Definition: In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.
Input: cally active but which do not bind antibody 259 have been prepared recently; cells transformed by such mutants were not altered morphologically, nor did they show greatly inhibited thymidine incorporation, after injection of antibody 259 26 • It is assumed that while viral oncogenes function without normal control, their mechanism of action is similar to that of related cellular genes. Here we have presented evidence to support this idea in the case of growth factor receptor-like molecules and related oncogenes. It is therefore possible that these data might aid in understanding the way in which cellular genes interact in the control of normal proliferation. Our results indicate that some receptor-like oncogenes depend on ras proteins while some cytoplasmic oncogenes do not. There are, of course, numerous oncogenes which we have not yet tested which might behave differently from those described here. With this limitation in mind and on the basis of our present data, we propose that an important class of proliferative signals are received at the cell surface by receptor molecules such as growth factor receptors, and the c-ras proteins are essential in the transfer of these signals to cytoplasmic effectors having serine kinase activity; the effectors then modify target molecules which are directly involved in initiating a proliferative cycle. Accordingly, if the cytoplasmic effector were mutated such that it functioned without activation, proliferation would continue independently of c-ras proteins. Receptor molecules, on the other hand, would always require c-ras to stimulate proliferation. While our data are consistent with the above scheme, they do not exclude many other possibilities involving multiple metabolic pathways and more complex interactions. For example, we have not reported results with nuclear oncogenes owing to their difficulty in transforming NIH 3T3 cells. The proposed scheme is primarily attractive because of its similarity to the carefully studied mechanism of signal transduction involving cyclic AMP. While it is unlikely that cyclic AMP itself regulates proliferation 27 , G-regulatory proteins with enzymatic similarities to c-ras proteins are involved. These regulatory proteins control signal transduction from cell-surface receptors to cytoplasmic serine kinase effector molecules by regulating adenyl cyclase activity28. While the present study has examined only one aspect of what is likely to be a highly complex system for regulating proliferation, it does provide a means of functionally comparing separate viral oncogenes. Injection of antibody has been used in other studies to characterize the types of molecules responsible for tumour cell proliferation. Like NIH 3T3 cells transformed by mos or raj genes, many tumour cells show no inhibition of proliferation when injected with anti-ras antibody. In this way their proliferation is distinct from that of the normal cell types studied, each of which was efficiently inhibited by the injected antibodyl6.

Viral particles induce Ia antigen expression on astrocytes