Reactome: A Curated Pathway Database
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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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Details on Person B3GAT3 (Ouzzine et al. 2000), along with B3GAT1 and 2, trans...

Class:IdSummation:3621743
_displayNameB3GAT3 (Ouzzine et al. 2000), along with B3GAT1 and 2, trans...
_timestamp2014-07-11 09:51:52
created[InstanceEdit:3621807] Jassal, B, 2013-05-24
modified[InstanceEdit:3656245] Jassal, B, 2013-05-31
[InstanceEdit:4006087] Jassal, B, 2013-07-26
[InstanceEdit:5607512] Jassal, Bijay, 2014-07-11
textB3GAT3 (Ouzzine et al. 2000), along with B3GAT1 and 2, transfers a glucuronate (GlcA) residue via a beta1,3-linkage to a terminal galactose to complete the tetrasaccharide linker sequence. The B3GAT3 mutant R277Q causes almost complete loss of activity (3-5% of wt) and results in the production of immature and lower numbers of dermatan sulfate (DS) and chondroitin sulfate (CS) chains (Baasanjav et al. 2011). This defect causes multiple joint dislocations, short stature, craniofacial dysmorphism, and congenital heart defects (JDSSDHD; MIM:245600).
(summation)[FailedReaction:3560802] Defective B3GAT3 does not transfer GlcA to tetrasaccharide linker [Homo sapiens]
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No pathways have been reviewed or authored by B3GAT3 (Ouzzine et al. 2000), along with B3GAT1 and 2, trans... (3621743)