germline and Somatic Mosaicism in a Female Carrier. Blood. 94(4). 1254–1260. 43 indexed citations
10.
Heiss, Nina S., S. W. Knight, Tom Vulliamy, et al.. (1998). X-linked dyskeratosis congenita is caused by mutations in a highly conserved gene with putative nucleolar functions. Nature Genetics. 19(1). 32–38. 708 indexed citations breakdown →
11.
Knight, S. W., Tom Vulliamy, Adrian Copplestone, et al.. (1998). Dyskeratosis Congenita (DC) Registry: identification of new features of DC. British Journal of Haematology. 103(4). 990–996. 133 indexed citations
12.
Knight, S. W., T. Vulliamy, Nina S. Heiss, et al.. (1998). 1.4 Mb candidate gene region for X linked dyskeratosis congenita defined by combined haplotype and X chromosome inactivation analysis.. Journal of Medical Genetics. 35(12). 993–996. 30 indexed citations
13.
Mijovic, C., Michelle A. Penny, David J.A. Jenkins, et al.. (1997). The Insulin Gene Region and Susceptibility to Insulin-Dependent Diabetes Mellitus in Four Races; New Insights from Afro-Caribbean Race-Specific Haplotypes. Autoimmunity. 26(1). 11–22. 7 indexed citations
14.
Vulliamy, T., S. W. Knight, Inderjeet Dokal, & Philip J. Mason. (1997). Skewed X-Inactivation in Carriers of X-Linked Dyskeratosis Congenita. Blood. 90(6). 2213–2216. 52 indexed citations
15.
Vulliamy, T., S. W. Knight, Inderjeet Dokal, & Philip J. Mason. (1997). Skewed X-Inactivation in Carriers of X-Linked Dyskeratosis Congenita. Blood. 90(6). 2213–2216. 5 indexed citations
16.
Knight, S. W., C. Mijovic, & Anthony Barnett. (1996). HLA‐DQB1 upstream regulatory region polymorphism and Type I diabetes. Tissue Antigens. 47(3). 231–236. 4 indexed citations
17.
Knight, S. W., T. Vulliamy, Gian Luca Forni, et al.. (1996). Fine mapping of the dyskeratosis congenita locus in Xq28.. Journal of Medical Genetics. 33(12). 993–995. 24 indexed citations
18.
Knight, S. W. & Kevin Docherty. (1992). RNA—protein interactions in the 5′ untranslated region of preproinsulin mRNA. Journal of Molecular Endocrinology. 8(3). 225–234. 8 indexed citations
19.
Docherty, Kevin, et al.. (1991). Metabolic control of insulin gene expression and biosynthesis. Proceedings of The Nutrition Society. 50(3). 553–558. 6 indexed citations
20.
Knight, S. W. & Kevin Docherty. (1991). The indentification of protein-RNA interactions within the 5′untranslated region of human preproinsulin mRNA. Biochemical Society Transactions. 19(2). 120S–120S. 3 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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