Activation of a Drosophila Janus kinase (JAK) causes hematopoietic neoplasia and developmental defects.
@article{Harrison1995ActivationOA, title={Activation of a Drosophila Janus kinase (JAK) causes hematopoietic neoplasia and developmental defects.}, author={Douglas A. Harrison and Richard Binari and Theresa Stines Nahreini and Michael Gilman and Norbert Perrimon}, journal={The EMBO Journal}, year={1995}, volume={14} }
In mammals, many cytokines and growth factors stimulate members of the Janus kinase (JAK) family to transduce signals for the proliferation and differentiation of various cell types, particularly in hematopoietic lineages. Mutations in the Drosophila hopscotch (hop) gene, which encodes a JAK, also cause proliferative defects. Loss‐of‐function alleles result in lethality and underproliferation of diploid tissues of the larva. A dominant gain‐of‐function allele, Tumorous‐lethal (hopTum‐l), leads…
487 Citations
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References
SHOWING 1-3 OF 3 REFERENCES
The Genetics and Biology of Drosophila
- BiologyHeredity
- 1976
This is the first attempt since 1925 to publish a comprehensive account of the biology and genetics of Drosophila and it aims to collate the dauntingly large literature on the subject and to make more accessible the private language ot the Dosophilist.
Molecular Cloning: A Laboratory Manual
- Biology
- 1983
The content has been entirely recast to include nucleic-acid based methods selected as the most widely used and valuable in molecular and cellular biology laboratories.
Antibodies: A
- Hanratty,W.P. and Ryerse,J.S
- 1981