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.

Details on Person UniProt:O05442 cpnT

Class:Id	ReferenceGeneProduct:9637681
_chainChangeLog	chain:1-846 for 9637681 added on Thu May 2 2019;chain:1- for 9637681 added on Thu May 2 2019;chain:-846 for 9637681 added on Thu May 2 2019
_displayName	UniProt:O05442 cpnT
_timestamp	2025-02-21 20:07:49
chain	chain:1-846 chain:1- chain:-846
checksum	CB7DF1D77C7C9A25
comment	FUNCTION Has a dual function in uptake of nutrients and induction of host cell death. The N-terminal domain (NTD) forms an outer membrane channel and is used for uptake of nutrients across the outer membrane. The secreted C-terminal toxic domain (TNT) acts as a glycohydrolase, which hydrolyzes the essential cellular coenzyme NAD(+) in the cytosol of infected macrophages, leading to necrotic host cell death. Both functions are required for survival, replication and cytotoxicity of M.tuberculosis in macrophages.CATALYTIC ACTIVITY NAD(+) + H2O = ADP-D-ribose + nicotinamide + H(+)ACTIVITY REGULATION Glycohydrolase activity is completely inhibited by interaction with the immunity factor for TNT (IFT). This inhibition protects M.tuberculosis from self-poisoning.BIOPHYSICOCHEMICAL PROPERTIES kcat is 52 sec(-1).SUBUNIT Interacts with the immunity factor for TNT (IFT) (PubMed:26237511). Oligomer formation is required for channel activity (PubMed:24753609).INTERACTION Secreted into the cytosol of infected macrophages while the bacteria are still confined to the phagosome. Access to the macrophage cytosol depends on the ESX-1 / type VII secretion system (T7SS).PTM The C-terminal toxic domain is cleaved, probably after integration of CpnT into the outer membrane.DISRUPTION PHENOTYPE Deletion reduces growth on glycerol and glucose as sole carbon sources. Deletion mutant does not replicate in differentiated THP-1 macrophages and lacks cytotoxicity (PubMed:24753609). Lack of cpnT does not increase drug resistance in vitro (PubMed:25645841). Deletion mutant does not decrease NAD(+) levels in infected macrophages (PubMed:26237511).
created	[InstanceEdit:9637696] Jassal, Bijay, 2019-02-19
description	recommendedName: fullName evidence="9"Outer membrane channel protein CpnT alternativeName: fullName evidence="7"Channel protein with necrosis-inducing toxin component recommendedName: fullName evidence="9"N-terminal channel domain /component component recommendedName: fullName evidence="8"Tuberculosis necrotizing toxin shortName evidence="8"TNT alternativeName: fullName evidence="8"NAD(+) glycohydrolase ecNumber evidence="6"3.2.2.5 /component
geneName	cpnT Rv3903c
identifier	O05442
isSequenceChanged	FALSE
keyword	3D-structure Cell outer membrane Host cytoplasm Hydrolase Ion transport Membrane NAD Porin Reference proteome Secreted Toxin Transmembrane Transmembrane beta strand Transport Virulence
modified	[InstanceEdit:9645038] Weiser, JD [InstanceEdit:9676415] Weiser, JD [InstanceEdit:9730071] Weiser, JD [InstanceEdit:9750299] Weiser, JD [InstanceEdit:9767224] Weiser, Joel [InstanceEdit:9852000] Weiser, Joel, 2023-11-03 [InstanceEdit:9939033] Weiser, Joel, 2025-02-21
name	cpnT
referenceDatabase	[ReferenceDatabase:2] UniProt
secondaryIdentifier	CPNT_MYCTU F2GDR4 I6Y4T3 Q7D4M4
sequenceLength	846
species	[Species:176806] Mycobacterium tuberculosis
(referenceEntity)	[EntityWithAccessionedSequence:9637692] CpnT [cytosol] [Mycobacterium tuberculosis]
[Change default viewing format]

No pathways have been reviewed or authored by UniProt:O05442 cpnT (9637681)