生长因子受体酪氨酸蛋白激酶及致癌性的阻遏

多肽生长因子（ＰＧＦ）介导之信号的特异性．在于它们能与特殊的细胞表面受体相结合，激发细胞内的一系列生理生化过程．生长因子受体都具有内在的酪氨酸蛋白激酶（ＴＰＫ）活性。生长因子与受体结合后能激活ＴＰＫ，导致各种细胞蛋白质的磷酸化和受体自身的磷酸化．许多癌基因产物都具有ＴＰＫ活性，ＴＰＫ的功能是使生长因子信号变为细胞内信号。肿瘤细胞受体ＴＰＫ区的突变体，虽然可能仍具有结合配体的能力，但丧失了刺激细胞内效应的能力。说明受体信号激活的关键是由一个功能性ＴＰＫ决定的，并通过一些ＴＰＫ的底物来介导细胞内的效应．这使人联想到肿瘤细胞之所以呈失控的增殖状态，与其受体ＴＰＫ的激活及细胞蛋白磷酸化密切相关。

TYROSINE PROTEIN KINASE OF GROWTH FACTOR RECEPTOR AND STEMMING OF CANCEROGENICITY

This is a review of recant progress on studies of Peptide growth factor(PGF) and itS receptor tyrosine protein kin(TPK). In this peper,the topicS discussed is PGF and its reeptor TPK Play imPOrtant role in cancer cells proliforation and tumorigenesis, and the questions stemming transmembrane traneduction of extracellular signal about cancer are also discussed. Recently, probes about Pathway of stopping cancer cell proliforation and inducing it differentiation devolp rapidlly in the field of molecular bilology and membrane biolcal chemistry. The first molecular event mdiated by groWth factor binding to their surface receptor is stimulation of tyrcoine residues Phosphoralation of cellular subetrace inclluding rapid growth faCtor receptor (OFR) autOPhosphorylation. Then, a serial of physiological and biochemical reaction are generated in cell. The proliferation and differentiation are physiologycal and biochemical processes of great coordination, the phesphorylation and dephcophorylation depend on each other for existence in normal call. Although TPK domain's mutation of cancer cell receptor is that can binding to ligand saal,but the function that stimchte intracellutar responsible are losed. Above, it had been confirmed by a number of research. A recent study disCovered that acute oncosen productS and the receptor for a lot of hormone and growth faCtor peers TPK activity. TheSe tindingy suggeSt that Phosphorytation of tryosine residuce of cellular Ptoteions Play a major of cell proliferation.