Targeting non-canonical NF-κB signalling in CYLD cutaneous syndrome by selective inhibition of IκB kinase alpha
Ontology highlight
ABSTRACT:
INSTRUMENT(S):
ORGANISM(S): Homo Sapiens (human)
TISSUE(S): Keratinocyte, Skin
SUBMITTER: 
Joseph Inns
LAB HEAD: Neil Rajan
PROVIDER: PXD053466 | Pride | 2026-05-13
REPOSITORIES: Pride
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| 20230810_JI_Exp7_C1.d.zip | Other | |||
| 20230810_JI_Exp7_C1.mzXML | Mzxml | |||
| 20230810_JI_Exp7_C2.d.zip | Other | |||
| 20230810_JI_Exp7_C2.mzXML | Mzxml | |||
| 20230810_JI_Exp7_C3.d.zip | Other |
Items per page: 5 1 - 5 of 25 |
Publications
Targeting non-canonical NF-κB signalling in CYLD cutaneous syndrome by selective inhibition of IκB kinase alpha.
Hodgson Kirsty K Inns Joseph J Reynolds Gary G Stephenson Emily E Paul Andrew A Sinclair Naomi N Berretta Giacomo G Lawson Christopher C Frey Andrew Michael AM Ivanova Iglika I Adam Eva E Lord Christopher J CJ Cockell Simon S Coxhead Jonathan J Nagy Nikoletta N Adams David D Szell Marta M Trost Matthias M Haniffa Muzlifah M Mackay Simon P SP Perkins Neil N Rajan Neil N
The British journal of dermatology 20260304
CYLD cutaneous syndrome (CCS) skin tumours develop from puberty onwards, can number in the hundreds and progressively grow over time. CCS patients lack medical therapies and require repeated surgery to control tumour burden. CYLD loss of heterozygosity (LOH) drives tumour growth, and CCS tumours have previously been shown to demonstrate increased canonical NF-κB and Wnt signalling. Here, we demonstrate evidence of non-canonical NF-κB signalling in CCS tumour keratinocytes, with increased p100 to ...[more]
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