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All of our services and products are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.

LITAF Antibody

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CAT. NO.: AMA-0285

Target Information
UniProt ID	Q99732

Product Details
Size	100 µL
Reactivity	Human
Storage	Store at -20°C. Do not aliquot the antibody.
Purification	Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues near the amino terminus of human LITAF protein. Antibodies were purified by peptide affinity chromatography.

Usage
Application	WB
Product Usage Information Dilution	Western Blotting (1:1000)
MW (Target)	23 kDa

Background
LITAF (PIG7/SIMPLE) is protein that contributes to the regulation of the inflammatory cytokine TNF-α. LITAF was identified as a transcription factor involved in LPS-induced TNF-α expression through interaction with the TNF-α promoter. The same protein, called PIG7, was independently described in a model for p53 regulation. A putative alternative spiced form of LITAF, named SIMPLE, encodes a protein with a unique carboxyl terminus. Studies on LITAF-deficient mice demonstrate that LITAF plays a significant role in the regulation of several inflammatory cytokines in response to LPS. The regulation of LITAF can occur through phosphorylation by p38α via the TLR pathway that leads to its nuclear translocation . Mutation in the LITAF/SIMPLE gene has been associated with an autosomal dominant demyelinating form of Charcot-Marie-Tooth disease.

Background

LITAF (PIG7/SIMPLE) is protein that contributes to the regulation of the inflammatory cytokine TNF-α. LITAF was identified as a transcription factor involved in LPS-induced TNF-α expression through interaction with the TNF-α promoter. The same protein, called PIG7, was independently described in a model for p53 regulation. A putative alternative spiced form of LITAF, named SIMPLE, encodes a protein with a unique carboxyl terminus. Studies on LITAF-deficient mice demonstrate that LITAF plays a significant role in the regulation of several inflammatory cytokines in response to LPS. The regulation of LITAF can occur through phosphorylation by p38α via the TLR pathway that leads to its nuclear translocation . Mutation in the LITAF/SIMPLE gene has been associated with an autosomal dominant demyelinating form of Charcot-Marie-Tooth disease.

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All of our services and products are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.