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About This Item
UNSPSC Code:
12352203
NACRES:
NA.41
biological source
rabbit
Quality Level
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
mol wt
antigen ~112 kDa
species reactivity
monkey, human
concentration
~1.5 mg/mL
technique(s)
western blot: 1.5-3.0 μg/mL using Jurkat and COS7 cell extracts
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... ITCH(83737)
General description
Itchy E3 ubiquitin protein ligase (ITCH), also known as atrophin 1-interacting protein 4, is encoded by the gene mapped to human 20q11.22. The encoded protein is a member of the Nedd4-like family of E3 ubiquitin ligases. ITCH is characterized by an N- terminal protein kinase C-related C2 domain, four WW domains and a HECT (homologous to the E6-associated protein carboxyl-terminus) ubiquitin protein ligase domain at the C-terminus.
Application
Anti-ITCH antibody produced in rabbit has been used in western blotting and immunoprecipitation.
Biochem/physiol Actions
Anti-ITCH specifically recognizes human and monkey ITCH.
ITCH can act as a transcriptional corepressor of nuclear factor erythroid 2 (NFE2)/p45. This protein may participate in mediating the immune responses by modifying Notch-mediated signaling.
Itchy E3 ubiquitin protein ligase (ITCH) in association with Ebola virus VP40 (eVP40), aids in virus-like particles (VLP) and virus budding. Overexpression of the gene is associated with the development of thyroid tumors, mainly anaplastic thyroid carcinoma (ATC). ITCH inhibits hippo tumor suppressor pathway and induce metastasis in breast cancer patients. The encoded protein is implicated in the positive regulation of transforming growth factor-β (TGF-β) signaling and of following epithelial-mesenchymal transition (EMT)-related gene expression. Down-regulated expression of the gene leads to syndromic multisystem autoimmune disease and severe morphologic and developmental abnormalities.
Physical form
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.
Preparation Note
Store at –20 °C. For continuous use, the product may be stored at 2–8 °C for up to one month. For extended storage, freeze in working aliquots at –20 °C. Repeated freezing and thawing, or storage in “frost-free” freezers, is not recommended. If slight turbidity occurs upon prolonged storage, clarify the solution by centrifugation before use. Working dilutions should be discarded if not used within 12 hours.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Storage Class Code
10 - Combustible liquids
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Regulatory Information
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ITCH E3 Ubiquitin Ligase Interacts with Ebola Virus VP40 To Regulate Budding
Han Z, et.al.
Journal of Virology, 90, 9163-9171 (2016)
L Qiu et al.
The Journal of biological chemistry, 275(46), 35734-35737 (2000-08-15)
Genetic studies identified Itch, which is a homologous to the E6-associated protein carboxyl terminus (Hect) domain-containing E3 ubiquitin-protein ligase that is disrupted in non-agouti lethal mice or Itchy mice. Itch-deficiency results in abnormal immune responses and constant itching in the
Kishu Ranjan et al.
Scientific reports, 6, 22787-22787 (2016-03-15)
Tumor Necrosis Factor-α canonically induces the activation of NF-κB and associated gene product cellular FLICE-like inhibitory protein (cFLIPL) to promote cell survival. Previously, we demonstrated that ectopic expression of the Fas associated death domain (FADD) diminishes the expression of cFLIPL
Human ITCH E3 ubiquitin ligase deficiency causes syndromic multisystem autoimmune disease.
Lohr NJ
American Journal of Human Genetics, 86, 447-453 (2010)
Ke-Jun Han et al.
Human molecular genetics, 25(7), 1392-1405 (2016-02-26)
Low levels of the survival motor neuron (SMN) protein cause spinal muscular atrophy, the leading genetic disorder for infant mortality. SMN is ubiquitously expressed in various cell types and localizes in both the cytoplasm and the nucleus, where it concentrates
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