A
Akira Imamoto
Researcher at University of Chicago
Publications - 35
Citations - 3890
Akira Imamoto is an academic researcher from University of Chicago. The author has contributed to research in topics: CRKL & Proto-oncogene tyrosine-protein kinase Src. The author has an hindex of 24, co-authored 35 publications receiving 3709 citations. Previous affiliations of Akira Imamoto include Baylor College of Medicine & University of Texas MD Anderson Cancer Center.
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Journal ArticleDOI
Disruption of overlapping transcripts in the ROSA βgeo 26 gene trap strain leads to widespread expression of β-galactosidase in mouse embryos and hematopoietic cells
Brian Zambrowicz,Akira Imamoto,Steve Fiering,Leonard A. Herzenberg,William G. Kerr,Philippe Soriano +5 more
TL;DR: Staining of ROSA26 tissues and fluorescence-activated cell sorter-Gal analysis of hematopoietic cells demonstrates ubiquitous expression of the proviral beta geo reporter gene, and bone marrow transfer experiments illustrate the general utility of this strain for chimera and transplantation studies.
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Disruption of the csk gene, encoding a negative regulator of Src family tyrosine kinases, leads to neural tube defects and embryonic lethality in mice
Akira Imamoto,Philippe Soriano +1 more
TL;DR: It is demonstrated that Src family kinase activity is critically dependent on phosphorylation by Csk and suggested that the regulation of Kinase activity may be essential during embryogenesis.
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The Adaptor Protein Paxillin Is Essential for Normal Development in the Mouse and Is a Critical Transducer of Fibronectin Signaling
Margit Hagel,Elizabeth George,Ann Kim,Rulla M. Tamimi,Sarah L. Opitz,Christopher E. Turner,Akira Imamoto,Sheila M. Thomas +7 more
TL;DR: Paxillin and fibronectin regulate some common embryonic developmental events, possibly due to paxillin modulation of fibronECTin-regulated focal adhesion dynamics and organization of the membrane cytoskeletal structures that regulate cell migration and spreading.
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Specific and redundant roles of Src and Fyn in organizing the cytoskeleton.
TL;DR: In this article, the role of activated Src family kinases in the csk- phenotype was determined by introducing mutations in the src and fyn genes into the Csk- mutant background, and the src- mutation can restore the normal distribution of cortactin and partly correct filamentous actin organization.
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Mice lacking the homologue of the human 22q11.2 gene CRKL phenocopy neurocristopathies of DiGeorge syndrome
TL;DR: It is reported that mice homozygous for a targeted null mutation at the CrkL locus exhibit defects in multiple cranial and cardiac neural crest derivatives including the cranial ganglia, aortic arch arteries, cardiac outflow tract, thymus, parathyroid glands and craniofacial structures.