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Charles W. Walker

Researcher at University of New Hampshire

Publications -  54
Citations -  1936

Charles W. Walker is an academic researcher from University of New Hampshire. The author has contributed to research in topics: Sea urchin & Strongylocentrotus droebachiensis. The author has an hindex of 26, co-authored 54 publications receiving 1802 citations. Previous affiliations of Charles W. Walker include Durham University.

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Comparative genomics explains the evolutionary success of reef-forming corals.

TL;DR: Transcriptome and genome data from twenty stony coral species and a selection of reference bilaterians were studied to elucidate coral evolutionary history and identify genes that encode the proteins responsible for the precipitation and aggregation of the aragonite skeleton on which the organisms live.
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Oxidative stress, DNA damage and p53 expression in the larvae of atlantic cod (Gadus morhua) exposed to ultraviolet (290-400 nm) radiation.

TL;DR: Cellular death caused by apoptosis is the most likely cause of mortality in embryos and larvae in these laboratory experiments, while the smaller size at hatching in those larvae that survived is caused by permanent cellular growth arrest in response to DNA damage.
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Manipulation of food and photoperiod promotes out-of-season gametogenesis in the green sea urchin, Strongylocentrotus droebachiensis: implications for aquaculture

TL;DR: Changes in the two principal cell types in the germinal epithelium of urchin gonads are described and indicate how knowledge of their population dynamics may be useful in aquaculture applications.
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Expression of homologues for p53 and p73 in the softshell clam (Mya arenaria), a naturally-occurring model for human cancer.

TL;DR: Structural and functional data for p53 and p73 cDNAs and gene products in a naturally occurring, non-mammalian disease model suggest that p53/p73-related molecular mechanisms that are held in common with Burkitt's lymphoma or other human cancers may be revealed.
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Mortalin-based cytoplasmic sequestration of p53 in a nonmammalian cancer model.

TL;DR: Leukemic clam hemocytes are introduced as novel and easily accessible, in vivo and in vitro models for human cancers displaying a similar mortalin-based phenotype and treatment of these models with novel chemotherapeutics may help reveal the molecular mechanism(s) involved in inactivating p53 by this form of cytoplasmic sequestration.