| Autor: |
Shilov ES; Lomonosov Moscow State University, Biological Faculty, Moscow, 119991, Russia. shilov_evgeny@inbox.ru., Kislyakov IV, Gorshkova EA, Zvartsev RV, Drutskaya MS, Mufazalov IA, Skulachev VP, Nedospasov SA |
| Jazyk: |
angličtina |
| Zdroj: |
Biochemistry. Biokhimiia [Biochemistry (Mosc)] 2014 Dec; Vol. 79 (12), pp. 1412-22. |
| DOI: |
10.1134/S0006297914120177 |
| Abstrakt: |
Cytochrome c is an indispensable electron carrier in the mitochondrial respiratory chain and also an important mediator of the internal pathway triggering apoptosis. Mice with a complete deficiency of the Cycs gene encoding the somatic cytochrome c die during the embryogenesis. Using the technology of LoxP-cre-dependent tissue-specific recombination, we obtained some mouse strains with significantly reduced expression of cytochrome c in certain cell types ("conditional genetic knockdown"). This knockdown was achieved by abrogation of the normal splicing of the Cycs locus pre-mRNA due to an additional acceptor site inside the stop-cassette neo(r). Previously, we observed embryonic lethality in homozygous mice with the same knockdown of cytochrome c in all cells of the organism. In the present work we studied two novel mouse strains with conditional knockdown of the Cycs gene in T lymphocytes and macrophages. Somewhat surprisingly, the mice of these two strains under normal conditions were not phenotypically different from the wild-type mice, either on the whole organism level or on the level of activity of individual target cells. Thus, the amount of cytochrome c in lymphomyeloid cells does not affect their development and normal functioning. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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