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Claire de la Cova, Ph.D.

Affiliations: 
2008 Columbia University, New York, NY 
 2018- University of Wisconsin-Milwaukee, Milwaukee, WI 
Area:
Genetics, Cell Biology
Website:
https://uwm.edu/biology/people/de-la-cova-claire/
Google:
"Claire de la Cova"
Bio:

https://uwm.edu/biology/wp-content/uploads/sites/21/2018/08/de-la-Cova-CV-2018.pdf

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Parents

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Laura A. Johnston grad student 2008 Columbia
 (Control of growth and cell competition by dMyc in Drosophila melanogaster.)
Iva Susan Greenwald post-doc 2008-2018 Columbia (GenetiTree)

Children

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Publications

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Rodriguez Torres CS, Wicker NB, Puccini de Castro V, et al. (2024) The Caenorhabditis elegans protein SOC-3 permits an alternative mode of signal transduction by the EGL-15 FGF receptor. Developmental Biology
Townley RA, Stacy KS, Cheraghi F, et al. (2024) The Raf/LIN-45 C-terminal distal tail segment negatively regulates signaling in . Biorxiv : the Preprint Server For Biology
Kodra AL, Sharma Singh A, de la Cova C, et al. (2024) The Drosophila TNF Eiger promotes Myc super-competition independent of canonical JNK signaling. Genetics
de la Cova CC. (2023) The Highs and Lows of FBXW7: New Insights into Substrate Affinity in Disease and Development. Cells. 12
Townley R, Deniaud A, Stacy KS, et al. (2023) The E3/E4 ubiquitin ligase UFD-2 suppresses normal and oncogenic signaling mediated by a Raf ortholog in . Science Signaling. 16: eabq4355
de la Cova CC, Townley R, Greenwald I. (2020) Negative feedback by conserved kinases patterns degradation of Raf in vulval fate patterning. Development (Cambridge, England)
Kodra A, de la Cova C, Gerhold AR, et al. (2020) Widely used mutants of , encoding the Tumor Necrosis factor, carry additional mutations in the NimrodC1 phagocytosis receptor. G3 (Bethesda, Md.)
de la Cova C, Townley R, Regot S, et al. (2017) A Real-Time Biosensor for ERK Activity Reveals Signaling Dynamics during C. elegans Cell Fate Specification. Developmental Cell
Meyer SN, Amoyel M, Bergantiños C, et al. (2014) An ancient defense system eliminates unfit cells from developing tissues during cell competition. Science (New York, N.Y.). 346: 1258236
de la Cova C, Senoo-Matsuda N, Ziosi M, et al. (2014) Supercompetitor status of Drosophila Myc cells requires p53 as a fitness sensor to reprogram metabolism and promote viability. Cell Metabolism. 19: 470-83
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