| protein
| NFE2, NOTCH |
|
E3 ubiquitin ligase that specifically targets SMAD7 for ubiquitin-dependent degradation without affecting the turnover of the activated TGF-beta type I receptor |
|
directly interacts with the amino-terminal half of nonvisual arrestin-2 (ARRB2)via its WW domains (activation of CXCR4 promotes this interaction that is consistent with a time when AIP4 co-localizes with arrestin-2 on endocytic vesicles) |
|
interacting with GLI1 and NUMB |
|
binding partner of USP9X (transient overexpression of FAM/USP9X resulted in the deubiquitylation of ITCH) |
|
interact with DTX3 and partially colocalize to endocytic vesicles, and ITCH targets DTX for lysosomal degradation |
|
interacting with SPG20 (spartin acts as an adaptor for WWP1 and ITCH) |
|
interacting with TXNIP, thus regulating intracellular reactive oxygene species levels and apoptosis |
|
interacting with atrophin-1 |
|
upon phosphorylation, can interact directly with CXCR4 and promotes its ubiquitination and degradation |
|
interacting with DRPLA, LMP2A, OCNL, NOTCH1, JUN, JUNB, ARHGEF7, RNF11, NFE2, FYN |
|
cooperation between USP8, ITCH, and the ESCRT-0 machinery in shaping receptor progression through the sorting endosome |
|
ITCH, a WW-domain containing protein, and LITAF strongly interact and this interaction depends on the two PPXY motifs in the N-terminus of LITAF |
|
LAPTM5 is a substrate of the ITCH-mediated degradation and its protein level is negatively regulated by ITCH |
|
interaction between ITCH and STAM and the ligase activity of ITCH are essential for ERK-1/2 activation |
|
NEDD4, NEDD4L and ITCH mediate poly-ubiquitination of AMOT/p130 |
|
NDFIP1 is an adaptor for the E3 ubiquitin ligase ITCH |
|
DVL1-binding protein (ITCH ubiquitinates the phosphorylated form of DVL1 and promotes its degradation via the proteasome pathway, thereby inhibiting canonical Wnt signaling |
|
a ubiquitin-regulated signaling network centered on ITCH and BIRC2 controls the strength of NOD2 signaling |
|
ITCH interacts with and targets pluripotency-associated transcription factor POU5F1 for ubiquitination |
|
interacts with mutant GBA variants and mediates their lysine 48 polyubiquitination and degradation |
|
AMOT promotes the ubiquitination of YAP1 by ITCH and prevents ITCH from binding to large tumor suppressor 1 |
|
bind and ubiquitinate AMOT at residue Lys-481 |
|
interacts with the deubiquitinating enzyme and is required for deubiquitination of TRAF6, thus limiting TNFSF11-induced osteoclast formation |
|
binds and ubiquitinates AMOT130, resulting in a reduction in AMOT130 residence at actin fibers and a significant enhancement of the stability of AMOT130 protein |
|
PDYN acts as a neuromodulator to inhibit ITCH in the dorsal horn of the spinal cord |
|
acts as an E3 ubiquitin ligase for SMAD7 polyubiquitination, and is an important regulator of SMAD7 activity and a positive regulator of TGFB1 signaling and of TGFB1-mediated biological processes |
|
NDFIP1 acts as an adaptor for UBE2L3 and ITCH |
|
TAX1BP1 functions as an adaptor molecule for ITCH to target MAVS during RNA virus infection and thus restrict virus-induced apoptosis |
|
mechanistically, YOD1 deubiquitinates ITCH, an E3 ligase of LATS, and enhances the stability of ITCH, which leads to reduced levels of LATS and a subsequent increase in the YAP/TAZ level |
|
YOD1 stabilizes ITCH and facilitates ITCH-mediated LATS1/2 ubiquitination and degradation, which results in increased YAP/TAZ level |
|
contributes to the differential ubiquitination of isoforms of the endocytic scaffold protein intersectin1 (ITSN1) |
|
regulates ITCH-mediated M1 ubiquitination of Influenza A Virus |
|
GRAMD4 inhibits the migration and metastasis of hepatocellular carcinoma, mainly by recruiting ITCH to promote the degradation of MAP3K7, which leads to the inactivation of MAPK and NFKB1 signalling pathways |
