Syringolin-Mediated Activation of the Pir7b Esterase Gene in Rice Cells Is Suppressed by Phosphatase Inhibitors

2000 ◽  
Vol 13 (3) ◽  
pp. 342-346 ◽  
Author(s):  
Paul Hassa ◽  
José Granado ◽  
Ernst Freydl ◽  
Urs Wäspi ◽  
Robert Dudler
Keyword(s):  
Signal Transduction ◽  
Pseudomonas Syringae ◽  
Kinase Inhibitors ◽  
De Novo ◽  
Signal Transduction Pathway ◽  
Defense Responses ◽  
Protein Kinase Inhibitors ◽  
Transcript Accumulation ◽  
Transcript Levels ◽  
Phosphatase Inhibitors

Inoculation of rice plants (Oryza sativa) with the nonhost pathogen Pseudomonas syringae pv. syringae leads to the activation of defense-related genes and ultimately to induced resistance against the rice blast fungus Pyricularia oryzae. One of the molecular determinants of P. syringae pv. syringae that is recognized by the plant cells and evokes these defense responses is syringolin A, an elicitor that is secreted by the bacteria under appropriate conditions. In order to investigate signal transduction events elicited by syringolin A, the response of cultured rice cells to syringolin A application was analyzed. Cultured rice cells were able to sense syringolin A at concentrations in the nanomolar range as observed by the transient accumulation of Pir7b esterase transcripts. Syringolin A-mediated Pir7b transcript accumulation was inhibited by cycloheximide, indicating that de novo protein synthesis was required. Calyculin and okadaic acid, two protein phosphatase inhibitors, blocked Pir7b gene induction, whereas the serine/threonine protein kinase inhibitors staurosporine and K-252a had no effect on Pir7b transcript levels. Actin transcript levels were essentially not affected by inhibitor treatments over the experimental time span. These results imply that dephosphorylation of a phosphoprotein is an important step in the syringolin A-triggered signal transduction pathway.

scholarly journals Radiotherapy and inhibition of the EGF family as treatment strategies for prostate cancer: combining theragnostics with theragates

2011 ◽  
Vol 5 (2) ◽  
pp. 119 ◽  
Author(s):  
Wolfgang Lilleby ◽  
Flavio Solca ◽  
Kathrine Røe
Keyword(s):  
Prostate Cancer ◽  
Signal Transduction ◽  
Solid Tumors ◽  
Kinase Inhibitors ◽  
Nuclear Translocation ◽  
Current Knowledge ◽  
Treatment Strategies ◽  
Signal Transduction Pathway ◽  
Protein Kinase Inhibitors ◽  
Treatment Modalities

Prostate cancer is one of the most common solid tumors affecting men. Localized stages can be cured, however, once disseminated to distant organs the median survival drops below 12 months. The challenge for the future consists of unifying gained insights of cellular signal dysfunctioning (‘‘theragates’’) with the knowledge of disease detection (‘‘theragnostics’’) in personalized therapy. In solid malignancies, multiple signal transduction molecules are often deregulated simultaneously, within the same tumor. A multi-targeted approach may possibly improve efficacy, but will also increase toxicity, thus, potentially limiting the use of various combinations. On the other hand, well-established treatment modalities in prostate cancer, such as radiotherapy with its known efficacy and limited toxicity, may be an attractive combination partner for protein kinase inhibitors. Deregulation of the epidermal growth factor receptor (EGFR) signal transduction pathway is observed in a variety of solid tumors, including prostate cancer. Furthermore, one important DNA repair mechanism is dependent on EGFR nuclear translocation, thus, providing a rationale for combining radiotherapy with EGFR inhibitors. This article reviews current knowledge regarding this combination paradigm, revealing an intriguing therapy option to be explored for patients with advanced prostate cancer.

scholarly journals Radiotherapy and inhibition of the EGF family as treatment strategies for prostate cancer: combining theragnostics with theragates

