Studies of the mechanism of action 1-aminocyclopentane-1-carboxylic acid.

doi:10.1016/0006-2952(63)90055-8

Paper

Studies of the mechanism of action 1-aminocyclopentane-1-carboxylic acid.

Published Apr 1, 1963 · W. Sterling, J. Henderson

Biochemical pharmacology

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23

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Abstract

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In Vitro Study

Study Snapshot

High concentrations of 1-aminocyclopentane-1-carboxylic acid (ACC) partially inhibit protein incorporation into ascites tumor cells in vitro, mainly due to inhibition of amino acid transport into the cells.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

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Paper

Studies of the mechanism of action 1-aminocyclopentane-1-carboxylic acid.

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References

Citations

Chemotherapeutic potential of methionine analogue inhibitors of tumor-derived methionine adenosyltransferases.

Methionine analogue inhibitors show potential as a cancer chemotherapy target due to their differential inhibitory activities between tumor-derived and normal rat liver isozymes.

Inhibition of the peptidyltransferase acceptor site by 2'(3')-O-cycloleucyl- and alpha-aminoisobutyryl derivatives of cytidylyl-(3'-5')adenosine.

Compounds 1c and 1d, which contain an anomalous amino acid with a substituted -hydrogen, can interfere with the peptidyltransferase A site but are not acceptors in the reaction due to a misfit of the -substituent.

NEUROTOXICITY OF A NON‐METABOLIZABLE AMINO ACID, 1‐AMINOCYCLOPENTANE‐l‐CARBOXYLIC ACID: REGIONAL PROTEIN LEVELS AND LIPID COMPOSITION OF NERVOUS TISSUE

ACPC injections in mice cause primary degeneration of axons in the cerebellum, spinal cord, and peripheral nerves, with significant protein deficits in the cerebellum and cervical spinal cord.

NEUROTOXICITY OF A NON‐METABOLIZABLE AMINO ACID, 1‐AMINOCYCLOPENTANE‐1‐CARBOXYLIC ACID: ANTAGONISM BY AMINO ACIDS IN CULTURES OF CEREBELLUM

Amino acids can protect nerve cell bodies from neurotoxicity caused by the non-metabolizable amino acid ACPC, suggesting defective protein metabolism in ACPC-treated mice.

Modifications de l'aminoacidurie aprés administration de cycloleucine chez le rat: analogies avec la cystinurie humaine

Cycloleucine administration in rats causes selective hyperaminoaciduria in basic amino acids and cystine, similar to human cystinuria-lysinuria, but its use is limited due to its toxicity.

Pathologic physiology and chemotherapy of Plasmodium berghei. IX. Gastric secretion and the influence of 1-aminocyclopentane carboxylic acid (WR 14, 997 or cycloleucine).

WR 14, 997 shows potential as an antimalarial drug, suppressing parasitemia in mice and showing minimal toxicity compared to other new compounds.