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Itch monoubiquitinates SMN (show STMN1 ELISA Kits) and monoubiquitination of SMN (show STMN1 ELISA Kits) plays an important role in regulating its cellular localization.
miR (show MLXIP ELISA Kits)-106b, which itself is down regulated in metastatic pancreatic cancer, directly interacts and inhibits ITCH expression.
LRAD3 is a component of pathways that function effectively to modulate Itch and Nedd4 auto-ubiquitination and levels.
Cytomegalovirus UL42 induced the ubiquitination and degradation of human Itch in virus-infected fibroblasts, and was partially colocalized with p62 (show GTF2H1 ELISA Kits), a ubiquitin-binding protein, and CD63 (show CD63 ELISA Kits), a marker of lysosome and multivesicular bodies.
catalytic activity of Itch toward different SH3 domain (show ITSN1 ELISA Kits)-containing proteins was similar, except for beta-PIX (show ARHGEF7 ELISA Kits) that was not readily ubiquitylated even though it could interact with an affinity comparable to those of other substrates tested
Cell proliferation of hepatocellular carcinoma cells mediated by miR (show MLXIP ELISA Kits)-411, is through suppression of ITCH expression.
In the absence of Ndfip1, the Nedd4 family member Itch can bind an E2 but cannot accept ubiquitin onto its catalytic cysteine.
These observations indicate that ITCH is involved in the cytosolic quality control pathway and may help to explain how abnormal proteins are targeted by QC ubiquitin-protein ligases.
Results suggest that Itch is a positive regulator of the TGF-beta (show TGFB1 ELISA Kits)-mediated Smad (show SMAD1 ELISA Kits) signaling pathway via Smad7 (show SMAD7 ELISA Kits) ubiquitination and protein degradation.
ITCH up-regulation and LATS1 down-regulation were closely associated with tumorigenesis and progression of SCC (show CYP11A1 ELISA Kits)
ITCH targets TXNIP (show TXNIP ELISA Kits) for ubiquitin-proteasome degradation in cardiomyocytes and ameliorates reactive oxygen species-induced cardiotoxicity through the thioredoxin (show TXN ELISA Kits) system.
CUL4B links two distinct spermatogenetic processes to a single E3 ligase, highlighting the significance of ubiquitin modification during spermatogenesis.
Impaired ITCH results in heightened TNF (show TNF ELISA Kits) signaling. ITCH-/- mouse's spontaneous lung inflammation and subsequent death can be delayed when TNF (show TNF ELISA Kits) signaling is genetically deleted.
ITCH modulates SIRT6 (show SIRT6 ELISA Kits) and SREBP2 (show SREBF2 ELISA Kits) to influence lipid metabolism and atherosclerosis in ApoE (show APOE ELISA Kits) null mice
The E3 ubiquitin ligase Itch inhibits p38alpha (show MAPK14 ELISA Kits) signaling and skin inflammation through the ubiquitylation of Tab1 (show TAB1 ELISA Kits).
Ndfip1 (show NDFIP1 ELISA Kits) regulates itch ligase activity and airway inflammation via UbcH7 (show UBE2L3 ELISA Kits).
The expression of Th2 cytokines by Treg cells was increased in the absence of Itch. Fate mapping revealed that a fraction of Treg cells lost Foxp3 (show FOXP3 ELISA Kits) expression independently of Itch.
identify Itch as a regulator of Oct4 (show POU5F1 ELISA Kits) stability and transcriptional activity, establishing a functional link between an E3 ligase and the regulation of pluripotency
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.
E3 ubiquitin-protein ligase Itchy homolog
, NFE2-associated polypeptide 1
, atrophin-1 interacting protein 4
, dJ468O1.1 (atrophin 1 interacting protein 4 (AIP4))
, itchy E3 ubiquitin protein ligase homolog
, E3 ubiquitin-protein ligase Itchy