2011 ◽  
pp. 119-128
Author(s):  
Wolfgang Lilleby ◽  
Flavio Solca ◽  
Kathrine Røe
Keyword(s):  
Prostate Cancer ◽  
Signal Transduction ◽  
Solid Tumors ◽  
Kinase Inhibitors ◽  
Nuclear Translocation ◽  
Current Knowledge ◽  
Treatment Strategies ◽  
Signal Transduction Pathway ◽  
Protein Kinase Inhibitors ◽  
Treatment Modalities

Prostate cancer is one of the most common solid tumors affecting men. Localized stages can be cured, however, once disseminated to distant organs the median survival drops below 12 months. The challenge for the future consists of unifying gained insights of cellular signal dysfunctioning (‘‘theragates’’) with the knowledge of disease detection (‘‘theragnostics’’) in personalized therapy. In solid malignancies, multiple signal transduction molecules are often deregulated simultaneously, within the same tumor. A multi-targeted approach may possibly improve efficacy, but will also increase toxicity, thus, potentially limiting the use of various combinations. On the other hand, well-established treatment modalities in prostate cancer, such as radiotherapy with its known efficacy and limited toxicity, may be an attractive combination partner for protein kinase inhibitors. Deregulation of the epidermal growth factor receptor (EGFR) signal transduction pathway is observed in a variety of solid tumors, including prostate cancer. Furthermore, one important DNA repair mechanism is dependent on EGFR nuclear translocation, thus, providing a rationale for combining radiotherapy with EGFR inhibitors. This article reviews current knowledge regarding this combination paradigm, revealing an intriguing therapy option to be explored for patients with advanced prostate cancer.

Two forms of long-term potentiation in area CA1 activate different signal transduction cascades

1996 ◽  
Vol 76 (5) ◽  
pp. 3038-3047 ◽  
Author(s):  
I. Cavus ◽  
T. Teyler
Keyword(s):  
Signal Transduction ◽  
Nmda Receptor ◽  
Kinase Inhibitors ◽  
Kinase Inhibitor ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Protein Kinase Inhibitors ◽  
Area Ca1 ◽  
Term Potentiation

1. The effects of protein kinase inhibitors on N-methyl-D-aspartate (NMDA)-receptor-mediated, voltage-dependent calcium channel (VDCC)-mediated, and 100-Hz long-term potentiation (LTP) were studied in area CA1 of rat hippocampal slices. 2. A 25-Hz tetanus induced a quickly developing potentiation that was blocked by the NMDA antagonist D,L-2-amino-5-phosphonovaleric acid (APV) and was not affected by the L-type VDCC inhibitor nifedipine, suggesting that it was mediated by NMDA receptors (NMDA-LTP). 3. Application of a 200-Hz tetanus in APV induced a slowly developing NMDA-receptor-independent potentiation that was blocked by nifedipine and thus named VDCC-LTP. NMDA- and VDCC-LTP reached comparable magnitudes despite their different induction parameters and developmental kinetics. 4. Bath perfusion of the broad-spectrum serine/threonine kinase inhibitor 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7) blocked NMDA-LTP but not VDCC-LTP, whereas the tyrosine kinase inhibitors genistein and lavendustin A blocked VDCC-LTP but not NMDA-LTP. These results suggest a differential involvement of H-7-sensitive serine/threonine kinases and tyrosine kinases in the two forms of LTP. 5. Tetanization of 200 Hz in control media resulted in a compound potentiation twice as large as NMDA- or VDCC-LTP, implying that the two forms of LTP did not facilitate or reduce each other's expression. The often-used 100-Hz tetanus (1 s twice) induced a potentiation that was comparable in size with the 200-Hz compound LTP. Nifedipine, genistein, and lavendustin A reduced the 100-Hz LTP by approximately 50%, suggesting that this LTP is also a compound potentiation consisting of NMDA- and VDCC-mediated components and their corresponding signal transduction pathways.

