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Digitale Medien

Studies of the type I cellular retinoic acid-binding protein mutants and their biological activities (1999)

Wei, Li-Na ; Chang, Liming ; Hu, Xinli

Springer

Molecular and cellular biochemistry 200 (1999), S. 69-76

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ISSN: 1573-4919

Schlagwort(e): CRABP-I ; RA induction ; RA binding ; mutagenesis

Quelle: Springer Online Journal Archives 1860-2000

Thema: Biologie , Chemie und Pharmazie , Medizin

Notizen: Abstract We have mutated the type I cellular retinoic acid binding protein (CRABP-I), individually at the Arg131 (into Ala) and the Tyr 133 (into Phe) residues which have been predicted to make direct contact with retinoic acid (RA) based upon previous structural studies. The RA-binding affinities of these mutants are examined and their biological effects on RA induction of reporter genes are determined. The R131A mutation drastically affects its ligand-binding property, but the Y133F mutation has little effect. By using an RA-inducible reporter, it is found that the wild type CRABP-I exerts biphasic effects on RA induction of the reporter. The early (at 12 h) effect is to enhance RA induction, whereas the delayed (at 24 h) effect is to suppress RA induction. In consistence with their RA binding property, the R 131A mutant loses both its early and delayed biological activities, whereas the Y133F mutant remains as effective as the wild type. It is concluded that CRABP-I over-expression exerts biphasic effects on RA-mediated gene expression, and that Arg131, but not Tyr 133, is essential for a high RA-binding affinity of this protein as well as its biological activity.

Materialart: Digitale Medien

URL: http://dx.doi.org/10.1023/A:1006906415388

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Digitale Medien

Homologous desensitization of ATP-stimulated mitogenesis: Mechanism involves desensitization of arachidonic acid release and cAMP elevation but not the activation of protein kinase A (1995)

Huang, Ning-Na ; Wang, Ding-Ji ; Heller, Elizabeth ; [weitere]

New York, NY [u.a.] : Wiley-Blackwell

Journal of Cellular Physiology 165 (1995), S. 667-675

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ISSN: 0021-9541

Schlagwort(e): Life and Medical Sciences ; Cell & Developmental Biology

Quelle: Wiley InterScience Backfile Collection 1832-2000

Thema: Biologie , Medizin

Notizen: Prolonged incubation of quiescent 3T3, 3T6, and A431 cells with the P2Y purinoceptor agonists ATP, ADP, or AMPPNP reduced the mitogenic responses of target cells to a further challenge by these agonists, as measured by [3H]thymidine incorporation. The mitogenic desensitization was agonist-specific, for no effect was seen on DNA synthesis stimulated by epidermal growth factor, insulin, bombesin, 12-0-tetradecanoyl-phorbol-12 acetate (TPA), or adenosine. The desensitization was completely reversible, since after a 24 hr incubation in the absence of ATP, the cells responded fully to the mitogenic action of ATP. The presence of a low level of cycloheximide blocked recovery, suggesting that down-regulation of the P2Y receptor may have occurred during desensitization. In Swiss 3T3 cells, stimulation of DNA synthesis occurs predominantly by activation of arachidonic acid release, followed by its oxidation to prostaglandin E2 and stimulation of adenylyl cyclase. Interestingly, prolonged preincubation with ATP produced a similar degree of desensitization of DNA synthesis and of ATP-dependent arachidonic acid release and cAMP accumulation. Furthermore, this was true for both wild type cells and mutants with a defective cAMP-dependent protein kinase (PKA). We conclude that homologous desensitization is likely due to uncoupling of the P2Y purinoceptor from phospholipase A2, and this process does not require activation of protein kinase A. © 1995 Wiley-Liss Inc.

Zusätzliches Material: 8 Ill.