ArticleProceedings of the National Academy of Sciences of the United States of America1994
Evidence for a regulatory protein involved in the increased activity of system A for neutral amino acid transport in osmotically stressed mammalian cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 45 citations in OpenAlex.
- Article
- Hypertonic stress and amino acid deprivation both increase expression of mRNA for amino Acid transport system A.The Journal of general physiology · 2005Article
- Mechanisms implicated in the response of system a to hypertonic stress and amino acid deprivation still can be different.The Journal of general physiology · 2005Article
- The osmoregulatory and the amino acid-regulated responses of system A are mediated by different signal transduction pathways.The Journal of general physiology · 2003Article
- Creatine and the creatine transporter: a review.Molecular and cellular biochemistry · 2001Review
- The proton-linked monocarboxylate transporter (MCT) family: structure, function and regulation.The Biochemical journal · 1999Review
- Lactate transport in skeletal muscle - role and regulation of the monocarboxylate transporter.The Journal of physiology · 1999Review
- Na+-dependent nucleoside transport in liver: two different isoforms from the same gene family are expressed in liver cells.The Biochemical journal · 1998Article
- Identification and partial characterization of a novel membrane glycoprotein induced by amino acid deprivation in renal epithelial cells.The Biochemical journal · 1997Article
- Regulation of Na+,K(+)-ATPase and the Na+/K+/Cl- co-transporter in the renal epithelial cell line NBL-1 under osmotic stress.The Biochemical journal · 1996Article
- Article
- Article
- Induction of the high-affinity Na(+)-dependent glutamate transport system XAG- by hypertonic stress in the renal epithelial cell line NBL-1.The Biochemical journal · 1995Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
System A for neutral amino acid transport is increased by hypertonic shock in NBL-1 cells previously induced to express system A activity by amino acid starvation. The hypertonicity-mediated effect can be blocked by cycloheximide but is insensitive to tunicamycin. The activity induced may be inactivated irreversibly by the addition of system A substrates, by a rapid mechanism insensitive to cycloheximide. In CHO-K1 cells, hypertonicity increases system A activity, as has been shown in NBL-1 cells. This effect is additive to the activity produced by derepression of system A by amino acid starvation and is insensitive to tunicamycin. Furthermore, the alanine-resistant mutant CHO-K1 alar4, which bears a mutation affecting the regulatory gene R1, involved in the derepression of system A activity after amino acid starvation, is still able to respond to the hypertonic shock by increasing system A activity to a level similar to that described in hypertonicity-induced derepressed CHO-K1 (wild type) cells. These results suggest (i) that the hypertonicity-mediated increase of system A activity occurs through a mechanism other than that involved in system A derepression and (ii) that a regulatory protein coded by an osmotically sensitive gene is responsible for further activation of preexisting A carriers.
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