Inhibition of the growth of mammalian cells in culture by amino acids and the isolation and characterization ofL-phenylalanine-resistant mutants modifyingL-phenylalanine transport

1976 ◽  
Vol 2 (5) ◽  
pp. 411-428 ◽  
Author(s):  
Ellis Englesberg ◽  
Richard Bass ◽  
William Heiser
In Vitro ◽  
1974 ◽  
Vol 9 (6) ◽  
pp. 414-420 ◽  
Author(s):  
Otto Grahl-Nielsen ◽  
P. Ødegaard ◽  
George L. Tritsch

Metabolites ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 481
Author(s):  
Gemma G. Martínez-García ◽  
Raúl F. Pérez ◽  
Álvaro F. Fernández ◽  
Sylvere Durand ◽  
Guido Kroemer ◽  
...  

Autophagy is an essential protective mechanism that allows mammalian cells to cope with a variety of stressors and contributes to maintaining cellular and tissue homeostasis. Due to these crucial roles and also to the fact that autophagy malfunction has been described in a wide range of pathologies, an increasing number of in vivo studies involving animal models targeting autophagy genes have been developed. In mammals, total autophagy inactivation is lethal, and constitutive knockout models lacking effectors of this route are not viable, which has hindered so far the analysis of the consequences of a systemic autophagy decline. Here, we take advantage of atg4b−/− mice, an autophagy-deficient model with only partial disruption of the process, to assess the effects of systemic reduction of autophagy on the metabolome. We describe for the first time the metabolic footprint of systemic autophagy decline, showing that impaired autophagy results in highly tissue-dependent alterations that are more accentuated in the skeletal muscle and plasma. These changes, which include changes in the levels of amino-acids, lipids, or nucleosides, sometimes resemble those that are frequently described in conditions like aging, obesity, or cardiac damage. We also discuss different hypotheses on how impaired autophagy may affect the metabolism of several tissues in mammals.


1988 ◽  
Vol 263 (22) ◽  
pp. 10817-10823
Author(s):  
H V Le ◽  
L Ramanathan ◽  
J E Labdon ◽  
C A Mays-Ichinco ◽  
R Syto ◽  
...  

1986 ◽  
Vol 42 (2) ◽  
pp. 185-186 ◽  
Author(s):  
K. Takahashi ◽  
I. Kaneko ◽  
M. Date ◽  
E. Fukada

1984 ◽  
Vol 4 (11) ◽  
pp. 2449-2454 ◽  
Author(s):  
E R Kaufman

A new protocol for inducing mutations in mammalian cells in culture by exposure to the thymidine analog 5-bromodeoxyuridine (BrdUrd) was established. This protocol, called "DNA-dependent" mutagenesis, involved the incorporation of BrdUrd into DNA under nonmutagenic conditions and the subsequent replication of the 5-bromouracil (BrUra)-containing DNA under mutagenic conditions but with no BrdUrd present in the culture medium. The mutagenic conditions were induced by allowing BrUra-containing DNA to replicate in the presence of high concentrations of thymidine. This generated high intracellular levels of dTTP and dGTP, causing nucleotide pool imbalance. The mutagenesis induced by this protocol was found to correlate with the level of BrUra substituted for thymine in DNA.


Biochemistry ◽  
1977 ◽  
Vol 16 (9) ◽  
pp. 1988-1996 ◽  
Author(s):  
Paul S. Miller ◽  
Lita T. Braiterman ◽  
Paul O. P. Ts'o

1998 ◽  
Vol 149 (1) ◽  
pp. 41 ◽  
Author(s):  
Hidehiko Kawai ◽  
Yukika Kitamura ◽  
Osamu Nikaido ◽  
Masaaki Tatsuka ◽  
Hiroko Hama-Inaba ◽  
...  

1988 ◽  
Vol 448 (1) ◽  
pp. 46-52 ◽  
Author(s):  
Ann Kingsbury ◽  
Vittorio Gallo ◽  
Robert Balazs

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