Mycotoxins

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  Subject Areas on Research

  • A 13-kilodalton maize mitochondrial protein in E. coli confers sensitivity to Bipolaris maydis toxin. 
  • Acylation of naturally occurring and synthetic 1-deoxysphinganines by ceramide synthase. Formation of N-palmitoyl-aminopentol produces a toxic metabolite of hydrolyzed fumonisin, AP1, and a new category of ceramide synthase inhibitor. 
  • Alteration of tissue and serum sphinganine to sphingosine ratio: an early biomarker of exposure to fumonisin-containing feeds in pigs. 
  • Alterations in reticulo-endothelial functions as produced by the administration of bacterial toxins. 
  • Cell cycle progression in G1 and S phases is CCR4 dependent following ionizing radiation or replication stress in Saccharomyces cerevisiae. 
  • Chronic toxicity of fumonisins from Fusarium moniliforme culture material (M-1325) to mink. 
  • Cross-linking of the cms-T maize mitochondrial pore-forming protein URF13 by N,N'-dicyclohexylcarbodiimide and its effect on URF13 sensitivity to fungal toxins. 
  • Dietary fumonisin B1 induces disruption of sphingolipid metabolism in Sprague-Dawley rats: a new mechanism of nephrotoxicity. 
  • Effect of nandrolone decanoate administration on recovery from bupivacaine-induced muscle injury. 
  • Effects of feeding Fusarium moniliforme culture material, containing known levels of fumonisin B1, on the young broiler chick. 
  • Endosymbiosis: the evil within. 
  • Evidence for disruption of sphingolipid metabolism as a contributing factor in the toxicity and carcinogenicity of fumonisins. 
  • Fluorescence staining of the actin cytoskeleton in living cells with 7-nitrobenz-2-oxa-1,3-diazole-phallacidin. 
  • Fumonisin B1 alters sphingolipid metabolism and disrupts the barrier function of endothelial cells in culture. 
  • Fumonisin B1 inhibits sphingosine (sphinganine) N-acyltransferase and de novo sphingolipid biosynthesis in cultured neurons in situ. 
  • Fumonisin inhibition of de novo sphingolipid biosynthesis and cytotoxicity are correlated in LLC-PK1 cells. 
  • Fumonisin toxicity and sphingolipid biosynthesis. 
  • Fumonisins and other inhibitors of de novo sphingolipid biosynthesis. 
  • Functional expression of the Aspergillus flavus PKS-NRPS hybrid CpaA involved in the biosynthesis of cyclopiazonic acid. 
  • Fungal toxins bind to the URF13 protein in maize mitochondria and Escherichia coli. 
  • Importance of sphingolipids and inhibitors of sphingolipid metabolism as components of animal diets. 
  • In vitro toxicology of fumonisins and the mechanistic implications. 
  • Increases in serum sphingosine and sphinganine and decreases in complex sphingolipids in ponies given feed containing fumonisins, mycotoxins produced by Fusarium moniliforme. 
  • Inflammatory cytokine gene expression in THP-1 cells exposed to Stachybotrys chartarum and Aspergillus versicolor. 
  • Inhibition of sphingolipid biosynthesis by fumonisins. Implications for diseases associated with Fusarium moniliforme. 
  • Mutations in the maize mitochondrial T-urf13 gene eliminate sensitivity to a fungal pathotoxin. 
  • Mycotoxins and interstitial lung disease. 
  • N,N'-dicyclohexylcarbodiimide cross-linking suggests a central core of helices II in oligomers of URF13, the pore-forming T-toxin receptor of cms-T maize mitochondria. 
  • Role of dietary sphingolipids and inhibitors of sphingolipid metabolism in cancer and other diseases. 
  • Sphingolipid biosynthesis de novo by rat hepatocytes in culture. Ceramide and sphingomyelin are associated with, but not required for, very low density lipoprotein secretion. 
  • Sphingolipids as biomarkers of fumonisin exposure and risk of esophageal squamous cell carcinoma in china. 
  • Sphingolipids--the enigmatic lipid class: biochemistry, physiology, and pathophysiology. 
  • Structural and functional analysis of separated strands of killer double-stranded RNA of yeast. 
  • The effect of fumonisin B1 on developing chick embryos: correlation between de novo sphingolipid biosynthesis and gross morphological changes. 
  • URF13, a ligand-gated, pore-forming receptor for T-toxin in the inner membrane of cms-T mitochondria.