RICERCA ITALIANA     

Programmi di ricerca simili:

• 1 - Modulazione dei meccanismi di apoptosi in corso di risposta immunitaria/infiammatoria: studio delle interazioni tra citochine della famiglia del TNF per la caratterizzazione di meccanismi molecolari e cellulari funzionali alla identificazione di nuovi target per la terapia di malattie croniche degenerative.
• 2 - Processi apoptotici nella differenziazione e degenerazione cellulare
• 3 - Il sistema GITR/GITRL nelle malattie a patogenesi autoimmunitaria/infiammatoria: un bersaglio per la terapia farmacologica
• 4 - Mitocondri e morte cellulare: identificazione di nuovi bersagli terapeutici
• 5 - Il fattore di trascrizione NF-kB nella regolazione del differenziamento ed apoptosi del sistema immune.
• 6 - L'autofagia nell'omeostasi del sistema immunitario: ruolo nella patogenesi e nella progressione delle malattie autoimmuni
• 7 - Identificazione di nuovi meccanismi molecolari dei glucocorticoidi nella regolazione di geni coinvolti nei processi infiammatori.
• 8 - Apoptosi e terapia del cancro: caratterizzazione di nuovi meccanismi e nuove molecole modulatrici dell'apoptosi
• 9 - I membri della famiglia del TNF nella modulazione del differenziamento cellulare e dell'attività antitumorale
• 10 - INTERRELAZIONI TRA LA PERMEABILITÀ IONICA DI MEMBRANA E LO STATO REDOX INTRACELLULARE NEI PROCESSI NEURODEGENERATIVI: AZIONE DEI PEPTIDI AMILOIDI IN CELLULE NEURONALI E GLIALI.

Classificazione scientifico-disciplinare

• Area scientifico disciplinare: Scienze biologiche
  • FARMACOLOGIA

Classificazione brevettuale

• CHEMISTRY; METALLURGY
  • BIOCHEMISTRY; BEER; SPIRITS; WINE; VINEGAR; MICROBIOLOGY; ENZYMOLOGY; MUTATION OR GENETIC ENGINEERING
    • MICRO-ORGANISMS OR ENZYMES; COMPOSITIONS THEREOF (biocides, pest repellants or attractants, or plant growth regulators, containing micro-organisms, viruses, microbial fungi, enzymes, fermentates or substances produced by or extracted from micro-organisms or animal material A01N63/00; food compositions A21, A23; medicinal preparations A61K; chemical aspects of, or use of materials for, bandages, dressings, absorbent pads or surgical articles A61L; fertilisers C05); PROPAGATING, PRESERVING OR MAINTAINING MICRO-ORGANISMS (preservation of living parts of humans or animals A01N1/02); MUTATION OR GENETIC ENGINEERING; CULTURE MEDIA (micro-biological testing media C12Q)
  • ORGANIC CHEMISTRY (such compounds as the oxides, sulfides, or oxysulfides of carbon, cyanogen, phosgene, hydrocyanic acid or salts thereof C01; products obtained from layered base-exchange silicates by ion-exchange with organic compounds such as ammonium, phosphonium or sulfonium compounds or by intercalation of organic compounds C01B33/44; macromolecular compounds C08; dyes C09; fermentation products C12; fermentation or enzyme-using processes to synthesise a desired chemical compound or composition or to separate optical isomers from a racemic mixture C12P; production of organic compounds by electrolysis or electrophoresis C25B3/00, C25B7/00)
    • PEPTIDES (peptides in foodstuffs A23; obtaining protein compositions for foodstuffs, working-up proteins for foodstuffs A23J; preparations for medicinal purposes A61K; peptides containing beta-lactam rings C07D; cyclic dipeptides not having in their molecule any other peptide link than those which form their ring, e.g. piperazine-2,5-diones, C07D; ergot alkaloids of the cyclic peptide type C07D519/02; macromolecular compounds having statistically distributed amino acid units in their molecules, i.e. when the preparation does not provide for a specific; but for a random sequence of the amino acid units, homopolyamides and block copolyamides derived from amino acids C08G69/00; macromolecular products derived from proteins C08H1/00; preparation of glue or gelatine C09H; single cell proteins, enzymes C12N; genetic engineering processes for obtaining peptides C12N15/00; compositions for measuring or testing processes involving enzymes C12Q; investigation or analysis of biological material G01N33/00)

