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.

If you have an ORCID ID that is not listed on this page, please forward this information to us and we will update your Reactome pathway records.

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Pathways authored by Khanna, Kum Kum (77152)

DB_ID Name
69580 p53-Dependent G1/S DNA damage checkpoint
69615 G1/S DNA Damage Checkpoints
69620 Cell Cycle Checkpoints

Pathways reviewed by Khanna, Kum Kum (77152)

DB_ID Name
73894 DNA Repair

Details on Person Khanna, Kum Kum

_displayNameKhanna, Kum Kum
_timestamp2017-08-22 20:36:55
affiliation[Affiliation:69510] Queensland Institute of Medical Research, Signal Transduction Laboratory
firstnameKum Kum
modified[InstanceEdit:1247344] D'Eustachio, P, 2011-04-01
[InstanceEdit:8932050] D'Eustachio, Peter, 2016-07-20
(author)[InstanceEdit:69508] Khanna, K, 2003-06-05 08:03:38
[InstanceEdit:69616] Hoffmann, I, Khanna, K, 2003-06-05 08:03:42
[InstanceEdit:69619] Hoffmann, I, Khanna, KK, Walworth, N, Yen, Tim, O'Donnell, M, 2005-01-01
[InstanceEdit:165097] Khanna, KK, Lindahl, T, West, SC, Wood, Richard D, 2004-06-01
[LiteratureReference:69530] ATM associates with and phosphorylates p53: mapping the region of interaction.
[LiteratureReference:69578] Ionizing radiation and UV induction of p53 protein by different pathways in ataxia-telangiectasia cells.
[LiteratureReference:83633] DNA double-strand breaks: signaling, repair and the cancer connection.
[LiteratureReference:5682124] Autophosphorylation of ataxia-telangiectasia mutated is regulated by protein phosphatase 2A
[LiteratureReference:6814900] The Integrator complex controls the termination of transcription at diverse classes of gene targets
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