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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

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)
Top mentioned proteins: Ubiquitin, CAN, V1a, HAD, Nedd4
Papers on Itch
Evolving understanding on the aetiology of thermally provoked itch.
Review
New
Katayama et al., Suita, Japan. In Eur J Pain, Jan 2016
BACKGROUND AND OBJECTIVES: Itch is one of the major symptoms in dermatology clinics, and severely impairs the quality of life.
Multiple Src Homology 3 Binding to the Ubiquitin Ligase Itch Conserved Proline-Rich Region.
New
Angers et al., Montréal, Canada. In Biochemistry, Jan 2016
Itch is a member of the C2-WW-HECT (CWH) family of ubiquitin ligases involved in the control of inflammatory signaling pathways, several transcription factors, and sorting of surface receptors to the degradative pathway.
WWOX modulates the ATR-mediated DNA damage checkpoint response.
New
Aqeilan et al., Jerusalem, Israel. In Oncotarget, Jan 2016
At the molecular level, we show that upon SSBs WWOX is modified at lysine 274 by ubiquitination mediated by the ubiquitin E3 ligase ITCH and interacts with ataxia telangiectasia-mutated (ATM).
GRPR/PI3Kγ: Partners in Central Transmission of Itch.
New
Campos et al., Porto Alegre, Brazil. In J Neurosci, Jan 2016
UNLABELLED: The gastrin-releasing peptide (GRP) and its receptor (GRPR) are important components of itch transmission.
Neuroimmune interactions in itch: Do chronic itch, chronic pain, and chronic cough share similar mechanisms?
Review
New
Ji, Durham, United States. In Pulm Pharmacol Ther, Dec 2015
Itch and pain are closely related but also clearly distinct sensations.
Negative correlation of ITCH E3 ubiquitin ligase and miRNA-106b dictates metastatic progression in pancreatic cancer.
New
Tang et al., Chengdu, China. In Oncotarget, Dec 2015
The E3 ubiquitin ligase ITCH has been previously reported to inhibit the tumor suppressive Hippo signaling by suppressing LATS1/2 in breast cancer and chronic lymphocytic leukemia.
Active IKKβ promotes the stability of GLI1 oncogene in diffuse large B-cell lymphoma.
New
Vega et al., Miami, United States. In Blood, Dec 2015
TNFα-mediated IKKβ activation impaired GLI1 binding with the E3 ubiquitin ligase-ITCH, leading to decreased K48-linked ubiquitination/degradation of GLI1.
G Protein-Coupled Receptors: Dynamic Machines for Signaling Pain and Itch.
Review
New
Bunnett et al., Florence, Italy. In Neuron, Dec 2015
G protein-coupled receptors (GPCRs) are the major class of sensory proteins and a primary therapeutic target in the pathways to pain and itch.
Trp channels and itch.
Review
New
Dong et al., Baltimore, United States. In Semin Immunopathol, Oct 2015
UNASSIGNED: Itch is a unique sensation associated with the scratch reflex.
The E3 ligase Itch in immune regulation and beyond.
Review
New
Liu et al., Beijing, China. In Immunol Rev, Jul 2015
Itch or itchy E3 ubiquitin ligase was initially discovered by genetic studies on the mouse coat color changes, and its deletion results in an itchy phenotype with constant skin scratching and multi-organ inflammation.
Chaperone-mediated autophagy regulates T cell responses through targeted degradation of negative regulators of T cell activation.
Impact
Macian et al., New York City, United States. In Nat Immunol, 2014
In activated T cells, CMA targeted the ubiquitin ligase Itch and the calcineurin inhibitor RCAN1 for degradation to maintain activation-induced responses.
The E3 ubiquitin ligase Itch is required for the differentiation of follicular helper T cells.
Impact
Liu et al., Los Angeles, United States. In Nat Immunol, 2014
Here we found that the E3 ubiquitin ligase Itch was essential for the differentiation of T(FH) cells, germinal center responses and immunoglobulin G (IgG) responses to acute viral infection.
The cells and circuitry for itch responses in mice.
Impact
Hoon et al., Bethesda, United States. In Science, 2013
Itch is triggered by somatosensory neurons expressing the ion channel TRPV1 (transient receptor potential cation channel subfamily V member 1), but the mechanisms underlying this nociceptive response remain poorly understood.
Aprepitant for management of severe pruritus related to biological cancer treatments: a pilot study.
Impact
Tonini et al., Roma, Italy. In Lancet Oncol, 2012
BACKGROUND: Itch is a common side-effect of treatment with anti-EGFR antibodies and tyrosine-kinase inhibitors.
The Nedd4-like ubiquitin E3 ligases target angiomotin/p130 to ubiquitin-dependent degradation.
GeneRIF
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.
GeneRIF
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.
TGF-β induces the expression of the adaptor Ndfip1 to silence IL-4 production during iTreg cell differentiation.
Impact
Oliver et al., Philadelphia, United States. In Nat Immunol, 2012
Once expressed, Ndfip1 promoted degradation of the transcription factor JunB mediated by the E3 ubiquitin ligase Itch, thus preventing IL-4 production.
HECT-type ubiquitin ligase ITCH targets lysosomal-associated protein multispanning transmembrane 5 (LAPTM5) and prevents LAPTM5-mediated cell death.
GeneRIF
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.
Impact
GeneRIF
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.
GeneRIF
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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