TIFA antibody (AA 51-150) (Cy7)

Catalog No. ABIN1707471

Product Details anti-TIFA Antibody (Cy7)

Target: TIFA (TRAF-Interacting Protein with Forkhead-Associated Domain (TIFA))

Binding Specificity: AA 51-150

Reactivity: Mouse

Host: Rabbit

Clonality: Polyclonal

Conjugate: This TIFA antibody is conjugated to Cy7

Application: Western Blotting (WB), Immunofluorescence (Cultured Cells) (IF (cc)), Immunofluorescence (Paraffin-embedded Sections) (IF (p))

Cross-Reactivity: Mouse

Predicted Reactivity: Human,Rat,Dog,Cow,Sheep,Pig,Chicken

Purification: Purified by Protein A.

Immunogen: KLH conjugated synthetic peptide derived from human TIFA

Isotype: IgG

Application Details

Application Notes: IF(IHC-P) 1:50-200
IF(IHC-F) 1:50-200
IF(ICC) 1:50-200

Restrictions: For Research Use only

Handling

Format: Liquid

Concentration: 1 μg/μL

Buffer: Aqueous buffered solution containing 0.01M TBS ( pH 7.4) with 1 % BSA, 0.03 % Proclin300 and 50 % Glycerol.

Preservative: ProClin

Precaution of Use: This product contains ProClin: a POISONOUS AND HAZARDOUS SUBSTANCE, which should be handled by trained staff only.

Storage: -20 °C

Storage Comment: Store at -20°C. Aliquot into multiple vials to avoid repeated freeze-thaw cycles.

Expiry Date: 12 months

Target Details for TIFA

Target: TIFA (TRAF-Interacting Protein with Forkhead-Associated Domain (TIFA))

Alternative Name: TIFA (TIFA Products)

Background:

Synonyms: Putative MAPK activating protein PM14, Putative MAPK-activating protein PM14, Putative NF kappa B activating protein 20, Putative NF-kappa-B-activating protein 20, T2BP, TA, TA_HUMAN, TRAF interacting protein with FHA domain containing protein A, TRAF-interacting protein with FHA domain-containing protein A, TRAF2 binding protein, TRAF2-binding protein.

Background: Adapter protein which mediates the IRAK1 and TRAF6 interaction following IL-1 stimulation, resulting in the downstream activation of NF-kappa-B and AP-1 pathways. Induces the oligomerization and polyubiquitination of TRAF6, which leads to the activation of TAK1 and IKK through a proteasome-independent mechanism.