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Cited by 296

The DOI matches its Crossref record; 51 of the 51 references it cites were found in a registry or an index.

Analysis of Ras-Induced Overproliferation in Drosophila Hemocytes

Asha, H, Nagy, Istvan, Kovacs, Gabor, Stetson, Daniel, Ando, Istvan, Dearolf, Charles R·2003·Genetics

Abstract

We use the Drosophila melanogaster larval hematopoietic system as an in vivo model for the genetic and functional genomic analysis of oncogenic cell overproliferation. Ras regulates cell proliferation and differentiation in multicellular eukaryotes. To further elucidate the role of activated Ras in cell overproliferation, we generated a collagen promoter-Gal4 strain to overexpress RasV12 in Drosophila hemocytes. Activated Ras causes a dramatic increase in the number of circulating larval hemocytes (blood cells), which is caused by cellular overproliferation. This phenotype is mediated by the Raf/MAPK pathway. The mutant hemocytes retain the ability to phagocytose bacteria as well as to differentiate into lamellocytes. Microarray analysis of hemocytes overexpressing RasV12 vs. Ras+ identified 279 transcripts that are differentially expressed threefold or more in hemocytes expressing activated Ras. This work demonstrates that it will be feasible to combine genetic and functional genomic approaches in the Drosophila hematopoietic system to systematically identify oncogene-specific downstream targets.

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Metadata

Authors
Asha, H., Nagy, I., Kovacs, G., Stetson, D., Ando, I., & Dearolf, C. R.
Venue
Genetics
Published
2003-01-01
Volume
163
Issue
1
Pages
203-215
ISSN
  • 0016-6731 (ISSN-L)
  • 1943-2631
OpenAlex
W1885479805
Cited by
296
References
51
FWCI
4.99
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Analysis of Ras-Induced Overproliferation in Drosophila Hemocytes. https://app.cochat.ai/papers/10.1093/genetics/163.1.203
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Asha, H., Nagy, I., Kovacs, G., Stetson, D., Ando, I., & Dearolf, C. R. (2003). Analysis of Ras-Induced Overproliferation in Drosophila Hemocytes. Genetics. https://doi.org/10.1093/genetics/163.1.203

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