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PERCC1, a new member of the Yap/TAZ/FAM181 transcriptional co-regulator family.
Sanchez-Pulido, Luis; Jia, Siyang; Hansen, Carsten Gram; Ponting, Chris P.
Afiliação
  • Sanchez-Pulido L; MRC Human Genetics Unit, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh EH4 2XU, UK.
  • Jia S; Centre for Inflammation Research, Institute for Regeneration and Repair, Queen's Medical Research Institute, Edinburgh bioQuarter, University of Edinburgh, Edinburgh EH16 4TJ, UK.
  • Hansen CG; Centre for Inflammation Research, Institute for Regeneration and Repair, Queen's Medical Research Institute, Edinburgh bioQuarter, University of Edinburgh, Edinburgh EH16 4TJ, UK.
  • Ponting CP; MRC Human Genetics Unit, Institute of Genetics and Cancer, University of Edinburgh, Edinburgh EH4 2XU, UK.
Bioinform Adv ; 2(1): vbac008, 2022.
Article em En | MEDLINE | ID: mdl-36699391
ABSTRACT
Motivation Disrupted PERCC1 gene expression causes an intractable congenital diarrhoea in infants. However, this gene's molecular mechanism is unknown and no homologous proteins have been reported.

Results:

Our detailed evolutionary analysis of PERCC1 sequence reveals it to be a previously unappreciated member of the YAP/TAZ/FAM181 family of homologous transcriptional regulators. Like YAP and TAZ, PERCC1 likely interacts with DNA via binding to TEA/ATTS domain transcription factors (TEADs) using its conserved interface-2 and -3 sequences. We compare the expression patterns of PERCC1 with those of YAP, TAZ, TEADs. Our report provides the identification and first in-depth bioinformatic analysis of a YAP/TAZ homologue, and a likely new regulator of the YAP/TAZ-TEAD transcriptional complex. Availability and implementation The data underlying this article are available in UniProt Database. Supplementary information Supplementary data are available at Bioinformatics Advances online.

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Tipo de estudo: Prognostic_studies Idioma: En Ano de publicação: 2022 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Tipo de estudo: Prognostic_studies Idioma: En Ano de publicação: 2022 Tipo de documento: Article