sepharose and benzo-1-2-3-thiadiazole

sepharose has been researched along with benzo-1-2-3-thiadiazole* in 1 studies

Other Studies

1 other study(ies) available for sepharose and benzo-1-2-3-thiadiazole

Article	Year
Identification of a 2,6-dichloroisonicotinic-acid-sensitive protein kinase from tobacco by affinity chromatography on benzothiadiazole-sepharose and NIM-metal chelate adsorbent. Pest management science, 2001, Volume: 57, Issue:8 In the search for the target site of inducers of systemic acquired resistance (SAR), a BTH-binding protein kinase (BBPK) has been identified from tobacco by affinity chromatography on benzothiadiazole-sepharose (CGA 324041-sepharose) and NIM-metal chelate affinity resin. The substrate selectivity of the isolated enzyme (phosphorylation of histone type III-S, I kappa B alpha,IkB alpha S32A/S36A and NIM1) suggested a possible BBPK-mediated regulation of NIM1 in tobacco. The measurement of the effect of different SAR-inducers showed an inhibition of BBPK by 2,6-dichloroisonicotinic acid (INA) and, to a lower extent, by benzothiadiazoles and salicylic acid. Comparison between BBPK cell-free inhibition and in vivo PR-1 induction revealed that BBPK could be the target site of INA. Topics: Chelating Agents; Chromatography, Affinity; Enzyme Inhibitors; Immunity, Innate; Isonicotinic Acids; Nicotiana; Phosphorylation; Plant Diseases; Protein Kinase Inhibitors; Protein Kinases; Salicylic Acid; Sepharose; Thiadiazoles	2001

Article

Year

Identification of a 2,6-dichloroisonicotinic-acid-sensitive protein kinase from tobacco by affinity chromatography on benzothiadiazole-sepharose and NIM-metal chelate adsorbent.

Pest management science, 2001, Volume: 57, Issue:8

In the search for the target site of inducers of systemic acquired resistance (SAR), a BTH-binding protein kinase (BBPK) has been identified from tobacco by affinity chromatography on benzothiadiazole-sepharose (CGA 324041-sepharose) and NIM-metal chelate affinity resin. The substrate selectivity of the isolated enzyme (phosphorylation of histone type III-S, I kappa B alpha,IkB alpha S32A/S36A and NIM1) suggested a possible BBPK-mediated regulation of NIM1 in tobacco. The measurement of the effect of different SAR-inducers showed an inhibition of BBPK by 2,6-dichloroisonicotinic acid (INA) and, to a lower extent, by benzothiadiazoles and salicylic acid. Comparison between BBPK cell-free inhibition and in vivo PR-1 induction revealed that BBPK could be the target site of INA.

Topics: Chelating Agents; Chromatography, Affinity; Enzyme Inhibitors; Immunity, Innate; Isonicotinic Acids; Nicotiana; Phosphorylation; Plant Diseases; Protein Kinase Inhibitors; Protein Kinases; Salicylic Acid; Sepharose; Thiadiazoles

2001