Reactome: A Curated Pathway Database

Query author contributions in Reactome

Reactome depends on collaboration between our curation team and outside experts to assemble and peer-review its pathway modules. The integration of ORCID within Reactome enables us to meet a key challenge with authoring, curating and reviewing biological information by incentivizing and crediting the external experts that contribute their expertise and time to the Reactome curation process. More information is available at ORCID and Reactome.

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Pathways authored by Comai, L (73731)

DB_ID Name
73728 RNA Polymerase I Promoter Opening
73762 RNA Polymerase I Transcription Initiation
73772 RNA Polymerase I Promoter Escape
73854 RNA Polymerase I Promoter Clearance
73864 RNA Polymerase I Transcription
73863 RNA Polymerase I Transcription Termination
74160 Gene expression (Transcription)

Details on Person Comai, L

Class:IdPerson:73731
_displayNameComai, L
_timestamp2017-08-22 20:36:50
created[InstanceEdit:73680] Gillespie, ME, 0000-00-00 00:00:00
crossReference[DatabaseIdentifier:5662816] ORCID:0000-0003-3109-1841
firstnameL
initialL
modified[InstanceEdit:5662814] Matthews, Lisa, 2015-01-13
surnameComai
(author)[InstanceEdit:73851] Comai, L, 2003-07-03 17:13:29
[InstanceEdit:73861] Comai, L, 2003-07-03 17:28:24
[InstanceEdit:75964] Comai, L, Conaway, JW, Conaway, RC, Gustafsson, CM, Hernandez, N, Hu, P, Larsson, N-G, Proudfoot, NJ, Reinberg, D, Timmers, HTM, 2003-09-11
[LiteratureReference:73730] The TATA-binding protein and associated factors are integral components of the RNA polymerase I transcription factor, SL1.
[LiteratureReference:73732] Reconstitution of transcription factor SL1: exclusive binding of TBP by SL1 or TFIID subunits.
[LiteratureReference:73740] Recruitment of TATA-binding protein-TAFI complex SL1 to the human ribosomal DNA promoter is mediated by the carboxy-terminal activation domain of upstream binding factor (UBF) and is regulated by UBF phosphorylation.
[LiteratureReference:73744] Repression of RNA polymerase I transcription by the tumor suppressor p53.
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