J.A. Maassen

402 total citations
10 papers, 325 citations indexed

About

J.A. Maassen is a scholar working on Molecular Biology, Cancer Research and Surgery. According to data from OpenAlex, J.A. Maassen has authored 10 papers receiving a total of 325 indexed citations (citations by other indexed papers that have themselves been cited), including 7 papers in Molecular Biology, 2 papers in Cancer Research and 1 paper in Surgery. Recurrent topics in J.A. Maassen's work include Metabolism, Diabetes, and Cancer (7 papers), Protein Kinase Regulation and GTPase Signaling (5 papers) and Cancer-related molecular mechanisms research (2 papers). J.A. Maassen is often cited by papers focused on Metabolism, Diabetes, and Cancer (7 papers), Protein Kinase Regulation and GTPase Signaling (5 papers) and Cancer-related molecular mechanisms research (2 papers). J.A. Maassen collaborates with scholars based in Netherlands, United Kingdom and India. J.A. Maassen's co-authors include Johannes L. Bos, W. Möller, D. Margriet Ouwens, Bentley Cheatham, C. Ronald Kahn, Gijsbertus J. Pronk, René H. Medema, Jeffrey S. Flier, David E. Moller and Anna Krook and has published in prestigious journals such as Journal of Biological Chemistry, Diabetologia and Biochimica et Biophysica Acta (BBA) - Molecular Cell Research.

In The Last Decade

J.A. Maassen

10 papers receiving 311 citations

Peers

J.A. Maassen
Rodolfo Battista Italy
Carmela Cisternino Italy
Luigi Zucaro Italy
RA Hegele Canada
Kyoko Tanimura Japan
L.B. Bäcklund Sweden
Amira Turki Tunisia
Yulia Antropova Australia
Stela Z. Berisha United States
Xiaojing Ma China
Rodolfo Battista Italy
J.A. Maassen
Citations per year, relative to J.A. Maassen J.A. Maassen (= 1×) peers Rodolfo Battista

Countries citing papers authored by J.A. Maassen

Since Specialization
Citations

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

Fields of papers citing papers by J.A. Maassen

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by J.A. Maassen. 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 J.A. Maassen. The network helps show where J.A. Maassen may publish in the future.

Co-authorship network of co-authors of J.A. Maassen

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

All Works

10 of 10 papers shown
1.
Bos, Johannes L., et al.. (2009). Changes in the signalling status of the small GTP-binding proteins Rac and Rho do not influence insulin-stimulated hexose transport. Experimental and Clinical Endocrinology & Diabetes. 105(5). 254–262. 4 indexed citations
2.
Maassen, J.A., et al.. (2009). The molecular basis and clinical characteristics of Maternally Inherited Diabetes and Deafness (MIDD), a recently recognized diabetic subtype. Experimental and Clinical Endocrinology & Diabetes. 104(3). 205–211. 2 indexed citations
3.
Fradkin, Lee G., Henk K. Koerten, J.A. Maassen, & Jasprien Noordermeer. (2006). Signalling in development and disease. 4 indexed citations
4.
Pijl, J.W. van der, H. H. P. J. Lemkes, Rudi GJ Westendorp, et al.. (1999). The DD genotype of the ACE gene polymorphism is associated with progression of diabetic nephropathy to end stage renal failure in IDDM.. PubMed. 51(3). 133–40. 50 indexed citations
5.
Krook, Anna, Jonathan P. Whitehead, Matthew R. Griffiths, et al.. (1997). Two Naturally Occurring Insulin Receptor Tyrosine Kinase Domain Mutants Provide Evidence That Phosphoinositide 3-Kinase Activation Alone Is Not Sufficient for the Mediation of Insulin's Metabolic and Mitogenic Effects. Journal of Biological Chemistry. 272(48). 30208–30214. 74 indexed citations
6.
McCarthy, Mark I., Paul G. Cassell, L Mathías, et al.. (1996). Evaluation of the Importance of Maternal History of Diabetes and of Mitochondrial Variation in the Development of NIDDM. Diabetic Medicine. 13(5). 420–428. 32 indexed citations
7.
8.
Vorm, Eric R. van der, et al.. (1993). Patients with lipodystrophic diabetes mellitus of the Seip-Berardinelli type, express normal insulin receptors. Diabetologia. 36(2). 172–174. 18 indexed citations
9.
Medema, René H., Johannes L. Bos, David E. Moller, et al.. (1992). Relation between the insulin receptor number in cells, autophosphorylation and insulin-stimulated Ras.GTP formation.. Journal of Biological Chemistry. 267(21). 14647–14653. 56 indexed citations
10.
Maassen, J.A., H. M. J. Krans, & Winfried Möller. (1987). The effect of insulin, serum and dexamethasone on mRNA levels for the insulin receptor in the human lymphoblastoic cell line IM-9. Biochimica et Biophysica Acta (BBA) - Molecular Cell Research. 930(1). 72–78. 17 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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