John G. Gilman

562 total citations
21 papers, 464 citations indexed

About

John G. Gilman is a scholar working on Genetics, Molecular Biology and Hematology. According to data from OpenAlex, John G. Gilman has authored 21 papers receiving a total of 464 indexed citations (citations by other indexed papers that have themselves been cited), including 14 papers in Genetics, 9 papers in Molecular Biology and 6 papers in Hematology. Recurrent topics in John G. Gilman's work include Hemoglobinopathies and Related Disorders (14 papers), Erythrocyte Function and Pathophysiology (6 papers) and Prenatal Screening and Diagnostics (4 papers). John G. Gilman is often cited by papers focused on Hemoglobinopathies and Related Disorders (14 papers), Erythrocyte Function and Pathophysiology (6 papers) and Prenatal Screening and Diagnostics (4 papers). John G. Gilman collaborates with scholars based in United States, Italy and Netherlands. John G. Gilman's co-authors include Oliver Smithies, Ronald L. Nagel, Thomas Wegmann, Giulio Superti‐Furga, Mary E. Fabry, Roberto Mantovani, George Stamatoyannopoulos, Daniel E. Goldberg, Leonid Grinberg and H L Shear and has published in prestigious journals such as Science, Nucleic Acids Research and Blood.

In The Last Decade

John G. Gilman

21 papers receiving 440 citations

Peers — A (Enhanced Table)

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

Name h Career Trend Papers Cites
John G. Gilman United States 11 251 169 151 109 67 21 464
M Patterson Canada 12 359 1.4× 148 0.9× 262 1.7× 163 1.5× 84 1.3× 27 505
G. V. Sciarratta Italy 11 292 1.2× 108 0.6× 193 1.3× 68 0.6× 40 0.6× 27 387
Lois B. Wilson United States 8 324 1.3× 349 2.1× 191 1.3× 41 0.4× 35 0.5× 10 632
Elizabeth R. Macari United States 8 174 0.7× 217 1.3× 105 0.7× 83 0.8× 39 0.6× 15 434
Surinder Safaya United States 12 316 1.3× 208 1.2× 260 1.7× 49 0.4× 15 0.2× 22 539
F E Cash United States 12 274 1.1× 468 2.8× 189 1.3× 57 0.5× 33 0.5× 12 683
J. M. Gonzalez‐Redondo United States 13 639 2.5× 131 0.8× 479 3.2× 98 0.9× 37 0.6× 20 702
B P Alter United States 7 135 0.5× 235 1.4× 222 1.5× 56 0.5× 20 0.3× 10 400
Shigeko Nishimura Japan 9 133 0.5× 323 1.9× 163 1.1× 84 0.8× 65 1.0× 31 543
Georgi D. Efremov North Macedonia 14 468 1.9× 239 1.4× 309 2.0× 176 1.6× 209 3.1× 31 852

Countries citing papers authored by John G. Gilman

Since Specialization
Citations

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

Fields of papers citing papers by John G. Gilman

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by John G. Gilman. 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 John G. Gilman. The network helps show where John G. Gilman may publish in the future.

Co-authorship network of co-authors of John G. Gilman

This figure shows the co-authorship network connecting the top 25 collaborators of John G. Gilman. A scholar is included among the top collaborators of John G. Gilman 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 John G. Gilman. John G. Gilman 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.
Fabry, Mary E., Sandra M. Suzuka, Rona Singer Weinberg, et al.. (2001). Second generation knockout sickle mice: the effect of HbF. Blood. 97(2). 410–418. 48 indexed citations
2.
Alami, Raouf, John G. Gilman, Yue Feng, et al.. (1999). Anti-βs-Ribozyme Reduces βs mRNA Levels in Transgenic Mice: Potential Application to the Gene Therapy of Sickle Cell Anemia. Blood Cells Molecules and Diseases. 25(2). 110–119. 19 indexed citations
3.
4.
Dixit, Mehul, John G. Gilman, Adrian Spitzer, Ira Greifer, & Daniel Glicklich. (1999). ACE Gene Polymorphism in Progression of Focal Segmental Glomerulosclerosis. Pediatric Research. 45(4, Part 2 of 2). 330A–330A. 1 indexed citations
5.
Shear, H L, Leonid Grinberg, John G. Gilman, et al.. (1998). Transgenic Mice Expressing Human Fetal Globin Are Protected From Malaria by a Novel Mechanism. Blood. 92(7). 2520–2526. 54 indexed citations
6.
Shear, H L, Leonid Grinberg, John G. Gilman, et al.. (1998). Transgenic Mice Expressing Human Fetal Globin Are Protected From Malaria by a Novel Mechanism. Blood. 92(7). 2520–2526. 5 indexed citations
7.
Bouhassira, Eric E., et al.. (1997). Properties of the mouse α-globin HS-26: Relationship to HS-40, the major enhancer of human α-globin gene expression. American Journal of Hematology. 54(1). 30–39. 13 indexed citations
8.
Frogheri, Laura, Laura Manca, Sylvain Doré, et al.. (1995). Fetal hemoglobin expression in compound heterozygotes for −117 (G→A) Aγ HPFH and β039 nonsense thalassemia. American Journal of Hematology. 49(4). 267–270. 7 indexed citations
9.
Gilman, John G., et al.. (1994). Mild β+(−87)‐thalassemia CACCC box mutation is associated with elevated fetal hemoglobin expression in cis. American Journal of Hematology. 45(3). 265–267. 10 indexed citations
10.
Gilman, John G., et al.. (1993). Direct demonstration that the AγT globin gene is linked to the 4 bp promoter deletion in the βA chromosome of sickle cell traits. American Journal of Hematology. 43(4). 312–315. 5 indexed citations
11.
Manca, Laura, et al.. (1990). Polymerase chain reaction amplification applied to the direct detection of a 4 bp deletion in the promoter region of the Aγ gene. American Journal of Hematology. 35(2). 131–133. 6 indexed citations
12.
13.
Gilman, John G., et al.. (1983). Modern Blood Banking and Transfusion Practices. Hemoglobin. 7(6). 617–618. 9 indexed citations
14.
Gilman, John G.. (1981). Red cell phosphofructokinase and pyruvate kinase activities correlate with genetic variation of 2,3-bisphosphoglycerate in rats. Biochemical and Biophysical Research Communications. 102(2). 766–774. 1 indexed citations
15.
Gilman, John G.. (1981). Red cells of newborn rats have low bisphosphoglyceromutase and high pyruvate kinase activities in association with low 2,3-bisphosphoglycerate. Biochemical and Biophysical Research Communications. 98(4). 1057–1062. 6 indexed citations
16.
Gilman, John G.. (1979). Carbon-13 nuclear magnetic resonance study of the motional behavior of ethyl isocyanide bound to myoglobin and hemoglobin. Biochemistry. 18(11). 2273–2279. 7 indexed citations
17.
Gilman, John G.. (1979). Evolutionary potential: A mathematical hypothesis of mouse hemoglobin beta chain evolution. Journal of Molecular Evolution. 13(1). 1–14. 5 indexed citations
18.
Gilman, John G.. (1972). Hemoglobin Beta Chain Structural Variation in Mice: Evolutionary and Functional Implications. Science. 178(4063). 873–874. 45 indexed citations
19.
Wegmann, Thomas & John G. Gilman. (1970). Chimerism for three genetic systems in tetraparental mice. Developmental Biology. 21(3). 281–291. 33 indexed citations
20.
Gilman, John G. & Oliver Smithies. (1968). Fetal Hemoglobin Variants in Mice. Science. 160(3830). 885–886. 56 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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