Tumor-bearing patients have defective TCR expression pattern that do not transduce signal from its membrane to nucleus [36]. Cytosolic PTK family proteins (syk) is mostly responsible for intracellular signalling as well as the Salinomycin function of CTL [36]. The ATP binding site of membrane PTK serves as the docking site for specific binding of cytoplasmic signalling protein containing SH2-domain and tyrosine-binding domains. These proteins recruit additional effector molecules having SH2, SH3 PTB and pleckstrin homology (PH) domain. The assembly of protein complexes thus activates signal transduction, which finally modulates (activation or repression) several genes [37]. Overexpression of PTK is reported in solid tumor, and the activated PTK activity is found in Philadelphia chromosome positive leukemia cells [38]. In our study higher PTK activity may be due to overexpression of non-receptor PTK or mutation of this protein. Excessive PTK activity brings about transmission of an abnormal signal to the nucleus contributing tumor development. After co-treatment with IL-3 and GM-CSF the activity is reduced, perhaps, due to inhibition of signal.
↧