TTP Antibody – Rabbit Polyclonal

TTP: a CCCH zinc finger protein that has anti-inflammatory and arthritis suppressor activity. Regulates inflammatory responses at the post-transcriptional level. TTP deficiency in mice causes a severe inflammatory syndrome that includes autoimmunity, myeloid hyperplasia, and erosive arthritis. Binds to and destabilizes mRNA molecules with AU-rich elements (AREs). Has a high affinity for UUAUUUAUU mRNA sequences. Destabilizes tumor necrosis factor-alpha (TNF??), interleukin 2 (IL2), granulocyte-macrophage colony-stimulating factor (GM-CSF), transcription factor E47, and cyclooxygenase 2 (COX2) mRNAs. TNF?? and GM-CSF mRNAs are stabilized in TTP-deficient mice, causing a severe inflammatory syndrome. Conversely, high levels of TTP reduce inflammatory responses. TTP is a very low abundance protein that is rapidly induced by insulin, glucocorticoids, lipopolysaccharide (LPS), fetal calf serum, zinc, herpes simplex virus 1, green tea, and cinnamon. Once induced, the TTP protein is relatively stable. Has been experimentaly shown to be able to bind zinc. TTP is extensively phosphorylated.

Protein type: DNA-binding; RNA-binding

Chromosomal Location of Human Ortholog: 19q13.1

Cellular Component: stress granule; cytoplasm; nucleus; cytosol

Molecular Function: mRNA binding; protein binding; single-stranded RNA binding; enzyme binding; DNA binding; metal ion binding; C-C chemokine binding; AU-rich element binding; protein kinase binding

Biological Process: response to starvation; poly(A) tail shortening; negative regulation of myeloid cell differentiation; negative regulation of inflammatory response; mRNA catabolic process; miRNA-mediated gene silencing, negative regulation of translation; regulation of tumor necrosis factor production; gene expression; negative regulation of transcription from RNA polymerase II promoter; RNA destabilization; mRNA catabolic process, deadenylation-dependent decay