Nabil Kaci

714 total citations
18 papers, 487 citations indexed

About

Nabil Kaci is a scholar working on Genetics, Molecular Biology and Oncology. According to data from OpenAlex, Nabil Kaci has authored 18 papers receiving a total of 487 indexed citations (citations by other indexed papers that have themselves been cited), including 17 papers in Genetics, 15 papers in Molecular Biology and 6 papers in Oncology. Recurrent topics in Nabil Kaci's work include Fibroblast Growth Factor Research (14 papers), Connective tissue disorders research (14 papers) and Bone health and treatments (3 papers). Nabil Kaci is often cited by papers focused on Fibroblast Growth Factor Research (14 papers), Connective tissue disorders research (14 papers) and Bone health and treatments (3 papers). Nabil Kaci collaborates with scholars based in France, United States and United Kingdom. Nabil Kaci's co-authors include Laurence Legeai‐Mallet, Catherine Benoist-Lasselin, Arnold Münnich, Federico Di Rocco, Emilie Mugniery, Davide Komla‐Ebri, Martin Biosse Duplan, Emilie Dambroise, Yann Heuzé and Ludovic Martin and has published in prestigious journals such as Journal of Clinical Investigation, The American Journal of Human Genetics and Human Molecular Genetics.

In The Last Decade

Nabil Kaci

17 papers receiving 484 citations

Peers — A (Enhanced Table)

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

Name h Career Trend Papers Cites
Nabil Kaci France 10 355 316 60 50 35 18 487
Changlin Ding United States 9 257 0.7× 249 0.8× 61 1.0× 36 0.7× 14 0.4× 12 453
Eva Maria Cutiongco Philippines 7 168 0.5× 180 0.6× 23 0.4× 26 0.5× 29 0.8× 7 327
Masaki Takagi Japan 14 236 0.7× 290 0.9× 66 1.1× 36 0.7× 13 0.4× 54 514
Ron Krofft United States 8 213 0.6× 129 0.4× 30 0.5× 23 0.5× 29 0.8× 8 486
Anenisia C. Andrade Sweden 13 344 1.0× 196 0.6× 51 0.8× 19 0.4× 39 1.1× 18 527
Rute A. Tomaz United Kingdom 13 291 0.8× 126 0.4× 54 0.9× 16 0.3× 18 0.5× 14 466
Daniel L. Shurman United States 6 249 0.7× 217 0.7× 51 0.8× 88 1.8× 40 1.1× 6 550
Juling Zhou United States 11 175 0.5× 131 0.4× 43 0.7× 30 0.6× 10 0.3× 14 381
Weipeng Zheng China 10 184 0.5× 186 0.6× 44 0.7× 66 1.3× 8 0.2× 17 428
Purificação Tavares Portugal 9 107 0.3× 121 0.4× 31 0.5× 37 0.7× 21 0.6× 18 301

Countries citing papers authored by Nabil Kaci

Since Specialization
Citations

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

Fields of papers citing papers by Nabil Kaci

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Nabil Kaci. 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 Nabil Kaci. The network helps show where Nabil Kaci may publish in the future.

Co-authorship network of co-authors of Nabil Kaci

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

All Works

18 of 18 papers shown
1.
Starrett, Jacqueline H., C. Lemoine, Nabil Kaci, et al.. (2025). TYRA-300, an FGFR3-selective inhibitor, promotes bone growth in two FGFR3-driven models of chondrodysplasia. JCI Insight. 10(9). 1 indexed citations
2.
Kaci, Nabil, et al.. (2024). Low–dose infigratinib increases bone growth and corrects growth plate abnormalities in an achondroplasia mouse model. Journal of Bone and Mineral Research. 39(6). 765–774. 3 indexed citations
3.
Komla‐Ebri, Davide, Yann Heuzé, Nabil Kaci, et al.. (2023). Hypochondroplasia gain-of-function mutation in FGFR3 causes defective bone mineralization in mice. JCI Insight. 8(12). 6 indexed citations
4.
Martin, Ludovic, Nabil Kaci, Catherine Benoist-Lasselin, et al.. (2022). Theobroma cacao improves bone growth by modulating defective ciliogenesis in a mouse model of achondroplasia. Bone Research. 10(1). 8–8. 7 indexed citations
5.
Moriceau, Stéphanie, Roman Hossein Khonsari, Yann Heuzé, et al.. (2022). FGFR3 overactivation in the brain is responsible for memory impairments in Crouzon syndrome mouse model.. PubMed. 219(4). 12 indexed citations
6.
Robinson, Jerid W., et al.. (2021). Prevention of guanylyl cyclase–B dephosphorylation rescues achondroplastic dwarfism. JCI Insight. 6(9). 12 indexed citations
7.
Shuhaibar, Leia C., Nabil Kaci, Jeremy R. Egbert, et al.. (2021). Phosphatase inhibition by LB-100 enhances BMN-111 stimulation of bone growth. JCI Insight. 6(9). 9 indexed citations
8.
Kaci, Nabil, et al.. (2020). Fgfr3 gain-of-function mutation impacts bone homeostasis in hypochondroplasia mouse model. Bone Reports. 13. 100691–100691. 1 indexed citations
9.
Dambroise, Emilie, et al.. (2019). Animal models of craniosynostosis. Neurochirurgie. 65(5). 202–209. 12 indexed citations
10.
Martin, Ludovic, Nabil Kaci, Nicolas Goudin, et al.. (2017). Constitutively-active FGFR3 disrupts primary cilium length and IFT20 trafficking in various chondrocyte models of achondroplasia. Human Molecular Genetics. 27(1). 1–13. 36 indexed citations
11.
Duplan, Martin Biosse, Davide Komla‐Ebri, Yann Heuzé, et al.. (2016). Meckel’s and condylar cartilages anomalies in achondroplasia result in defective development and growth of the mandible. Human Molecular Genetics. 25(14). ddw153–ddw153. 32 indexed citations
12.
Komla‐Ebri, Davide, Emilie Dambroise, Ina Krämer, et al.. (2016). Tyrosine kinase inhibitor NVP-BGJ398 functionally improves FGFR3-related dwarfism in mouse model. Journal of Clinical Investigation. 126(5). 1871–1884. 78 indexed citations
13.
Mehawej, Cybel, Agnès Delahodde, Laurence Legeai‐Mallet, et al.. (2014). The Impairment of MAGMAS Function in Human Is Responsible for a Severe Skeletal Dysplasia. PLoS Genetics. 10(5). e1004311–e1004311. 31 indexed citations
14.
Rocco, Federico Di, Martin Biosse Duplan, Yann Heuzé, et al.. (2014). FGFR3 mutation causes abnormal membranous ossification in achondroplasia. Human Molecular Genetics. 23(11). 2914–2925. 63 indexed citations
15.
Duplan, Martin Biosse, Yann Heuzé, Davide Komla‐Ebri, et al.. (2014). Disturbed cartilages of the mandible in achondroplasia are associated with defective mandible shape and position. Bone Abstracts.
16.
Lorget, Florence, Nabil Kaci, Jeff Peng, et al.. (2012). Evaluation of the Therapeutic Potential of a CNP Analog in a Fgfr3 Mouse Model Recapitulating Achondroplasia. The American Journal of Human Genetics. 91(6). 1108–1114. 140 indexed citations
17.
Mugniery, Emilie, Catherine Benoist-Lasselin, Nabil Kaci, et al.. (2011). A novel tyrosine kinase inhibitor restores chondrocyte differentiation and promotes bone growth in a gain-of-function Fgfr3 mouse model. Human Molecular Genetics. 21(4). 841–851. 39 indexed citations
18.

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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