scholarly journals Platelet-conditioned medium increases endothelial electrical resistance independently of cAMP/PKA and cGMP/PKG

2001 ◽  
Vol 281 (5) ◽  
pp. H1992-H2001 ◽  
Author(s):  
Jonathan P. Gainor ◽  
Christine A. Morton ◽  
Jared T. Roberts ◽  
Peter A. Vincent ◽  
Fred L. Minnear
Keyword(s):  
Signal Transduction ◽  
Conditioned Medium ◽  
Pertussis Toxin ◽  
Electrical Resistance ◽  
Tyrosine Kinases ◽  
Kinase Inhibitors ◽  
Pulmonary Arteries ◽  
Signal Transduction Pathway ◽  
Transduction Pathway

Platelets release a soluble factor into blood and conditioned medium (PCM) that decreases vascular endothelial permeability. The objective of this study was to determine the signal-transduction pathway that elicits this decrease in permeability. Permeability-decreasing activity of PCM was assessed by the real-time measurement of electrical resistance across cell monolayers derived from bovine pulmonary arteries and microvessels. Using a desensitization protocol with cAMP/protein kinase A (PKA)-enhancing agents and pharmacological inhibitors, we determined that the activity of PCM is independent of PKA and PKG. Genistein, an inhibitor of tyrosine kinases, prevented the increase in endothelial electrical resistance. Because lysophosphatidic acid (LPA) has been proposed to be responsible for this activity of PCM and is known to activate the Giprotein, inhibitors of the G protein pertussis toxin and of the associated phosphatidylinositol 3-kinase (PI3K) wortmannin were used. Pertussis toxin and wortmannin caused a 10- to 15-min delay in the characteristic rise in electrical resistance induced by PCM. Inhibition of phosphorylation of extracellular signal-regulated kinase with the mitogen-activated kinase kinase inhibitors PD-98059 and U-0126 did not prevent the activity of PCM. Similar findings with regard to the cAMP protocols and inhibition of Giand PI3K were obtained for 1-oleoyl-LPA. These results demonstrate that PCM increases endothelial electrical resistance in vitro via a novel, signal transduction pathway independent of cAMP/PKA and cGMP/PKG. Furthermore, PCM rapidly activates a signaling pathway involving tyrosine phosphorylation, the Giprotein, and PI3K.

scholarly journals Induction of Chalcone Synthase Expression by Rhizobia and Nod factors in Root Hairs and Roots

1997 ◽  
Vol 10 (3) ◽  
pp. 388-393 ◽  
Author(s):  
Andrea Krause ◽  
Vo T. T. Lan ◽  
William J. Broughton
Keyword(s):  
Chalcone Synthase ◽  
Root Hairs ◽  
Signal Transduction Pathway ◽  
Defense Responses ◽  
Nod Factors ◽  
Nod Factor ◽  
Transcript Levels ◽  
Gene Transcripts ◽  
Infection Pathway ◽  
Rhizobium Sp

Chalcone synthase (CHS) of Vigna unguiculata is encoded by a gene family that is abundantly transcribed in leaves and nodules. Inoculation with Rhizobium sp. NGR234, which nodulates V. unguiculata, or with NGRΔnodABC, a mutant deficient in Nod factor production, induced rapid accumulation of CHS mRNAs in roots and root hairs. As both Nod+ and Nod- bacteria provoke responses, induction of CHS gene expression may involve symbiotic or defense responses. Four days after inoculation with the wild-type Rhizobium sp., the transcript levels increased in roots but decreased in root hairs. Use of a region unique to the 5′ end of a specific CHS gene (VuCHS1) showed that increases of transcript levels in root hairs 24 h after inoculation with both rhizobia were specific to this gene. Transcripts of this gene in roots were only detectable 4 days after treatment with NGR234. It is possible therefore that accumulation of VuCHS1 follows the infection pathway of rhizobia entering legume roots. Purified Nod factors induced accumulation of transcripts, showing that they might be part of the signal transduction pathway leading to CHS expression.

