Purified anti-ITCH Antibody, ITCH, W19229A,BioLegend,611452
For immunocytochemistry (ICC), we suggest fixation with 4% PFA followed by permeabilization with ice-cold methanol or fixation and permeabilization with ice-cold methanol. Fixation with 4% PFA followed by permeabilization with Triton X-100 results in dimmer staining in comparison to the other two methods.Clone W19229A is not suitable for IHC.
Host
Rat
Reactivity
Human, Mouse
Application
WB - Quality testedICC - Verified
Platform ID
BAB396132967

BioLegend
Contact
Tel: 1-858-455-9588
Fax: +49 (4131) 7023913
Email:
Specifications
Scientific Background
ITCH, Itchy E3 Ubiquitin Protein Ligase or atrophin-1 interacting protein 4 (AIP4), receives ubiquitin from E2 ubiquitin-conjugating enzymes and transfers them to their target proteins for lysosomal degradation. The degradation regulated by ITCH is involved in a broad array of biological functions, including T helper cell inflammatory signaling, T lymphocyte differentiation, immune response, tumor cell death, and skin keratinocyte differentiation. In animal models, ITCH mutant mice develop spontaneous autoimmune disease symptoms including skin scratching, lymphoproliferation, and chronic pulmonary inflammation. ITCH suppresses IL-4 levels by degrading JUNB and maintains the attenuation of differentiation of T helper cells type 2. To maintain peripheral immune tolerance, ITCH monoubiquitinates protein kinase θ and phospholipase C-γ1 through lysosome degradation near immunological synapse for T cell energy. ITCH modulates trafficking of receptor CXCR4 from the cell surface to the endosome through endocytosis. The transcription factor targets of ITCH, such as JUN, JUNB, TP63, NOTCH1, and GLI1, participate in epidermal keratinocyte development and differentiation. In addition to a role in proteolysis, the polyubiquitination of BRAF by ITCH sustains its activity and elevates the MEK/ERK signaling pathway to promote proliferation and invasion in melanoma cells.
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