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Itchy E3 ubiquitin protein ligase homolog

Itch, AIP4, AIF4
This gene encodes a member of the Nedd4 family of HECT domain E3 ubiquitin ligases. HECT domain E3 ubiquitin ligases transfer ubiquitin from E2 ubiquitin-conjugating enzymes to protein substrates, thus targeting specific proteins for lysosomal degradation. The encoded protein plays a role in multiple cellular processes including erythroid and lymphoid cell differentiation and the regulation of immune responses. Mutations in this gene are a cause of syndromic multisystem autoimmune disease. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene. [provided by RefSeq, Mar 2012] (from NCBI)
Papers on Itch
The Nedd4-like ubiquitin E3 ligases target angiomotin/p130 to ubiquitin-dependent degradation.
Yu et al., Shanghai, China. In Biochem J, 2012
Knockdown of Nedd4, Nedd4-2 and Itch causes an accumulation of steady-state level of AMOT/p130.
Novel roles for the E3 ubiquitin ligase atrophin-interacting protein 4 and signal transduction adaptor molecule 1 in G protein-coupled receptor signaling.
Marchese et al., Maywood, United States. In J Biol Chem, 2012
Overexpression of an AIP4 catalytically inactive mutant and a mutant that shows poor binding to STAM-1 fails to enhance CXCR4-induced ERK-1/2 signaling.
HECT-type ubiquitin ligase ITCH targets lysosomal-associated protein multispanning transmembrane 5 (LAPTM5) and prevents LAPTM5-mediated cell death.
Inazawa et al., Tokyo, Japan. In J Biol Chem, 2012
LAPTM5 is a substrate of the ITCH-mediated degradation and its protein level is negatively regulated by ITCH
The E3 ligase Itch and deubiquitinase Cyld act together to regulate Tak1 and inflammation.
Venuprasad et al., Detroit, United States. In Nat Immunol, 2011
we have identified an Itch-Cyld-mediated regulatory mechanism in innate inflammatory cells.
The role of ITCH protein in human T-cell leukemia virus type 1 release.
Heidecker et al., Frederick, United States. In J Biol Chem, 2011
Only silencing of ITCH, but not of WWP1, WWP2, and Nedd4, resulted in a reduction of HTLV-1 budding from 293T cells
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