Classificazione geografica

• Regione: Sicilia

Bibliografia

1. LeBlanc AC. 2003 Natural cellular inhibitors of caspases. Prog Neuropsychopharmacol Biol Psychiatry. 2:215-29
2. Kaufmann SH, et al.2001.Programmed cell death: alive and well in the new millennium.Trends Cell Biol 11:526.
3. Jaattela M,et al.2003.Caspase-independent cell death in T lymphocytes.Nat Immunol. 4:416.
4. Mandic A, et al.2002.Calpain-mediated Bid cleavage and calpain-independent Bak modulation: two separate pathways in cisplatin-induced apoptosis. Mol Cell Biol 22:3003.
5. Nitsch R, et al.2000. Human brain-cell death induced by tumour-necrosis-factor-related apoptosis-inducing ligand (TRAIL). Lancet 2 356 : 827
6. Almasan A, et al.2003 Apo2L/TRAIL: apoptosis signaling, biology, and potential for cancer therapy. Cytokine & Growth factor Reviews. 14: 337-348.
7. Wiley SR, et al.1995. Identification and characterization of a new member of the TNF family that induces apoptosis. Immunity. 6:673-82.
8. Sheridan JP, et al. 1999 Control of TRAIL-induced apoptosis by a family of signaling and decoy receptors. Science. 277:818-21.
9. D'Adamio F, et al. 1997.A new dexamethasone-induced gene of the leucine zipper family protects T lymphocytes from TCR/CD3-activated cell death.Immunity 7:803
10. Delfino DV, et al 2004. Decrease of Bcl-xL and augmentation of thymocyte apoptosis in GILZ overexpressing transgenic mice. Blood 104 ;13 :4134-41
11. Yang B.Y., et al 1995 Fas and activation-induced Fas ligand mediate apoptosis of T cell hybridomas :. Inhibition of Fas ligand expression by retinoic acid and glucocorticoids J.Exp.Med. 181 : 1673-1682
12. Sprent J., et al.2002 The thymus and negative selection. Immunol Rev. 185:126-135.
13. Fridkis-Hareli M., et al..2004 New approaches to eliciting protective immunity through T cell repertoire manipulation: the concept of thymic vaccination. Med Immunol.:10.1186/1476-9433-3-2.
14. Lamhamedi-Cherradi S-E., et al.2003 Defective thymocyte apoptosis and accellerated autoimmune diseases in TRAIL-/- mice. Nat Immunol. 4:255-260.
15. Bouillet P., et al.(2002) BH3-only Bcl-2 family member Bim is required for apoptosis of autoreactive thymocytes. Nature 415:922-926
16. Lewis CE et al.. 1992.The Macrophage, ed. Oxford University Press. IRL Press,.1-415.
17. Perlman H, , et al.1999.FLICE-inhibitory protein expression during macrophage differentiation confers resistance to Fas-mediated apoptosis.J Exp Med 190:1679.
18. Pagliari LJ, et al. 2000.Macrophages require constitutive NF-kB activation to maintain A1 expression and mitochondrial homeostasis.Mol Cell Biol 20:8855.
19. Kausalya S, , et al. 2001.Requirement of A1-a for bacillus Calmette-Guerin-mediated protection of macrophages against nitric oxide-induced apoptosis. J Immunol 166:4721.
20. Zhou P, L, et al.1997.Mcl-1, a Bcl-2 family member, delays the death of hematopoietic cells under a variety of apoptosis-inducing conditions. Blood 89:630.
21. Liu H, et al. 2001.Constitutively activated Akt-1 is vital for the survival of human monocyte-differentiated macrophages.Role of Mcl-1, independent of nuclear factor (NF)-kappaB, Bad, or caspase activation. J Exp Med 194:113.
22. Grassme H, et al 2001 .Molecular mechanisms of bacteria induced apoptosis.Apoptosis 6:441.
23. Spellerberg B .2000. Pathogenesis of neonatal Streptococcus agalactiae infections.Microbes Infect 2:1733.
24. Fettucciari K, et al 2000 .Group B Streptococcus induces apoptosis in macrophages.J Immunol 165:3923.
25. Fettucciari K et al.2003.Involvement of mitogen-activated protein kinases in Group B Streptococcus-induced macrophage apoptosis.Pharmacol Res 47:355.
26. Mancuso G, et al. 2002.Mitogen-activated protein kinases and NF-kappa B are involved in TNF-alpha responses to group B streptococci.J Immunol 169:1401.
27. Cornacchione P, et al.1998.Group B streptococci persist inside macrophages.Immunology 93:86
28. Halaas Ø, et al 2004.Monocytes Stimulated with Group B Streptococci or Interferons Release Tumour Necrosis Factor-Related Apoptosis-Inducing Ligand.Scand J Immunol 60:74
29. .Halaas Ø,.2000.Lipopolysaccharide induces expression of APO2 ligand/TRAIL in human monocytes and macrophages.Scand J Immunol 51:244
