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Samples were acidified with phosphoric acid to 1% v/v. Proteins were precipitated with 90% Methanol, 10% TEAB v/v, and the resulting mixture added to ProtiFi micro S-Trap column following the manufacturer’s protocol. Briefly, samples were passed through a column by centrifugation at 4,000 x g for 1 min and washed with 90% Methanol, 10% TEAB v/v 5 times by centrifugation. Column bound proteins were digested with 1:20 trypsin at 47 °C for 2 h. Resulting peptides were serialy eluted with 40 μL of 50 mM TEAB pH 8.0, 0.2% FA in water and 0.2% FA in 50% acetonitrile, 50% water. Eluates were dried by vacuum concentration and resuspended in 0.1% formic acid in water. 500 ng of digest was analysed on a Bruker TIMS-TOF HT mass spectrometer in line with the EvoSep One LC system. Samples were separated by elution in a gradient of  MS solvent A ( 0.1 % formic acid in HPLC water) and MS solvent B (0.1 % formic acid  in HPLC grade acetonitrile), by the manufacturer-defined Evosep One Whisper 20 samples per day method. The mass spectrometer was operated in positive-ion, data independent acquisition parallel accumulation serial fragmentation (DIA-PASEF) mode. Precursor ion scans (full scan, MS1) were performed in the range of 100-1,700 m/z,   for DIA-PASEF (MS2 scans),  mass and IM ranges were from 300-1200 m/z and 0.6-1.4 1/K0, DIA-PASEF was performed using 16 variable width IM-m/z windows, designed using py_diAID. Collision energy was applied as a linear gradient from 20-59 eV, to precursors with mobilities from  0.60-1.60 V.s/cm2. The ramp and accumulation time were set to 100 ms, with a ramp rate of 9.42 Hz, the total cycle time was ~1.8 sec."],"repository":["Pride"],"quantification_method":["Not available"],"modification":[""],"data_protocol":["Data files were searched against an in-silico digest of SwissProt Homo sapiens database performed in DIA-NN 1.8.1. Analysis of protein groups intensities was performed in the R statistical computing environment v4.3.0; including data filtering, clustering, principal component analysis, t-tests and graphics generation. The packages employed included limma, tidyverse, and ggplot2."],"omics_type":["Proteomics"],"labhead":["Neil Rajan"],"instrument_platform":[""],"submission_type":["PARTIAL"],"labhead_affiliation":["Newcastle University, Translational and cliniclal research institute, UK"],"species":["Homo Sapiens (human)"],"publication":["41779628 Hodgson K, Inns J, Reynolds G, Stephenson E, Paul A, Sinclair N, Berretta G, Lawson C, Frey AM, Ivanova I, Adam E, Lord CJ, Cockell S, Coxhead J, Nagy N, Adams D, Szell M, Trost M, Haniffa M, Mackay SP, Perkins N, Rajan N. Targeting non-canonical NF-κB signalling in CYLD cutaneous syndrome by selective inhibition of IκB kinase alpha. Br J Dermatol. 2026:ljag044 10.1093/bjd/ljag044"],"submitter_mail":["joe.inns.ac@gmail.com"],"submitter_affiliation":["Newcastle University"],"submitter_country":["United Kingdom"],"pubmed_abstract":["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 p52 processing and RelB protein expression compared to normal skin. Utilizing complementary transcriptomics and proteomics on patient derived CCS tumour cell fractions, we identify IκB kinase alpha (IKKα) as a candidate target in the non-canonical NF-κB signalling pathway. A novel, highly selective, IKKα inhibitor (SU1644) used in patient derived CCS tumour spheroid cultures demonstrated that IKKα inhibition reduced tumour spheroid viability. These data provide the pre-clinical rationale for the assessment of topical IKKα inhibitors as a novel preventative treatment for CCS."],"pubmed_title":["Targeting non-canonical NF-κB signalling in CYLD cutaneous syndrome by selective inhibition of IκB kinase alpha."],"pubmed_authors":["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"],"additional_accession":[]},"is_claimable":false,"name":"Targeting non-canonical NF-κB signalling in CYLD cutaneous syndrome by selective inhibition of IκB kinase alpha","description":"Proteome of CD45- sorted healthy skin (C1-C5) and CD45-/CD200+ CYLD cutaneous syndrome tumour samples 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