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ITCH / AIP4 Antibody (FITC), Mouse MAb
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ITCH / AIP4 Antibody (FITC), Mouse MAb PDF Download

Catalog   Size (Price) Quantity In Stock Operation
11131-MM01-F  
YES   
 

Primary antibody | Secondary antibody | Tag antibody | Isotype control antibody | Loading control antibody | Antibody Purification

ITCH / AIP4 Antibody Datasheet

  Order or Inquire for ITCH / AIP4 Antibody product Quality antibodies Antibody production services
 

ITCH / AIP4 Antibody Product Information

Immunogen :

Recombinant Human ITCH / AIP4 protein (Catalog#11131-HNCE)

Reagents : FITC-conjugated mouse monoclonal antibody

Clone ID :

01

Ig Type :

Mouse IgG1

Concentration :

10 μl/Test, 0.1 mg/ml

Formulation : Aqueous solution containing 0.5% BSA and 0.09% sodium azide
Preparation :

This antibody was produced from a hybridoma resulting from the fusion of a mouse myeloma with B cells obtained from a mouse immunized with purified, recombinant Human ITCH / AIP4 (rh ITCH / AIP4; Catalog#11131-HNCE; NP_113671.3; Arg 526-Glu 903) and conjugated with FITC under optimum conditions, the unreacted FITC was removed.

ITCH / AIP4 Antibody Usage Guide

Specificity :

Human ITCH / AIP4

Flow Cytometry :
ITCH / AIP4 Flow Cytometry

Flow cytometric analysis of Human ITCH expression in HeLa cells. The cells were treated according to manufacturer’s manual (BD Pharmingen™ Cat. No. 554714), and then stained with FITC Mouse anti-ITCH (11131-MM01-F). The fluorescence histograms were derived from gated events with the forward and side light-scatter characteristics of intact cells.

Flow cytometry was performed on a BD FACSCalibur flow cytometry system

Please refer to www.sinobiological.com/Flow-Cytometry-FACS-Protocols-a-750.html for technical protocols.

Storage : This antibody is stable for 12 months from date of receipt when stored at 2℃-8℃. Protected from prolonged exposure to light. Do not freeze !
Sodium azide is toxic to cells and should be disposed of properly. Flush with large volumes of water during disposal.

ITCH / AIP4 Antibody Related Products & Topics

ITCH / AIP4 Antibody Related Areas:

Neuroscience>>Neurodegenerative Disease>>Ubiquitin-proteasome pathway>>ITCH/AIP4

Proteins:

Molecule Species Description //For Detailed Info. and Price------CLICK! Cat. No
ITCH/AIP4 Human ITCH/AIP4 (aa 526 - 903) Protein, Recombinant 11131-HNCE

Antibodies:

Molecule Application Description //For Detailed Info. and Price------CLICK! Cat. No
Human ITCH/AIP4 WB, ELISA ITCH / AIP4 Antibody 11131-RP01
Human ITCH/AIP4 WB, ELISA ITCH / AIP4 Antibody (Antigen Affinity Purified) 11131-RP02
Human ITCH/AIP4 FCM ITCH / AIP4 Antibody ( FITC ) 11131-MM01-F

ITCH / AIP4 Antibody Background

E3 ubiquitin-protein ligase Itchy homolog, also known as Atrophin-1-interacting protein 4, NFE2-associated polypeptide 1, NAPP1 and ITCH, is a cell membrane protein which contains oneC2 domain, oneHECT (E6AP-type E3 ubiquitin-protein ligase) domain and contains fourWW domains. ITCH acts as an E3 ubiquitin-protein ligase which accepts ubiquitin from an E2 ubiquitin-conjugating enzyme in the form of a thioester and then directly transfers the ubiquitin to targeted substrates. It catalyzes 'Lys-29'-, 'Lys-48'- and 'Lys-63'-linked ubiquitin conjugation. ITCH is involved in the control of inflammatory signaling pathways. It is an essential component of a ubiquitin-editing protein complex, comprising also TNFAIP3, TAX1BP1 and RNF11, that ensures the transient nature of inflammatory signaling pathways. ITCH promotes the association of the complex after TNF stimulation. Once the complex is formed, TNFAIP3 deubiquitinates 'Lys-63' polyubiquitin chains on RIPK1 and catalyzes the formation of 'Lys-48'-polyubiquitin chains. This leads to RIPK1 proteosomal degradation and consequently termination of the TNF- or LPS-mediated activation of NFKB1. Defects in ITCH are the cause of syndromic multisystem autoimmune disease (SMAD) which is characterized by organomegaly, failure to thrive, developmental delay, dysmorphic features and autoimmune inflammatory cell infiltration of the lungs, liver and gut.

References

  1. Marchese A. et al., 2003, Dev. Cell 5:709-22.
  2. Wang Y. et al., 2006, EMBO J. 25: 5058-70.
  3. Bhandari D. et al., 2009, Mol. Biol. Cell 20: 1324-39.
  4. Edwards TL. et al., 2009, Biochem. J. 423: 31-9.
  5. Zhang P. et al., 2010, J. Biol. Chem. 285: 8869-79.
  6. Azakir B.A. et al., 2010, FEBS J. 277: 1319-30.
 

 

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