30. Diehl GE, et al. 2004 .TRAIL-R as a negative regulator of innate immune cell responses.Immunity 21:877.
31. Deng Y, et al. 2002. TRAIL-induced apoptosis requires Bax-dependent mitochondrial release of Smac/DIABLO.Genes Dev. 16 : 33–45.
32. Lamothe B, et al.2002. Ectopic expression of Bcl-2 and Bcl-xL inhibits apoptosis induced by TNF-related apoptosis inducing ligand (TRAIL) through suppression of caspases-8, 7, and 3 and BID cleavage in human acute myelogenous leukemia cell line HL-60.J Interferon Cytokine Res 22:269.
33. Berrebi D, et al.2003.Synthesis of glucocorticoid-induced leucine zipper (GILZ) by macrophages: an anti-inflammatory and immunosuppressive mechanism shared by glucocorticoids and IL-10.Blood 101:729.
34. Selkoe DJ 1994 Normal and abnormal biology of the beta-amyloid precursor protein. Annu Rev Neurosci, 17:489-517
35. Yan SD, et al 1996 RAGE and amyloid-beta peptide neurotoxicity in Alzheimer's disease. Nature 382:685-91
36. Yaar M, et al 1997 Binding of beta-amyloid to the p75 neurotrophin receptor induces apoptosis. A possible mechanism for Alzheimer's disease. J Clin Invest. 100:2333-40.
37. Lorenzo A, et al 2000 Amyloid beta interacts with the amyloid precursor protein: a potential toxic mechanism in Alzheimer's disease. Nat Neurosci. 3:460-4.
38. Ivins KJ, et al 1999 Neuronal apoptosis induced by beta-amyloid is mediated by caspase-8. Neurobiol Dis 6:440-449
39. Dong Y.et al 2001 Immune function of astrocytes. Glia. 36:180-90.
40. Solà C et al 2002. Astrocytes enhance lypopolisaccharide-induced nitric oxide production by microglial cells. Eur J Neurosci. 16: 1275-83
41. Meda L, et al 1995 Activation of microglial cells by beta-amyloid protein and interferon-gamma. Nature 374:647-50.
42. Meda L, et al 1996 Beta-amyloid (25-35) peptide and IFN-gamma synergistically induce the production of the chemotactic cytokine MCP-1/JE in monocytes and microglial cells. J Immunol. 157:1213-8.
43. Araujo DM, et al 1992 Beta-amyloid stimulates glial cells in vitro to produce growth factors that accumulate in senile plaques in Alzheimer's disease. Brain Res. 569:141-5.
44. Bonaiuto C, et al 1997. Activation of nuclear factor-kappa B by beta-amyloid peptides and interferon-gamma in murine microglia J Neuroimmunol 77:51-6
45. Bianca VD, et al 1999 Beta-amyloid activates the O-2 forming NADPH oxidase in microglia, monocytes, and neutrophils. A possible inflammatory mechanism of neuronal damage in Alzheimer's disease. J Biol Chem. 274:15493-9.
46. Coyle JT,et al. 1993 Oxidative stress, glutamate, and neurodegenerative disorders. Science 262: 689-694
47. Mattson MP, et al. 2001 Dysregulation of cellular calcium homeostatis in Alzheimer's disease: bad genes and bad habits. J. Mol. Neurosci. 17: 205-224
48. Zucconi GG, et al.2002 Microglia activation and cell death in response to diethyl-dithiocarbamate acute administration J Comp Neurol 446; 2 :135-50
49. Ghezzi P, et al 1998 Tumor necrosis factor is increased in the spinal cord of an animal model of motor neuron degeneration. Eur Cytokine Netw. 9:139-44
50. Kwon D, et al 2001 Hydrogen peroxide triggers the expression of Fas/FasL in astrocytoma cell lines and augments apoptosis.J Neuroimmunol. 113:1-9.
51. Sprick MR, et al 2000 FADD/MORT1 and caspase-8 are recruited to TRAIL receptors 1 and 2 and are essential for apoptosis mediated by TRAIL receptor 2. Immunity. 12:599-609.
52. Villa P, et al 1997 Caspases and caspases inhibitors. TIBS, 22: 388-92.
53. Dziedzic T, et al 2003 Dexamethasone inhibits TNF-alpha synthesis more effectivelyin Alzheimer's disease patients than in healthy individuals. Dement Geriatr CognDisord. 16; 4:283-6.
54. Amsterdam A., et al 2002 The anti-inflammatory action of glucorticoids is mediated by cell type specific regulation of apoptosis Mol.Cell.Endocrin.189 : 1-9

Parole Chiave

TUMOR NECROSIS FACTOR RELATED APOPTOSIS INDUCING LIGAND (TRAIL); GLUCOCORTICOID INDUCED LEUCINE ZIPPER (GILZ); PROTEINE DELLA FAMIGLIA BCL-2; APOPTOSI; STREPTOCOCCO DI GRUPPO B (GBS); GLIA; MACROFAGI; TIMOCITI; PROCESSI IMMUNITARI/INFIAMMATORI