Mouse Gli1 mutants are viable but have defects in SHH signaling in combination with a Gli2 mutation
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doi.org/10.1242/dev.127.8.1593 →Countries where authors are citing Mouse Gli1 mutants are viable but have defects in SHH signaling in combination with a Gli2 mutation
This map shows the geographic impact of Mouse Gli1 mutants are viable but have defects in SHH signaling in combination with a Gli2 mutation. 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 Mouse Gli1 mutants are viable but have defects in SHH signaling in combination with a Gli2 mutation with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Mouse Gli1 mutants are viable but have defects in SHH signaling in combination with a Gli2 mutation more than expected).
Fields of papers citing Mouse Gli1 mutants are viable but have defects in SHH signaling in combination with a Gli2 mutation
This network shows the impact of Mouse Gli1 mutants are viable but have defects in SHH signaling in combination with a Gli2 mutation. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the Mouse Gli1 mutants are viable but have defects in SHH signaling in combination with a Gli2 mutation.
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.
This paper is also available at doi.org/10.1242/dev.127.8.1593.