Jean‐Pierre Abita

1.3k total citations
40 papers, 1.1k citations indexed

About

Jean‐Pierre Abita is a scholar working on Molecular Biology, Oncology and Immunology. According to data from OpenAlex, Jean‐Pierre Abita has authored 40 papers receiving a total of 1.1k indexed citations (citations by other indexed papers that have themselves been cited), including 26 papers in Molecular Biology, 10 papers in Oncology and 7 papers in Immunology. Recurrent topics in Jean‐Pierre Abita's work include Retinoids in leukemia and cellular processes (9 papers), Mast cells and histamine (6 papers) and Drug Transport and Resistance Mechanisms (5 papers). Jean‐Pierre Abita is often cited by papers focused on Retinoids in leukemia and cellular processes (9 papers), Mast cells and histamine (6 papers) and Drug Transport and Resistance Mechanisms (5 papers). Jean‐Pierre Abita collaborates with scholars based in France, United States and Israel. Jean‐Pierre Abita's co-authors include Michel Lazdunski, Christian Gespach, Seymour Kaufman, M Delaage, Sheldon Milstien, J. Šavrda, Christine Chomienne, Michael A. Parniak, N Balitrand and A. Zimber and has published in prestigious journals such as Proceedings of the National Academy of Sciences, Journal of Biological Chemistry and Cancer Research.

In The Last Decade

Jean‐Pierre Abita

39 papers receiving 992 citations

Peers — A (Enhanced Table)

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

Name h Career Trend Papers Cites
Jean‐Pierre Abita France 19 660 163 162 160 155 40 1.1k
Roger L. Hudgin Canada 15 1.2k 1.9× 196 1.2× 253 1.6× 217 1.4× 234 1.5× 16 1.8k
Walther Vogt Germany 17 658 1.0× 326 2.0× 121 0.7× 232 1.4× 59 0.4× 27 1.4k
Gérard Crémel France 21 950 1.4× 164 1.0× 184 1.1× 153 1.0× 353 2.3× 59 1.6k
Barry R. Ganong United States 15 1.2k 1.9× 155 1.0× 261 1.6× 205 1.3× 65 0.4× 24 1.7k
Çelík Kayalar United States 16 1.1k 1.7× 114 0.7× 152 0.9× 99 0.6× 92 0.6× 22 1.4k
Yumiko Nishinaka Japan 20 1.1k 1.7× 274 1.7× 193 1.2× 154 1.0× 118 0.8× 24 1.6k
Richard C. Hresko United States 20 1.3k 2.0× 179 1.1× 211 1.3× 219 1.4× 139 0.9× 29 1.6k
Alexander Kaplun Russia 21 780 1.2× 147 0.9× 50 0.3× 96 0.6× 190 1.2× 96 1.4k
Hubert A. Scoble United States 14 595 0.9× 87 0.5× 80 0.5× 160 1.0× 104 0.7× 18 1.2k
Edward L. Kean United States 20 1.3k 2.0× 134 0.8× 232 1.4× 247 1.5× 58 0.4× 66 1.7k

Countries citing papers authored by Jean‐Pierre Abita

Since Specialization
Citations

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

Fields of papers citing papers by Jean‐Pierre Abita

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Jean‐Pierre Abita. 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 Jean‐Pierre Abita. The network helps show where Jean‐Pierre Abita may publish in the future.

