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153. Kidins220/ARMS mediates the integration of the neurotrophin and VEGF pathways in the vascular and nervous systems

Author

Cesca, F, primary, Yabe, A, additional, Spencer-Dene, B, additional, Scholz-Starke, J, additional, Medrihan, L, additional, Maden, C H, additional, Gerhardt, H, additional, Orriss, I R, additional, Baldelli, P, additional, Al-Qatari, M, additional, Koltzenburg, M, additional, Adams, R H, additional, Benfenati, F, additional, and Schiavo, G, additional

Published
2011
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171. cAMP induced modifications of HOX D gene expression in prostate cells allow the identification of a chromosomal area involved in vivo with neuroendocrine differentiation of human advanced prostate cancers

Author

Cantile, M., primary, Kisslinger, A., additional, Cindolo, L., additional, Schiavo, G., additional, D'antò, V., additional, Franco, R., additional, Altieri, V., additional, Gallo, A., additional, Villacci, A., additional, Tramontano, D., additional, and Cillo, C., additional

Published
2005
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172. CLOSTRIDIAL NEUROTOXINS

Author

Verastegui, C., primary, Lalli, G., additional, Bohnert, S., additional, Meunier, F. A., additional, and Schiavo, G., additional

Published
2002
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173. Synaptic vesicle endocytosis mediates the entry of tetanus neurotoxin into hippocampal neurons

Author

Matteoli, M, Verderio, C, Rossetto, O, Iezzi, N, Coco, S, Schiavo, G, Montecucco, C, Montecucco, C., COCO, SILVIA, Matteoli, M, Verderio, C, Rossetto, O, Iezzi, N, Coco, S, Schiavo, G, Montecucco, C, Montecucco, C., and COCO, SILVIA

Abstract

Tetanus neurotoxin causes the spastic paralysis of tetanus by blocking neurotransmitter release at inhibitory synapses of the spinal cord. This is due to the penetration of the toxin inside the neuronal cytosol where it cleaves specifically VAMP/synaptobrevin, an essential component of the neuroexocytosis apparatus. Here we show that tetanus neurotoxin is internalized inside the lumen of small synaptic vesicles following the process of vesicle reuptake. Vesicle acidification is essential for the toxin translocation in the cytosol, which results in the proteolytic cleavage of VAMP/ synaptobrevin and block of exocytosis

Published
1996

174. The effects of pH on the interaction of anthrax toxin lethal and edema factors with phospholipid vesicles.

Author

Kochi, S K, Martin, Isabelle, Schiavo, G, Mock, M, Cabiaux, Véronique, Kochi, S K, Martin, Isabelle, Schiavo, G, Mock, M, and Cabiaux, Véronique

Abstract

Bacillus anthracis secretes three distinct proteins which interact in binary combinations to produce two toxins. The two effector moieties, edema factor (EF) and lethal factor (LF), interact competitively with the cell receptor-binding moiety, protective antigen (PA), to produce biologically distinct effects. The passage of the toxins through an acidified endosomal compartment is an essential step in the intoxication process, and it has been shown that low pH triggers the insertion of the activated form of PA, PA63, into model lipid bilayers. In this study, we have examined the effects of pH on the interaction of LF and EF with a model membrane system. Protein labeling by radioactive phospholipid probes indicated that both LF and EF are able to insert into asolectin lipid bilayers in a pH-dependent manner. For LF, the extent of insertion into the bilayer was accompanied in parallel by the release of calcein from preloaded LUV (large unilamellar vesicles). The transition pH for protein insertion, however, was somewhat higher than that for membrane destabilization. The extent of protein radiolabeling and the release of calcein from LUV incubated with EF was similar to that seen with LF; however, the pH dependency was significantly less. Low pH-induced membrane insertion by both proteins was accompanied by only a minimal change in conformation. These results suggest that LF and EF may be actively involved in the process of toxin translocation., In Vitro, Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S., SCOPUS: ar.j, info:eu-repo/semantics/published

Published
1994

191. Identification an d association analysis of several hundred single nucleotide polymorphisms within candidate genes for back fat thickness in Italian Large White pigs using a selective genotyping approach.

Author

Fontanesi, L., Galimberti, G., Calò, D. G., Fronza, R., Martelli, P. L., Scotti, E., Colombo, M., Schiavo, G., Casadio, R., Buttazzoni, L., and Russo, V.

