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Katherine A. Murphy

Researcher at University of California, Davis

Publications -  16
Citations -  750

Katherine A. Murphy is an academic researcher from University of California, Davis. The author has contributed to research in topics: Circadian clock & Internal medicine. The author has an hindex of 7, co-authored 12 publications receiving 578 citations. Previous affiliations of Katherine A. Murphy include Stanford University.

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Highly evolvable malaria vectors: The genomes of 16 Anopheles mosquitoes

Daniel E. Neafsey, +133 more
- 02 Jan 2015 - 
TL;DR: The authors investigated the genomic basis of vectorial capacity and explore new avenues for vector control, sequenced the genomes of 16 anopheline mosquito species from diverse locations spanning ~100 million years of evolution Comparative analyses show faster rates of gene gain and loss, elevated gene shuffling on the X chromosome, and more intron losses, relative to Drosophila.
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Ingestion of genetically modified yeast symbiont reduces fitness of an insect pest via RNA interference.

TL;DR: This is the first study to show that yeast can be used to deliver dsRNA to an insect pest, and it is demonstrated that this biopesticide decreases larval survivorship, and reduces locomotor activity and reproductive fitness in adults, which are indicative of general health decline.
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CK1α Collaborates with DOUBLETIME to Regulate PERIOD Function in the Drosophila Circadian Clock.

TL;DR: The results indicate that CK1α collaborates with the key clock kinase DOUBLETIME (DBT) in both the cytoplasm and the nucleus to regulate the timing of PER-dependent repression of the circadian transcriptome.
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CD58 Aberrations Limit Durable Responses to CD19 CAR in Large B Cell Lymphoma Patients Treated with Axicabtagene Ciloleucel but Can be Overcome through Novel CAR Engineering

TL;DR: This work evaluated CD58 status in fifty-one R/R LBCL patients treated at Stanford with commercial axicabtagene ciloleucel (axi-cel) through immunohistochemistry (IHC) on tumor biopsy samples and/or deep sequencing of circulating tumor DNA by CAPP-Seq, and identified that CAR T cell response to tumors lacking functional CD58 is likely to be overcome.