Mohammed S. Ikram

1.2k total citations
12 papers, 932 citations indexed

About

Mohammed S. Ikram is a scholar working on Molecular Biology, Dermatology and Genetics. According to data from OpenAlex, Mohammed S. Ikram has authored 12 papers receiving a total of 932 indexed citations (citations by other indexed papers that have themselves been cited), including 8 papers in Molecular Biology, 6 papers in Dermatology and 5 papers in Genetics. Recurrent topics in Mohammed S. Ikram's work include Hedgehog Signaling Pathway Studies (7 papers), Genetic and rare skin diseases. (5 papers) and Cancer and Skin Lesions (5 papers). Mohammed S. Ikram is often cited by papers focused on Hedgehog Signaling Pathway Studies (7 papers), Genetic and rare skin diseases. (5 papers) and Cancer and Skin Lesions (5 papers). Mohammed S. Ikram collaborates with scholars based in United Kingdom, Austria and United States. Mohammed S. Ikram's co-authors include Graham W. Neill, Anna‐Maria Frischauf, Fritz Aberger, Thomas Eichberger, Gerhard Regl, Anthony Quinn, Michael P. Philpott, Lucy Ghali, Alan Storey and O. Djahanbakhch and has published in prestigious journals such as The Journal of Clinical Endocrinology & Metabolism, Oncogene and British Journal of Cancer.

In The Last Decade

Mohammed S. Ikram

12 papers receiving 906 citations

Peers

Mohammed S. Ikram

PHEOH

GENET

ONCOL

H Salazar United States

Marc Leushacke Singapore

Jeffrey M. Cloutier United States

Christine Hoyle United Kingdom

Enrica Rampazzo Italy

Gönül Oğur Türkiye

Önder Bozdoğan Türkiye

Anette Szczepny Australia

Priscilla Wong China

Lihua Sun China

H Salazar United States

Mohammed S. Ikram

368 ×0.6

261 ×1.3

92 ×0.5

PHEOH

133 ×0.8

GENET

120 ×0.8

ONCOL

Citations per year, relative to Mohammed S. Ikram Mohammed S. Ikram (= 1×) peers H Salazar

Countries citing papers authored by Mohammed S. Ikram

Since Specialization

Citations

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

Fields of papers citing papers by Mohammed S. Ikram

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

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

Co-authorship network of co-authors of Mohammed S. Ikram

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

All Works

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12 of 12 papers shown

Gemenetzidis, Emilios, Giuseppe Trigiante, Gary Warnes, et al.. (2014). GLI2 induces genomic instability in human keratinocytes by inhibiting apoptosis. Cell Death and Disease. 5(1). e1028–e1028. 20 indexed citations

Neill, Graham W., Wesley J. Harrison, Mohammed S. Ikram, et al.. (2008). GLI1 repression of ERK activity correlates with colony formation and impaired migration in human epidermal keratinocytes. Carcinogenesis. 29(4). 738–746. 28 indexed citations

Das, Mukul K., O. Djahanbakhch, Burak Hacıhanefioğlu, et al.. (2008). Granulosa Cell Survival and Proliferation Are Altered in Polycystic Ovary Syndrome. Obstetrical & Gynecological Survey. 63(9). 579–580. 14 indexed citations

Das, Mukul K., O. Djahanbakhch, Burak Hacıhanefioğlu, et al.. (2007). Granulosa Cell Survival and Proliferation Are Altered in Polycystic Ovary Syndrome. The Journal of Clinical Endocrinology & Metabolism. 93(3). 881–887. 218 indexed citations

Wan, Hong, Ming Yuan, Cathy A. Simpson, et al.. (2007). Stem/Progenitor Cell-Like Properties of Desmoglein 3dim Cells in Primary and Immortalized Keratinocyte Lines. Stem Cells. 25(5). 1286–1297. 28 indexed citations

Green, Judith L., Mohammed S. Ikram, Charlotte M. Proby, et al.. (2006). Overexpression of the Axl tyrosine kinase receptor in cutaneous SCC-derived cell lines and tumours. British Journal of Cancer. 94(10). 1446–1451. 39 indexed citations

Ikram, Mohammed S., Graham W. Neill, Gerhard Regl, et al.. (2004). GLI2 Is Expressed in Normal Human Epidermis and BCC and Induces GLI1 Expression by Binding to its Promoter. Journal of Investigative Dermatology. 122(6). 1503–1509. 140 indexed citations

Eichberger, Thomas, Gerhard Regl, Mohammed S. Ikram, et al.. (2004). FOXE1, A New Transcriptional Target of GLI2 Is Expressed in Human Epidermis and Basal Cell Carcinoma. Journal of Investigative Dermatology. 122(5). 1180–1187. 71 indexed citations

Neill, Graham W., Lucy Ghali, Judith L. Green, et al.. (2003). Loss of protein kinase Calpha expression may enhance the tumorigenic potential of Gli1 in basal cell carcinoma.. PubMed. 63(15). 4692–7. 52 indexed citations

10.

Regl, Gerhard, Maria Kasper, Harald Schnidar, et al.. (2003). The zinc-finger transcription factor GLI2 antagonizes contact inhibition and differentiation of human epidermal cells. Oncogene. 23(6). 1263–1274. 70 indexed citations

11.

Regl, Gerhard, Graham W. Neill, Thomas Eichberger, et al.. (2002). Human GLI2 and GLI1 are part of a positive feedback mechanism in Basal Cell Carcinoma. Oncogene. 21(36). 5529–5539. 167 indexed citations

12.

Iles, Ray K., et al.. (2000). True. British Journal of Cancer. 82(9). 1553–1556. 85 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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