The coastal zone provides foraging opportunities for insular populations of terrestrial mammals, allowing for expanded habitat use, increased dietary breadth, and locally higher population densities. We examined the use of sandy beach resources by the threatened island fox (Urocyon littoralis) on the California Channel Islands using scat analysis, surveys of potential prey, beach habitat attributes, and stable isotope analysis. Consumption of beach invertebrates, primarily intertidal talitrid amphipods (Megalorchestia spp.) by island fox varied with abundance of these prey across sites. Distance-based linear modeling revealed that abundance of giant kelp (Macrocystis pyrifera) wrack, rather than beach physical attributes, explained the largest amount of variation in talitrid amphipod abundance and biomass across beaches. δ13C and δ15N values of fox whisker (vibrissae) segments suggested individualism in diet, with generally low δ13C and δ15N values of some foxes consistent with specializing on primarily terrestrial foods, contrasting with the higher isotope values of other individuals that suggested a sustained use of sandy beach resources, the importance of which varied over time. Abundant allochthonous marine resources on beaches, including inputs of giant kelp, may expand habitat use and diet breadth of the island fox, increasing population resilience during declines in terrestrial resources associated with climate variability and long-term climate change.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8553077 | PMC |
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0258919 | PLOS |
Cancer Res
June 2012
Department of Biochemistry and Cancer Biology, College of Medicine, Health Science Campus, University of Toledo, Toledo, Ohio, USA.
Epigenetic modifications such as histone methylation play an important role in human cancer metastasis. Enhancer of zeste homolog 2 (EZH2), which encodes the histone methyltransferase component of the polycomb repressive complex 2 (PRC2), is overexpressed widely in breast and prostate cancers and epigenetically silences tumor suppressor genes. Expression levels of the novel tumor and metastasis suppressor Raf-1 kinase inhibitor protein (RKIP) have been shown to correlate negatively with those of EZH2 in breast and prostate cell lines as well as in clinical cancer tissues.
View Article and Find Full Text PDFFEBS Lett
November 2006
Medical University of Ohio, Department of Biochemistry and Cancer Biology, 3035 Arlington Avenue, Toledo, OH 43614-5804, USA.
The Raf kinase inhibitory protein (RKIP) binds to Raf-1 interfering with binding of the MEK substrate and potentially also Raf-1 activation. In response to mitogen stimulation RKIP dissociates from Raf-1 and later re-associates. Here, using a combination of mutational approaches, biochemical studies, peptide arrays and plasmon surface resonance (BIAcore), we fine map and characterize a minimal 24 amino acid long RKIP binding domain in the Raf-1 N-region, which consists of constitutive elements at both flanks and a center element that is regulated by phosphorylation and enhances the re-binding of RKIP to Raf-1 in the later phase of mitogen stimulation.
View Article and Find Full Text PDFOncogene
May 2005
Medical College of Ohio, Department of Biochemistry & Cancer Biology, 3035 Arlington Avenue, Toledo, OH 43614-5804, USA.
The Raf-MEK-ERK protein kinase cascade is a highly conserved signaling pathway that is pivotal in relaying environmental cues from the cell surface to the nucleus. Three Raf isoforms, which share great sequence and structure similarities, have been identified in mammalian cells. We have previously identified Raf kinase inhibitor protein (RKIP) as a negative regulator of the Raf-MEK-ERK signaling pathway by specifically binding to the Raf-1 isoform.
View Article and Find Full Text PDFJ Biol Chem
April 2004
Department of Medicine, Brown University and Rhode Island Hospital, Providence, Rhode Island 02903, USA.
Cancer cells are more susceptible to chemotherapeutic agent-induced apoptosis than their normal counterparts. Although it has been demonstrated that the increased sensitivity results from deregulation of oncoproteins during cancer development (Evan, G. I.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!