Kidney Research and Clinical Practice : eISSN 2211-9140 / pISSN 2211-9132

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Fig. 1. A genetic disease is caused by a defective protein or specific protein deficiency (A). In the PHS hypothesis, the PHS of organisms can induce alternative proteins (AP) in various organ cells in need (B). Thus, the patients who produce more proper AP might have a less severe clinical course and a better prognosis in a familial genetic disease. Also, it is possible that prolonged activation of transformed proteins or AP is associated with the substances that are toxic to host cells in natural course of some genetic diseases (C). A cancer cell originates from a gene defect of an intracellular protein which may be essential for cell survival (D). AP are produced within the cells with new gene activation, and these proteins may also be controlled by the intracellular PHS if the cell avoids cell death. During this process in replicating cells or stem cells, serial activation of genes affecting cell-replication cycles, including embryonic transcriptional factors, occurs and an eventual self-reproducing cell can be established (E). In tumor growth in most cancers, the stop signals (proteins) may not function, because of ongoing new proteins that are produced from renewal cancer cells and cannot be controlled by the systemic PHS in the host (F). Whereas normal organogenesis of stem cells such as embryonic development and organ repair is strictly controlled by stop signals (proteins) under the PHS in the host. TP, transformed proteins.
Kidney Research and Clinical Practice 2017;36:132~144
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