Phosphorylation regulates the assembly of NuMA in a mammalian mitotic extract

1997 ◽  
Vol 110 (11) ◽  
pp. 1287-1297 ◽  
Author(s):  
A. Saredi ◽  
L. Howard ◽  
D.A. Compton
Keyword(s):  
Mitotic Spindle ◽  
Kinase Inhibitors ◽  
Cultured Cells ◽  
Protein Kinase Inhibitors ◽  
Structural Function ◽  
Interphase Nuclei ◽  
Phosphatase Inhibitors ◽  
Insoluble Particles ◽  
Protein Phosphatase Inhibitors ◽  
Protein Dephosphorylation

NuMA is a 236 kDa nuclear protein that is required for the organization of the mitotic spindle. To determine how NuMA redistributes in the cell during mitosis, we have examined the behavior of NuMA in a mammalian mitotic extract under conditions conducive to the reassembly of interphase nuclei. NuMA is a soluble protein in mitotic extracts prepared from synchronized cultured cells, but forms insoluble structures when the extract becomes non-mitotic (as judged by the inactivation of cdc2/cyclin B kinase and the disappearance of mpm-2-reactive antigens). These NuMA-containing structures are irregularly shaped particles of 1–2 microm in diameter and their assembly is specific because other nuclear components such as the lamins remain soluble in the extract under these conditions. NuMA is dephosphorylated during this assembly process, and the assembly of these NuMA-containing structures is catalyzed by protein dephosphorylation because protein kinase inhibitors enhance their formation and protein phosphatase inhibitors block their formation. Finally, immunodepletion demonstrates that NuMA is an essential structural component of these insoluble particles, and electron microscopy shows that the particles are composed of a complex interconnected network of foci. These results demonstrate that phosphorylation regulates the solubility of NuMA in a mammalian mitotic extract, and the spontaneous assembly of NuMA into extensive structures upon dephosphorylation supports the conclusion that NuMA serves a structural function.

scholarly journals Fungal Elicitation of Signal Transduction-Related Plant Genes Precedes Mycorrhiza Establishment and Requires the dmi3 Gene in Medicago truncatula

2004 ◽  
Vol 17 (12) ◽  
pp. 1385-1393 ◽  
Author(s):  
Stéphanie Weidmann ◽  
Lisa Sanchez ◽  
Julie Descombin ◽  
Odile Chatagnier ◽  
Silvio Gianinazzi ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Medicago Truncatula ◽  
Sinorhizobium Meliloti ◽  
Expressed Sequence Tag ◽  
Signal Transduction Pathway ◽  
Suppressive Subtractive Hybridization ◽  
Cell Contact ◽  
Transduction Pathway ◽  
Transcript Accumulation ◽  
Plant Genes

Suppressive subtractive hybridization and expressed sequence tag sequencing identified 29 plant genes which are upregulated during the appressorium stage of mycorrhiza establishment between Medicago truncatula J5 (Myc+) and Glomus mosseae. Eleven genes coding plant proteins with predicted functions in signal transduction, transcription, and translation were investigated in more detail for their relation to early events of symbiotic interactions. Expression profiling showed that the genes are activated not only from the appressorium stage up to the fully established symbiosis in the Myc+ genotype of M. truncatula, but also when the symbionts are not in direct cell contact, suggesting that diffusible fungal molecules (Myc factors) play a role in the induction of a signal-transduction pathway. Transcript accumulation in roots of a mycorrhiza-defective Myc- dmi3 mutant of M. truncatula is not modified by appressorium formation or diffusible fungal molecules, indicating that the signal transduction pathway is required for a successful G. mosseae-M. truncatula interaction leading to symbiosis development. The symbiotic nodulating bacterium Sinorhizobium meliloti does not activate the 11 genes, which supposes early discrimination by plant roots between the microbial symbionts.

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