Friday, September 27, 2013


One of the function of the Glycan coverage of protein receptor is not only to be a an integral part of the Glycopeptide nature of the receptor as it is recognized, but to also induce Antigenic like recognition by the immune system when the cell is altered as it occurs during a neoplastic transformation of the cell.  During such a transformation, it is believed that cyclines and altered FAK abnormally produced may cause membrane alterations which include alterations at cellular receptors that will dampen cellular induction of chemokines that could be naturally induced.  This effect will reduce normal recognition of cellular abnormality, and dampen caspase 3 stimulation as well as allowing the changed cell to escape immune recognition.   There is indeed a cascade of maneuvers that allow the cell to survive a neoplastic transformation.  Aside for an uncontrolled DNA duplication and cellular proliferation, gene alterations and mistakes must be tolerated through suppression of control genetic mechanisms, gen repair must fail, BRCA genes and the like of them must be "mutated" and Breaks such as P53 must be 'MUTATED" to let the neoplastic process advance. Suppressor gene such as Rb1 must be silenced!  Receptors under the attack of cytokines, will have their Glycan portion altered.  the Receptor consequently become resistant to its stimulant growth factor, a fact which under normal considition will stimulate further growth factor to try to conquer the resistance, this increase will stimulate intact secondary factor and dampen some pathway genes (PTEN) an break to the PI3K pathway.  further stressful action will start the HSP family of Heat stroke Protein and cause the c-JUN/c-fos, increasing further epigenetic events....Again glycopeptide alteration is a critical step in cellular tolerance of malignant transformed cell (IT IS BELIEVED)
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