Co-authorship network of co-authors of Jean‐Pierre Abita

This figure shows the co-authorship network connecting the top 25 collaborators of Jean‐Pierre Abita. A scholar is included among the top collaborators of Jean‐Pierre Abita 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 Jean‐Pierre Abita. Jean‐Pierre Abita 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.
Zimber, A., et al.. (1994). Inhibition of proliferation and induction of monocytic differentiation in HL60 human promyelocytic leukemia cells treated with bile acids In vitro. International Journal of Cancer. 59(1). 71–77. 19 indexed citations
2.
Geny, Blandine, et al.. (1991). The differentiating agent, retinoic acid, causes an early inhibition of inositol lipid-specific phospholipase C activity in HL-60 cells. Cellular Signalling. 3(1). 11–23. 18 indexed citations
3.
Crémoux, Patricia de, A. Zimber, Fabien Calvo, et al.. (1991). Gsα availability to cholera toxin-catalysed ADP-ribosylation is decreased in membranes of retinoic acid-treated leukemic cell lines HL-60 and THP-1. Biochemical Pharmacology. 42(11). 2141–2146. 9 indexed citations
4.
Powis, Garth, John A. Hickman, Paul Workman, et al.. (1990). The Cell Membrane and Cell Signals as Targets in Cancer Chemotherapy AACR, EORTC, and BACR Special Conference in Cancer Research. Cancer Research. 50(7). 2203–2211. 7 indexed citations
5.
Giacchetti, Sylvie, Patricia de Crémoux, L. Bertin, et al.. (1990). Characterization, in some human breast cancer cell lines, of gastrin‐releasing peptide‐like receptors which are absent in normal breast epithelial cells. International Journal of Cancer. 46(2). 293–298. 82 indexed citations
6.
Ogunkolade, B, et al.. (1990). Interactions between the human monocytic leukaemia THP-1 cell line and Old and New World species of Leishmania. Acta Tropica. 47(3). 171–176. 35 indexed citations
7.
8.
Faille, A, et al.. (1987). Changes in the patterns of protein phosphorylation associated with granulocytic and monocytic-induced differentiation of HL-60 cells.. PubMed. 6(5). 1053–63. 15 indexed citations
9.
Ladoux, Annie, Jean‐Pierre Abita, & Blandine Geny. (1987). Retinoic-acid-induced differentiation of HL-60 cells is associated with biphasic activation of the Na+ — K+ pump. Differentiation. 33(3). 142–147. 1 indexed citations
10.
Ladoux, Annie, Jean‐Pierre Abita, & Blandine Geny. (1986). Retinoic-acid-induced differentiation of HL-60 cells is associated with biphasic activation of the Na+ − K+ pump. Differentiation. 33(2). 142–147. 11 indexed citations
11.
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13.
Gespach, Christian, et al.. (1981). Effect of indomethacin on the binding of the chemotactic peptide formyl‐Met—Leu—Phe on human polymorphonuclear leukocytes. FEBS Letters. 132(1). 85–88. 19 indexed citations
14.
Abita, Jean‐Pierre. (1981). Indomethacin is a competitive inhibitor of the binding of the chemotactic peptide formyl-Met-Leu-Phe to human polymorphonuclear leukocytes. Inflammation Research. 11(6-7). 610–612. 11 indexed citations
15.
Abita, Jean‐Pierre, et al.. (1980). Hormonal control of phenylalanine hydroxylase activity in isolated rat hepatocytes. Biochemical and Biophysical Research Communications. 92(3). 912–918. 16 indexed citations
16.
17.
Abita, Jean‐Pierre, et al.. (1972). Zymogen‐Enzyme Transformations. European Journal of Biochemistry. 30(1). 37–47. 55 indexed citations
18.
Abita, Jean‐Pierre, M Delaage, Michel Lazdunski, & J. Šavrda. (1969). The Mechanism of Activation of Trypsinogen. The Role of the Four N-Terminal Aspartyl Residues. European Journal of Biochemistry. 8(3). 314–324. 135 indexed citations
19.
Abita, Jean‐Pierre, S. Maroux, M Delaage, & Michel Lazdunski. (1969). The reactivity of carboxyl groups in chymotrypsinogen. FEBS Letters. 4(3). 203–206. 17 indexed citations
20.
Abita, Jean‐Pierre & Michel Lazdunski. (1969). On the structural and functional role of carboxylates in chymotrypsinogen A a comparison with chymotrypsin, trypsinogen and trypsin. Biochemical and Biophysical Research Communications. 35(5). 707–712. 30 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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