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The Protein Kinase Inhibitor, H-7, Suppresses Heat Induced Activation of Heat Shock Transcription Factor 1

The Protein Kinase Inhibitor, H-7, Suppresses Heat Induced Activation of Heat Shock Transcription Factor 1

K Ohnishi, X Wang, A Takahashi, H Matsumoto, T Ohnishi

Mol Cell Biochem. 1999 Jul;197(1-2):129-35.

PMID: 10485332

Abstract:

We investigated the effects of a protein kinase (PK) inhibitor, H-7 (1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride), on the regulation of heat shock protein (hsp)72 gene expression in a human glioblastoma cell line (A-172) using a gel mobility-shift assay and Western blot analysis. Heat shock transcription factor 1 (HSF1) was phosphorylated immediately after heat treatment (44 degrees C, 30 min) and the phosphorylation of HSF1 was suppressed by H-7. The increase in DNA binding ability of HSFI to heat shock element (HSE) by heat shock was significantly suppressed by the addition of H-7 in a dose-dependent manner. Similarly, the accumulation of hsp72 by heat shock was suppressed by the addition of H-7 in a dose-dependent manner. Since H-7 is known to be a potent inhibitor of some PKs, especially calcium-dependent PK (PKC), cyclicAMP-dependent PK (PKA) and cyclicGMP-dependent PK (PKG), it is possible that the activation of HSF1 by phosphorylation and subsequent hsp72 gene expression are dependent on some of those PKs. The nature of H-7 as a non-specific inhibitor for PKs is discussed in relation to its availability for regulation of heat sensitivity of cells depending on cellular level of hsp72.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP108930172-A	H-7 dihydrochloride		108930-17-2	Price

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