Ontology highlight
ABSTRACT:
INSTRUMENT(S): Q Exactive Plus
ORGANISM(S): Homo Sapiens (human)
TISSUE(S): Epithelial Cell, Cell Culture
DISEASE(S): Warburg Micro Syndrome
SUBMITTER: Mark Handley
LAB HEAD: Mark Handley
PROVIDER: PXD016336 | Pride | 2024-01-26
REPOSITORIES: Pride
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45_02_1-CTRL.raw | Raw | |||
45_03_2-WT.raw | Raw | |||
45_04_3-GAP1.raw | Raw | |||
45_05_4-GAP2.raw | Raw | |||
45_06_5-TBC1D20.raw | Raw |
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Kiss Robert S RS Chicoine Jarred J Khalil Youssef Y Sladek Robert R Chen He H Pisaturo Alessandro A Martin Cyril C Dale Jessica D JD Brudenell Tegan A TA Kamath Archith A Kyei-Boahen Jeffrey J Hafiane Anouar A Daliah Girija G Alecki Célia C Hopes Tayah S TS Heier Martin M Aligianis Irene A IA Lebrun Jean-Jacques JJ Aspden Julie J Paci Emanuele E Kerksiek Anja A Lütjohann Dieter D Clayton Peter P Wills Jimi C JC von Kriegsheim Alex A Nilsson Tommy T Sheridan Eamonn E Handley Mark T MT
The Journal of biological chemistry 20230928 11
Loss of functional RAB18 causes the autosomal recessive condition Warburg Micro syndrome. To better understand this disease, we used proximity biotinylation to generate an inventory of potential RAB18 effectors. A restricted set of 28 RAB18 interactions were dependent on the binary RAB3GAP1-RAB3GAP2 RAB18-guanine nucleotide exchange factor complex. Twelve of these 28 interactions are supported by prior reports, and we have directly validated novel interactions with SEC22A, TMCO4, and INPP5B. Con ...[more]