Dataset Information


Systemic Comparison of Heat Shock Response Induced by Heat Shock and a Proteasome Inhibitor in Mouse Fibrosarcoma Cells and Their Thermotolerant Counterparts

ABSTRACT: Heat shock response (HSR) is a cellular defense mechanism against various stresses. Both heat shock and proteasome inhibitor MG132 cause the induction of heat shock proteins, a distinct feature of HSR. To better understand the molecular basis of HSR, we subjected the mouse fibrosarcoma cell line, RIF-1, and its thermotolerant variant, TR-RIF-1 cells, to heat shock and MG132. We compared mRNA expressions using microarray analysis during recovery after heat shock and MG132 treatment. This study led us to group the 3,245 up-regulated genes by heat shock and MG132 into three families: genes regulated 1) by both heat shock and MG132 (e.g. chaperones); 2) by heat shock (e.g. DNA-binding proteins including histones); and 3) by MG132 (e.g. innate immunity and defense-related molecules). RIF-1 and TR cells were heat shock treated or MG132 treated and harvested after various times of recovery. mRNA expressions were compared to untreated samples. Biological replication was done.

ORGANISM(S): Mus musculus  

SUBMITTER: Kong-Joo Lee   Hee-Jung Kim 

PROVIDER: E-GEOD-24197 | ArrayExpress | 2011-11-09



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Systemic analysis of heat shock response induced by heat shock and a proteasome inhibitor MG132.

Kim Hee-Jung HJ   Joo Hye Joon HJ   Kim Yung Hee YH   Ahn Soyeon S   Chang Jun J   Hwang Kyu-Baek KB   Lee Dong-Hee DH   Lee Kong-Joo KJ  

PloS one 20110630 6

The molecular basis of heat shock response (HSR), a cellular defense mechanism against various stresses, is not well understood. In this, the first comprehensive analysis of gene expression changes in response to heat shock and MG132 (a proteasome inhibitor), both of which are known to induce heat shock proteins (Hsps), we compared the responses of normal mouse fibrosarcoma cell line, RIF-1, and its thermotolerant variant cell line, TR-RIF-1 (TR), to the two stresses. The cellular responses we e  ...[more]

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