LITAF, Polyclonal Antibody

Anti-LITAF Antibody IHC-plus; LITAF; PIG7; TP53I7; p53-induced gene 7 protein; SIMPLE; CMT1C; LPS-induced TNF-alpha factor; Human LITAF

For Research Use Only. Not for use in diagnostic procedures.

Polyclonal

Rabbit

Human LITAF. Predicted cross-reactivity based on amino acid sequence homology: mouse (85%), rat (86%), bovine (86%).

Immunoaffinity Purified

0.1 M Tris-glycine, pH 7, 10% Glycerol, 0.01% Thimerosal

1 mg/ml (lot specific)

Aliquot and store at -20 degree C. Minimize freezing and thawing.

Small volumes of anti-LITAF antibody vial(s) may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice and additional dry ice fee may apply.

Immunohistochemistry (IHC - Paraffin), Western Blot (WB)

IHC-P (10 ug/ml), WB (1:500 - 1:3000)

Anti-LITAF antibody IHC staining of human spleen. Immunohistochemistry of formalin-fixed, paraffin-embedded tissue after heat-induced antigen retrieval.

Sample (30 ug of whole cell lysate). A: Hep G2. 12% SDS PAGE. LITAF antibody diluted at 1:1000

15,824 Da

lipopolysaccharide-induced TNF factor

lipopolysaccharide-induced tumor necrosis factor-alpha factor; p53-induced gene 7 protein; LPS-induced TNF-alpha factor; tumor protein p53 inducible protein 7; lipopolysaccharide-induced TNF-alpha factor; small integral membrane protein of lysosome/late endosome

Lipopolysaccharide-induced tumor necrosis factor-alpha factor

PIG7; SIMPLE; LPS-induced TNF-alpha factor  [Similar Products]

LITAF_HUMAN

Lipopolysaccharide is a potent stimulator of monocytes and macrophages, causing secretion of tumor necrosis factor-alpha (TNF-alpha) and other inflammatory mediators. This gene encodes lipopolysaccharide-induced TNF-alpha factor, which is a DNA-binding protein and can mediate the TNF-alpha expression by direct binding to the promoter region of the TNF-alpha gene. The transcription of this gene is induced by tumor suppressor p53 and has been implicated in the p53-induced apoptotic pathway. Mutations in this gene cause Charcot-Marie-Tooth disease type 1C (CMT1C) and may be involved in the carcinogenesis of extramammary Paget's disease (EMPD). Multiple alternatively spliced transcript variants have been found for this gene. [provided by RefSeq, Dec 2014]

LITAF: Probable role in regulating transcription of specific genes. May regulate through NFKB1 the expression of the CCL2/MCP-1 chemokine. May play a role in tumor necrosis factor alpha (TNF- alpha) gene expression. Interacts with NEDD4. Interacts with WWOX. Isoform 2 may interact with STAT6. By bacterial lipopolysaccharides (LPS) or p53/TP53. In monocytes by the Bacillus Calmette-Guerin (BCG). Ubiquitously and abundantly expressed. Expressed predominantly in the placenta, peripheral blood leukocytes, lymph nodes and spleen. 2 isoforms of the human protein are produced by alternative splicing.

Protein type: Oncoprotein; Transcription factor

Chromosomal Location of Human Ortholog: 16p13.13

Cellular Component: nucleoplasm; Golgi apparatus; intracellular membrane-bound organelle; lysosomal membrane; cytoplasm; plasma membrane

Molecular Function: signal transducer activity; protein binding; WW domain binding

Biological Process: regulation of transcription from RNA polymerase II promoter; positive regulation of I-kappaB kinase/NF-kappaB cascade; transcription, DNA-dependent; apoptosis; negative regulation of NF-kappaB import into nucleus; signal transduction; aging; regulation of cytokine production

Disease: Charcot-marie-tooth Disease, Demyelinating, Type 1c

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