Anti-Phospho-TICAM2 Antibody (FITC)
|Name:||Anti-Phospho-TICAM2 Antibody (FITC)|
|Description:||Rabbit polyclonal antibody to Phospho-TICAM2 (FITC)|
|Applications:||ELISA, IP, WB|
|Dilutions:||DB: 1:10,000; ELISA: 1:10,000; Western Blot: 1:500-1:750|
|Reactivity:||Human, Mouse, Rat|
|Immunogen:||Phosphorylated synthetic peptide corresponding to unique amino acid sequences on TRIF-related adapter molecule protein.|
|Concentration:||0.50-0.75 µg/µl in antibody stabilization buffer|
|Storage:||-20⁰C for long term storage|
Target (Information from UniProt)
|Function:||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.|
|Tissue Specificity:||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).|
|Post-Translational Modification:||Phosphorylated by PRKCE in response to LPS. Phosphorylation is essential for its function. It is depleted from the membrane upon phosphorylation.|
|Cellular Location:||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.