Does cytosolic entry of Shiga-like toxin a chain from the yeast endoplasmic reticulum require catalytically active Hrd1p?
The fraction of SLTxA1 that disengages from the ERAD pathway thus does so upstream of Cdc48p interactions and downstream of Hrd1p interactions, in a step that possibly involves de-ubiquitylation. Mechanistically therefore, the dislocation of this toxin is quite distinct from that of conventional ERAD substrates that are normally degraded, and the toxins partially characterised to date that do not require the catalytic cysteine of the major Hrd1p component of the dislocation apparatus.
Though the agreement between adolescents' and parents' reports on the three SES measures is generally judged to be good in most cases, using adolescents reports for family SES may still be biased if analysis is not stratified by family financial stress.