ERR family members

The most profound difference between the ER and ERR families is their ligandbinding profile [35]. No endogenous ligand has been identified for any of the ERRs, leaving them as orphan receptors for now. Members of the ERR family do not bind to estradiol and many of their activities appear to be ligand independent, but they can bind to synthetic ligands. All three ERR family members bind to DES at much higher... 

Selective tools have helped determine possible roles of each ERR family member. ERRa knockout mice show relatively normal anatomical features, but have much lower fat deposits than wild-type mice and are resistant to high-fat diet-induced obesity, suggesting a role for ERRoc in metabolic regulation [39]. The mice also lack the ability to maintain body temperature due to defects in mitochondrial function [39]. ERRp knockout mice die before birth, suggesting an important role for ERRP during embryonic development [40]. The ERRy knockout mice die within 1 week after birth due to faulty oxidative metabolism in the heart [41]. 

Overall, the ERR family members do not appear to be true ERs , but it is clear that there is some overlap between E R and ERR ligand-binding preferences and the genes regulated by the receptors in tissues such as bone and certain forms of cancer [47,48]. 

The knockout mice and selective ligands also suggest that ERR family members are involved in processes distinct from the ER family that could lead to new therapeutic opportunities. 

Such is the lability of TMS ethers, that they can usually be removed selectively in the presence of other members of the silyl ether family. For example, in Car-reira s synthesis of Zaragozic Acid C, a tertiary TMS ether was removed in the presence of a primary /err-butyldimethylsilyl (TBS) ether with chloroacetic acid in methanol [ heme 4.2] moreover, tertiary TMS ethers can be removed in the presence of primary triisopropyl (TIPS) ethers using pyridinium p-toluene-sulfonate in methanol [Scheme 4.3]. ... 

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