Disease relevance of TBCEL

• These mutations comprised a single Glu replacement for Gly at the N-terminus ("El" mutant) or at position 4 ("E4") of the HA2 subunit and were shown to produce striking alterations in virus-induced hemolysis and syncytia formation, especially for E1 [1].

Psychiatry related information on TBCEL

• This is attributed primarily to the permissiveness of HEK293 to rhAd infection and their ability to support viral DNA replication by providing the missing El proteins [2].

High impact information on TBCEL

• Degradation of functional tubulin dimers as well as the alteration of the cellular content of stable microtubules through El might regulate the distribution and organization of organelles in vivo [3].
• Investigations of 38 different V. cholerae strains by Southern blotting, PCR, and sequencing analyses showed that the O1 El Tor wav gene cluster type is prevalent among clinical isolates of different serogroups associated with cholera and environmental O1 strains [4].
• Preliminary evidence that the genes encoded by this cluster are involved in core OS biosynthesis came from analysis of the recently released O1 El Tor V. cholerae genome sequence and sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis of O1 El Tor mutant strains defective in three genes (waaF, waaL, and wavB) [4].
• A novel Y243S mutation in the pyruvate dehydrogenase El alpha gene subunit: correlation with thiamine pyrophosphate interaction [5].

Anatomical context of TBCEL

• Suppression of El expression seems to increase the cellular content of stable, posttranslationally modified microtubules by an unknown mechanism [3].

References