Psychiatry related information on Hsp67Ba

• In most cases, the disease results from transcriptional silencing of fragile mental retardation gene 1, fmr1, which encodes FMRP [1].

High impact information on Hsp67Ba

• By DNA sequencing of gene 1, the homology was localized within the same two regions already conserved between the small hsp genes: a central region of 83 amino acids, homologous with the mammalian alpha crystallin and the first 15 N-terminal amino acids [2].
• Codons 1 through 257 of gene 2 occupied 833 nucleotides and contained only one intron, whereas the corresponding region of gene 1 occupied 17.5 kilobases and was interrupted by eight introns [3].
• Functionally, gene 1 was considerably more complex than gene 2; it was active in both muscle and nonmuscle cell lineages, had at least five variable exons, and specified a minimum of five developmentally regulated isoforms [3].
• The zinc finger transcription factor transforming growth factor beta-inducible early gene-1 confers myeloid-specific activation of the leukocyte integrin CD11d promoter [4].
• WT1 bound to the endogenous sprouty1 promoter in vivo and directly regulated sprouty1 through an early growth response gene-1 binding site [5].

Biological context of Hsp67Ba

• Expression of gene 1 was substantially increased by heat shock in pupae, but was one to two orders of magnitude lower in adults or in embryos [6].
• Furthermore, S1 nuclease mapping analysis revealed several gene 1 mRNA species, which are generated by the use of alternative polyadenylation sites and by the use of differentially regulated transcriptional initiation sites [6].

Other interactions of Hsp67Ba

• The data obtained strongly suggest that the cis-acting elements delimited within the hsp23-gene 1 intergenic region respond to ecdysone in a secondary manner, presumably by requiring interaction with the product(s) of primary ecdysone-responsive genes [7].

References