Subjects
SINGLE nucleotide polymorphisms, SWINE genetics, GENOTYPE-environment interaction, NUCLEOTIDE sequence, GENETIC markers, OBESITY
Abstract

Combining different approaches (rese-quencing of portions of 54 obesity candidate genes, literature mining for pig markers associated with fat deposition or related traits in 77 genes, and in silico mining of porcine expressed sequence tags and other sequences available in databases), we identified and analyzed 736 SNP within candidate genes to identify markers associated with back fat thickness (BFT) in Italian Large White sows. Animals were chosen using a selective genotyping approach according to their EBV for BFT (276 with most negative and 279 with most positive EBV) within a population of ∼12,000 pigs. Association analysis between the SNP and BFT has been carried out using the MAX test proposed for case-control studies. The designed assays were successful for 656 SNP: 370 were excluded (low call rate or minor allele frequency <5%), whereas the remaining 286 in 212 genes were taken for subsequent analyses, among which 64 showed a Pnominal value <0.1. To deal with the multiple testing problem in a candidate gene approach, we applied the proportion of false positives (PFP) method. Thirty-eight SNP were significant (PPFP < 0.20). The most significant SNP was the IGF2 intron3-g.3072G>A polymorphism (Pnominal < 1.0E-50). The second most significant SNP was the MC4R c.l426A>G polymorphism (nominal = 8.0E-05). The third top SNP (nominal = 6.2E-04) was the intronic TBCIDI g.219G>A polymorphic site, in agreement with our previous results obtained in an independent study. The list of significant markers also included SNP in additional genes (ABHD16A, ABHD5, ACP2, ALMS1, APOA2, ATP1A2, CALR, COL14A1, CTSF, DARS, DECR1, ENPP1, ESR1, GHl, GHRL, GNMT, 1KBKB, JAK3, MTTP, NFKB1A, NT5E, PLAT, PPARG, PPP2R5D, PRLR, RRAGD, RFC2, SDHD, SER-PINF1, UBE2H, VCAM1, and WAT). Functional relationships between genes were obtained using the Ingenuity Pathway Analysis (IPA) Knowledge Base. The top scoring pathway included 19 genes with a Pnominal < 0.1,2 of which (IKBKB and NFKBIA) are involved in the hypothalamic IKKβ/NFκB program that could represent a key axis to affect fat deposition traits in pigs. These results represent a starting point to plan marker-assisted selection in Italian Large White nuclei for BFT. Because of similarities between humans and pigs, this study might also provide useful clues to investigate genetic factors affecting human obesity. [ABSTRACT FROM AUTHOR]

Published
2012
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192. Kidins220/ARMS mediates the integration of the neurotrophin and VEGF pathways in the vascular and nervous systems.

Author

Cesca, F, Yabe, A, Spencer-Dene, B, Scholz-Starke, J, Medrihan, L, Maden, C H, Gerhardt, H, Orriss, I R, Baldelli, P, Al-Qatari, M, Koltzenburg, M, Adams, R H, Benfenati, F, and Schiavo, G

Subjects
PROTEIN-tyrosine kinases, CELL differentiation, NEUROTROPHINS, VASCULAR endothelial growth factors, PREGNANCY
Abstract

Signaling downstream of receptor tyrosine kinases controls cell differentiation and survival. How signals from different receptors are integrated is, however, still poorly understood. In this work, we have identified Kidins220 (Kinase D interacting substrate of 220 kDa)/ARMS (Ankyrin repeat-rich membrane spanning) as a main player in the modulation of neurotrophin and vascular endothelial growth factor (VEGF) signaling in vivo, and a primary determinant for neuronal and cardiovascular development. Kidins220−/− embryos die at late stages of gestation, and show extensive cell death in the central and peripheral nervous systems. Primary neurons from Kidins220−/− mice exhibit reduced responsiveness to brain-derived neurotrophic factor, in terms of activation of mitogen-activated protein kinase signaling, neurite outgrowth and potentiation of excitatory postsynaptic currents. In addition, mice lacking Kidins220 display striking cardiovascular abnormalities, possibly due to impaired VEGF signaling. In support of this hypothesis, we demonstrate that Kidins220 constitutively interacts with VEGFR2. These findings, together with the data presented in the accompanying paper, indicate that Kidins220 mediates the integration of several growth factor receptor pathways during development, and mediates the activation of distinct downstream cascades according to the location and timing of stimulation. [ABSTRACT FROM AUTHOR]

Published
2012
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198. CLOSTRIDIAL NEUROTOXINS

Author

Verastegui, C., Lalli, G., Bohnert, S., Meunier, F. A., and Schiavo, G.

Abstract

Tetanus (TeNT) and botulinum (BoNTs) neurotoxins are powerful toxins endowed with a specific zinc-endopeptidase activity. Targets of these neurotoxins have been identified as synaptic members of the SNARE proteins, which are involved in the exocytosis of neurotransmitters at the synapse. Despite this identical intracellular mechanism of action, TeNT and BoNTs target different neurons in vivo. After binding at the neuromuscular junction, BoNTs block neurotransmitter release at this site, whereas TeNT is retrogradely transported through motor neurons and inhibits exocytosis in inhibitory interneurons. Recently, several studies have reported the structure of these neurotoxins and clarified important aspects of the intoxication process. However, important questions on the mechanism responsible for the binding specificity and for the targeting of TeNT and BoNTs remain to be addressed. Once elucidated, this novel information would enables us to use CNTs more efficiently as therapeutic tools in neuronal disorders.

Published
2002
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