Arado Ar 240 by Gerhard Lang

By Gerhard Lang

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Cell 21:669–679 Inouye S, Katsuki K, Izu H, Fujimoto M, Sugahara K, Yamada S, Shinkai Y, Oka Y, Katoh Y, Nakai A (2003) Activation of heat shock genes is not necessary for protection by heat shock transcription factor 1 against cell death due to a single exposure to high temperatures. Mol Cell Biol 23:5882–5895 Iqbal J, Qureshi SA (2010) Selective depletion of Sulfolobus solfataricus transcription factor E under heat shock conditions. J Bacteriol 192:2887–2891 Jakobsen BK, Pelham HR (1991) A conserved heptapeptide restrains the activity of the yeast heat shock transcription factor.

Although HSF2 is unstable in severe heat shock conditions such as 42  C (Sistonen et al. 1994), it is stable and acquires a DNA-binding activity through trimerization in febrile-range, mild heat shock conditions such as 40  C (Shinkawa et al. 2011). Mammalian HSF4 lacks the HR-A/B domain and therefore forms a DNA-binding trimer constitutively in the lens and other tissues including the brain and lung (Fujimoto et al. 2004; Tanabe et al. 1999). HSF3 may exist as a trimer in unstressed mouse cells, because sequences of the heptad repeats of hydrophobic amino acids in the HR-C domain are not well conserved (Fujimoto et al.

8 Members of vertebrate HSF gene family. (a). Evolution of the vertebrates. Phylogenetic tree among main groups of the vertebrates is shown (Patterson 2001). Two rounds (2R) of wholegenome duplication (WGD) may have occurred in vertebrate ancestral cells more than 440 million years (Myr) ago. (b) HSF genes in vertebrate species. gov/), are shown. 1 HSF1; 2 HSF2; 3 HSF3; 4 HSF4. HSF3 protein is not registered in chimpanzee, zebra fish, medaka, and coelacanth (x). Human HSF3 is a pseudogene (white circle).

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