Cells in the Human Genome
Heat shock is regulated in cells in the mammalian genome, and this response has a shock transcription factor 1. This factor acts as the main factor that responds during heat stress in a mammalian cell. The role is properly elaborated and it is clear that the research backing this study carried out is of the standards of a proper cell biology research. This is indicated clearly as all the stages of examination were all well done. The main methods used involved collecting 437 genes that were used in the study based on their promoter HSF1 of the human promoter microarray and chromatin IP, human promoters with HSE, microarray expression data and measuring the binding of HSF1 and transcript levels (Trinklein et al. 1255). In this way finding the correlation between binding and expression, between binding and HSE occurrence and the promoter activities of heat shock promoters. In examining the effects of heat shock transcription, translation, DNA repair, and replication to explain further why some genes cannot be affected by the shock despite binding of HSF1 to their promoters while others are affected without binding of the HSF1(Trinklein et al. 1256). The materials and methods used are the main contributors to the paper as they profoundly determine the results.
The paper provided was well done considering the level of research and experiments carried out with consistent results and the level of detail it has carried is evidence of proper conduct of research. Errors were nil in the paper although it was confusing that the HSF1 binding was not sufficient for induction despite the fact that heat-induced expression predicted HSF1 binding. It would be wise in future for the author to research more on the definition of targets of other transcriptional factors for a more comprehensive look.
Work Cited
Trinklein, D. Nathan et al. “The Role of Heat Shock Transcription Factor 1 in the Genome-wide
Regulation of the Mammalian Heat Shock Response.” Molecular Biology of the Cell, vol. 15, 2004, pp. 1254–1261.
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