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anti-Human ITCH Anticorps:
anti-Mouse (Murine) ITCH Anticorps:
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Dog (Canine) Polyclonal ITCH Primary Antibody pour ELISA, WB - ABIN547858
Di Marcotullio, Ferretti, Greco, De Smaele, Po, Sico, Alimandi, Giannini, Maroder, Screpanti, Gulino: Numb is a suppressor of Hedgehog signalling and targets Gli1 for Itch-dependent ubiquitination. dans Nature cell biology 2006
Human Polyclonal ITCH Primary Antibody pour ICC, IF - ABIN4327763
Bozóky, Savchenko, Csermely, Korcsmáros, Dúl, Pontén, Székely, Klein: Novel signatures of cancer-associated fibroblasts. dans International journal of cancer 2013
Study defined ITCH as a direct and functional downstream target of miR-10b, and showed that there was an inverse correlation between the expression of ITCH and miR-10b on melanoma tissues. Its down-regulation alleviates inhibitory effects of miR-10b inhibitor on melanoma cell proliferation, migration and invasion.
Different modes of ubiquitination regulated by AIP4 have opposite effects on ITSN1 isoform stability.
the expression of cir_ITCH and circHIPK3 were significantly downregulated in gastric cancer tumoral tissues compared with their paired adjacent nonneoplastic counterparts; further analyses showed that cir_ITCH and circHIPK3 expression levels were related with numerous clinicopathological features of tumoral tissues
Study reports that in melanoma cells in response to proinflammatory cytokines, BRAF is poly-ubiquitinated at lysine 27 by the ITCH ubiquitin E3 ligase in response to JNK-mediated phosphorylation. K27-linked ubiquitination of BRAF abolishes 14-3-3-mediated suppression of BRAF kinase activity, leading to sustained BRAF/MuEK/ERK signaling, which contributes to the pro-tumoral cytokine-facilitated survival of melanoma cells.
Circ-ITCH correlates with small tumor size, decreased FIGO stage and prolonged OS, and it inhibits cells proliferation while promotes cells apoptosis in epithelial ovarian cancer
CypA regulates the cellular localization of M1 via inhibition of AIP4-mediated M1 ubiquitination at K102 and K104, which results in the reduced replication of influenza A virus.
The results indicated that circ-ITCH was significantly decreased in BCa and correlated with poor prognosis of BCa patients. Moreover, circ-ITCH suppressed cell proliferation, migration and invasion in vitro and tumorigenesis in vivo.
Itch/beta-arrestin2 complex binds SuFu and induces its Lys63-linked polyubiquitylation without affecting its stability.
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.
JunB neddylation mediated by Itch promotes its ubiquitination-dependent degradation.
Describe an autoinhibitory mechanism for ITCH ubiquitin ligase involving a linker-HECT domain interaction. This intramolecular interaction traps the HECT enzyme in its inactive state and can be relieved by linker phosphorylation.
Data show that the E3 ubiquitin ligase Itch forms a complex with tricellulin and thereby enhances its ubiquitination.
ASPP2 suppresses invasion, peritoneal dissemination and TGF-beta1-induced EMT by inhibiting Smad7 degradation mediated by ITCH in gastric cancer cells.
WBP2/ITCH signaling functions to link the intricate Wnt and Hippo signaling networks in breast cancer.
The cellular ubiquitin ligase, Itch, is required for Kaposi's sarcoma herpesvirus RTA induced degradation of vFLIP.
Results indicate that TAX1BP1 functions as an adaptor molecule for Itch to target MAVS during RNA virus infection and thus restrict virus-induced apoptosis.
These data demonstrate that Itch, ubiquitin, and Alix control the BFRF1-mediated modulation of the nuclear envelope and human herpesvirus 4 maturation, uncovering novel regulatory mechanisms of nuclear egress of viral nucleocapsids.
The authors demonstrate that the PPxY L domain motif of ebolavirus VP40 interacts specifically with the WW domain of the host E3 ubiquitin ligase ITCH.
Molecular basis of interactions between SH3 domain-containing proteins and the proline-rich region of the ubiquitin ligase Itch.
cir-ITCH may play an inhibitory role in lung cancer progression by enhancing its parental gene, ITCH, expression
Itch and WWP2 cooperate to regulate TH2 differentiation by enhancing the strength of the TCR signal via inducing atypical ubiquitination of the phosphatase SHP-1.
this paper shows that IL-17-driven intestinal fibrosis is inhibited by Itch-mediated ubiquitination of HIC-5
beta-Arrestin2 increases the Itch-mediated ubiquitylation of SuFu.
findings show that the WW domains proceeding the catalytic HECT domain play an inhibitory role by binding directly to HECT in Itch; study provides a new mechanism governing the regulation of Itch
this study identified a previously unknown role for Itch in regulating IL-17-mediated colonic inflammation and carcinogenesis
Itch monoubiquitinates SMN and monoubiquitination of SMN plays an important role in regulating its cellular localization.
ITCH targets TXNIP for ubiquitin-proteasome degradation in cardiomyocytes and ameliorates reactive oxygen species-induced cardiotoxicity through the thioredoxin system.
CUL4B links two distinct spermatogenetic processes to a single E3 ligase, highlighting the significance of ubiquitin modification during spermatogenesis.
The Itch plays a role in epidermal homeostasis and remodelling and this feature does not seem to depend on immunological alterations.
Impaired ITCH results in heightened TNF signaling. ITCH-/- mouse's spontaneous lung inflammation and subsequent death can be delayed when TNF signaling is genetically deleted.
ITCH modulates SIRT6 and SREBP2 to influence lipid metabolism and atherosclerosis in ApoE null mice
Upregulated microRNA-214 enhances cardiac injury by targeting ITCH during coxsackievirus infection.
In the absence of Ndfip1, the Nedd4 family member Itch can bind an E2 but cannot accept ubiquitin onto its catalytic cysteine.
The E3 ubiquitin ligase Itch inhibits p38alpha signaling and skin inflammation through the ubiquitylation of Tab1.
Ndfip1 regulates itch ligase activity and airway inflammation via UbcH7.
Itch acts as an essential positive regulator in the differentiation of follicular T cells.
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 expression independently of Itch.
identify Itch as a regulator of Oct4 stability and transcriptional activity, establishing a functional link between an E3 ligase and the regulation of pluripotency
Itch interacts with the deubiquitinating enzyme and is required for deubiquitination of TRAF6, thus limiting RANKL-induced osteoclast formation
Itch directly associates with and ubiquitinates PI4KIIalpha, and both proteins colocalize on endosomes containing Wnt-activated frizzled 4 (Fz4) receptor
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