These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Breakdown of endocytosis in the oncogenic activation of receptor tyrosine kinases.
    Author: Abella JV, Park M.
    Journal: Am J Physiol Endocrinol Metab; 2009 May; 296(5):E973-84. PubMed ID: 19240253.
    Abstract:
    There is increasing evidence to support the concept that the malignant behavior of many tumors is sustained by the deregulated activation of growth factor receptors. Activation of receptor tyrosine kinases (RTKs) by their respective ligand(s) initiates cellular signals that tightly modulate cell proliferation, survival, differentiation and migration to ensure normal tissue patterning. Therefore, uncontrolled activation of such signals can have deleterious effects, leading to oncogenesis. To date, deregulation of most RTKs has been implicated in the development of cancer, although the mechanisms that lead to their deregulation are not yet fully understood (10). RTK endocytosis, the internalization and trafficking of receptors inside the cell, has long been established as a mechanism to attenuate RTK signaling. However, RTKs have been demonstrated to continue to signal along the endocytic pathway, which contributes to the spatio-temporal regulation of signal transduction. This review will focus on recent advances linking defective endocytosis of RTKs in the development of cancer.
    [Abstract] [Full Text] [Related] [New Search]