Anti-TIRP TICAM2 Antibody

TIRP is a member of the Toll/interleukin-1 receptor (TIR) family, a group of proteins that include the Toll-like receptors (TLRs) . TLRs are signaling molecules that recognize different pathogen-associated molecular patterns (PAMPs) and serve as an important link between the innate and adaptive immune responses. TIRP, along with other molecules such as TRIF, MAL, and MyD88, serves as an adaptor protein that allows for the interaction and activation of the IL-1R-associated kinase (IRAK) family, the subsequent activation of TNF receptor associated factor (TRAF) -6, and ultimately the activation of NF-κB. Expression of TIRP appears to be essential for TLR4 signalling.

TIRP antibody was raised against a peptide corresponding to 16 amino acids at the C-terminus of human TIRP. The immunogen is located within the last 50 amino acids of TIRP.

Expressed in spleen, prostate, testis, uterus, small intestine, colon, peripheral blood leukocytes, heart, placenta, lung, liver, skeletal muscle, and pancreas Isoform 2 is ubiquitously expressed (at lower levels than isoform 1) .

Functions as sorting adapter in LPS-TLR4 signaling to regulate the MYD88-independent pathway during the innate immune response to LPS. Physically bridges TLR4 and TICAM1 and functionally transmits LPS-TRL4 signal to TICAM1; signaling is proposed to occur in early endosomes after endocytosis of TLR4. May also be involved in IL1-triggered NF-kappa-B activation, functioning upstream of IRAK1, IRAK2, TRAF6, and IKBKB; however, reports are controversial. Involved in IL-18 signaling and is proposed to function as a sorting adaptor for MYD88 in IL-18 signaling during adaptive immune response.

TIRP antibody can be stored at 4°C for three months and -20°C, stable for up to one year. Avoid repeated freeze-thaw cycles. Antibodies should not be exposed to prolonged high temperatures.

Isoform 1: Cytoplasm. Golgi apparatus. Cell membrane. Endoplasmic reticulum. Early endosome membrane. Late endosome membrane. Localized to the plasma membrane as a result of myristoylation. Phosphorylation on Ser-16 leads to its depletion from the membrane. Upon LPS stimulation colcoalizes with isoform 2 in late endosomes.