Hypothesis of evolutionary origin of several human and animal diseases
Studies of our Laboratory in the field of molecular and evolutionary endocrinology have allowed us to put forward a hypothesis about evolutionary origin of endocrine and other diseases of human and animals. This hypothesis is considered using a model of hormonal signaling systems. It is based on the...
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Published in | Journal of evolutionary biochemistry and physiology Vol. 46; no. 3; pp. 312 - 320 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
Dordrecht
Dordrecht : SP MAIK Nauka/Interperiodica
01.06.2010
SP MAIK Nauka/Interperiodica Springer Nature B.V |
Subjects | |
Online Access | Get full text |
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Summary: | Studies of our Laboratory in the field of molecular and evolutionary endocrinology have allowed us to put forward a hypothesis about evolutionary origin of endocrine and other diseases of human and animals. This hypothesis is considered using a model of hormonal signaling systems. It is based on the concept formulated by the authors about molecular defects in hormonal signaling systems as the key causes of endocrine diseases; on evolutionary conservatism of hormonal signaling systems, which stems logically from the authors' concept of the prokaryotic genesis and endosymbiotic emergence in the course of evolution of chemosignaling systems in the higher eukaryotes; from the fact that the process of formation of hormonal signaling systems with participation of endosymbiosis including the horizontal transfer of genes is accompanied by transfer not only of normal, but also of the defected genetic material. There are considered examples of the principal possibility of transfer of defected genes between bacteria and eukaryotic organisms. Analysis of the current literature allows suggesting inheritance of pathogenic factors from evolutionary ancestors in the lineage prokaryotes—lower eukaryotes—higher eukaryotes. |
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Bibliography: | http://dx.doi.org/10.1134/S0022093010030130 |
ISSN: | 0022-0930 1608-3202 |
DOI: | 10.1134/S0022093010030130 |