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3 results on '"Portero-Robles I"'

1. A fruit-specific putative dihydroflavonol 4-reductase gene is differentially expressed in strawberry during the ripening process.

Author

Moyano, E, Portero-Robles, I, Medina-Escobar, N, Valpuesta, V, Muñoz-Blanco, J, and Caballero, J L

Abstract

A cDNA clone encoding a putative dihydroflavonol 4-reductase gene has been isolated from a strawberry (Fragaria x ananassa cv Chandler) DNA subtractive library. Northern analysis showed that the corresponding gene is predominantly expressed in fruit, where it is first detected during elongation (green stages) and then declines and sharply increases when the initial fruit ripening events occur, at the time of initiation of anthocyanin accumulation. The transcript can be induced in unripe green fruit by removing the achenes, and this induction can be partially inhibited by treatment of de-achened fruit with naphthylacetic acid, indicating that the expression of this gene is under hormonal control. We propose that the putative dihydroflavonol 4-reductase gene in strawberry plays a main role in the biosynthesis of anthocyanin during color development at the late stages of fruit ripening; during the first stages the expression of this gene could be related to the accumulation of condensed tannins.

Published
1998
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3. Inhibition of phosphotyrosine phosphatase 1B causes resistance in BCR-ABL-positive leukemia cells to the ABL kinase inhibitor STI571.

Author

Koyama N, Koschmieder S, Tyagi S, Portero-Robles I, Chromic J, Myloch S, Nürnberger H, Rossmanith T, Hofmann WK, Hoelzer D, and Ottmann OG

Subjects
Apoptosis drug effects, Benzamides, Cell Differentiation drug effects, Cell Line, Tumor, Cell Proliferation drug effects, Dose-Response Relationship, Drug, Fusion Proteins, bcr-abl metabolism, Humans, Imatinib Mesylate, K562 Cells, Phosphorylation, Piperazines antagonists & inhibitors, Protein Tyrosine Phosphatase, Non-Receptor Type 1, Protein Tyrosine Phosphatases metabolism, Pyrimidines antagonists & inhibitors, Structure-Activity Relationship, Vanadates pharmacology, Antineoplastic Agents pharmacology, Drug Resistance, Neoplasm drug effects, Enzyme Inhibitors pharmacology, Fusion Proteins, bcr-abl drug effects, Piperazines pharmacology, Protein Tyrosine Phosphatases antagonists & inhibitors, Protein-Tyrosine Kinases antagonists & inhibitors, Pyrimidines pharmacology
Abstract

Protein tyrosine phosphatase 1B (PTP1B) is a negative regulator of BCR-ABL-mediated transformation in vitro and in vivo. To investigate whether PTP1B modulates the biological effects of the abl kinase inhibitor STI571 in BCR-ABL-positive cells, we transfected Philadelphia chromosome-positive (Ph+) chronic myeloid leukemia cell-derived K562 cells with either wild-type PTP1B (K562/PTP1B), a substrate-trapping dominant-negative mutant PTP1B (K562/D181A), or empty vector (K562/mock). Cells were cultured with or without STI571 and analyzed for its effects on proliferation, differentiation, and apoptosis. In both K562/mock and K562/PTP1B cells, 0.25 to 1 mumol/L STI571 induced dose-dependent growth arrest and apoptosis, as measured by a decrease of cell proliferation and an increase of Annexin V-positive cells and/or of cells in the sub-G(1) apoptotic phase. Western blot analysis showed increased protein levels of activated caspase-3 and caspase-8 and induction of poly(ADP-ribose) polymerase cleavage. Low concentrations of STI571 promoted erythroid differentiation of these cells. Conversely, K562/D181A cells displayed significantly lower PTP1B-specific tyrosine phosphatase activity and were significantly less sensitive to STI571-induced growth arrest, apoptosis, and erythroid differentiation. Pharmacologic inhibition of PTP1B activity in wild-type K562 cells, using bis(N,N-dimethylhydroxamido)hydroxooxovanadate, attenuated STI571-induced apoptosis. Lastly, comparison of the STI571-sensitive Ph+ acute lymphoblastic leukemia cell line SupB15 with a STI571-resistant subline revealed significantly decreased PTP1B activity and enhanced BCR-ABL phosphorylation in the STI571-resistant SupB15 cells. In conclusion, functional PTP1B is involved in STI571-induced growth and cell cycle arrest, apoptosis, and differentiation, and attenuation of PTP1B function may contribute to resistance towards STI571.

Published
2006
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