The HECT-type E3 ubiquitin ligase (E3) Itch is absent in the non-agouti-lethal 18H or Itchy mice, which develop a severe immunological disease, including lung and stomach inflammation and hyperplasia of lymphoid and hematopoietic cells. The involvement of Itch in multiple signaling pathways and pathological conditions is presently an area of extensive scientific interest. This review aims to bring together a growing body of work exploring Itch-regulated biological processes, and to highlight recent discoveries on the regulatory mechanisms modulating its catalytic activity and substrate recognition capability. Our contribution is also an endeavor to correlate Itch substrate specificity with the pathological defects manifested by the mutant Itchy mice.

Melino, G., Gallagher, E., Aqeilan, R.i., Knight, R., Peschiaroli, A., Rossi, M., et al. (2008). Itch: A HECT-type E3 ligase regulating immunity, skin and cancer. CELL DEATH AND DIFFERENTIATION, 15(7), 1103-1112 [10.1038/cdd.2008.60].

Itch: A HECT-type E3 ligase regulating immunity, skin and cancer

MELINO, GENNARO;ROSSI, MARIACRISTINA;BERNASSOLA, FRANCESCA
2008-01-01

Abstract

The HECT-type E3 ubiquitin ligase (E3) Itch is absent in the non-agouti-lethal 18H or Itchy mice, which develop a severe immunological disease, including lung and stomach inflammation and hyperplasia of lymphoid and hematopoietic cells. The involvement of Itch in multiple signaling pathways and pathological conditions is presently an area of extensive scientific interest. This review aims to bring together a growing body of work exploring Itch-regulated biological processes, and to highlight recent discoveries on the regulatory mechanisms modulating its catalytic activity and substrate recognition capability. Our contribution is also an endeavor to correlate Itch substrate specificity with the pathological defects manifested by the mutant Itchy mice.
2008
Pubblicato
Rilevanza internazionale
Articolo
Sì, ma tipo non specificato
Settore BIO/11 - BIOLOGIA MOLECOLARE
English
Con Impact Factor ISI
adaptor protein; cytokine; mutant protein; Notch receptor; protein c jun; protein Itch; regulator protein; transcription factor; transforming growth factor beta; ubiquitin protein ligase E3; apoptosis; autoimmune disease; autoimmunity; binding affinity; carboxy terminal sequence; cell differentiation; cell fate; cell growth; cell proliferation; cell renewal; cell stress; clonal anergy; disease course; DNA damage; enzyme activation; enzyme activity; enzyme analysis; enzyme localization; enzyme specificity; enzyme substrate; epidermis cell; gene expression regulation; gene mutation; growth regulation; human; immune response; immunological tolerance; immunopathogenesis; immunopathology; immunoregulation; inflammation; keratinocyte; lung disease; lymphocyte differentiation; malignant neoplastic disease; malignant transformation; mutational analysis; nonhuman; pathophysiology; priority journal; protein binding; protein degradation; protein expression; protein family; protein phosphorylation; protein processing; protein protein interaction; protein stability; regulatory mechanism; review; signal transduction; skin disease; T lymphocyte activation; transcription regulation; ubiquitination; Animals; Cell Death; Immune System; Keratinocytes; Mice; Mice, Mutant Strains; Neoplasms; Phosphorylation; Protein Transport; Receptor, Epidermal Growth Factor; Receptors, Chemokine; Repressor Proteins; Signal Transduction; Skin; Substrate Specificity; Transforming Growth Factor beta; TRPC Cation Channels; Ubiquitin; Ubiquitin-Protein Ligases; Agouti; Mus
Melino, G., Gallagher, E., Aqeilan, R.i., Knight, R., Peschiaroli, A., Rossi, M., et al. (2008). Itch: A HECT-type E3 ligase regulating immunity, skin and cancer. CELL DEATH AND DIFFERENTIATION, 15(7), 1103-1112 [10.1038/cdd.2008.60].
Melino, G; Gallagher, E; Aqeilan, Ri; Knight, R; Peschiaroli, A; Rossi, M; Scialpi, F; Malatesta, M; Zocchi, L; Browne, G; Ciechanover, A; Bernassola, F
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/30419
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