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C-terminal amides mark proteins for degradation via SCF/FBXO31 - Interaction Proteomics of FBXO31 in HEK293T cells

ABSTRACT: FBXO31 is a substrate adapter for the SCF-type ubiquitin ligase complex SCF/FBXO31 which ubiquitylates C-terminal amide-bearing proteins (CTAPs), thereby triggering their proteasomal degradation in human cells. Immunoprecipitation followed by MS (IP-MS) was performed on HA-tagged cDNA-expressed variants of FBXO31 from HEK293T cells to identify putative clients.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture

SUBMITTER: Matthias Muhar

LAB HEAD: Prof. Jacob

PROVIDER: PXD055535 | Pride | 2024-11-05

REPOSITORIES: Pride

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			Action	DRS
	20221215_C30303_002_S437002_MFM-X216-1_Control.raw	Raw
	20221215_C30303_003_S437003_MFM-X216-2_Control.raw	Raw
	20221215_C30303_004_S437004_MFM-X216-3_Control.raw	Raw
	20221215_C30303_005_S437005_MFM-X216-4_HA-IP.raw	Raw
	20221215_C30303_006_S437006_MFM-X216-5_HA-IP.raw	Raw

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C-terminal amides mark proteins for degradation via SCF/FBXO31 – CTAP discovery

Project description:FBXO31 is a substrate adapter for the SCF-type ubiquitin ligase complex SCF/FBXO31 which ubiquitylates C-terminal amide-bearing proteins (CTAPs), thereby triggering their proteasomal degradation in human cells. CTAPs can arise from internal protein cleavage events during which the N-terminal fragment is left with an amidated C-terminus (-0.984016 Da). We searched for such cleavage events (semi-enzymatic C-terminus and C-terminal amidation) in previously published datasets and in own experimental data. These include: - Re-analysis of tissue samples from a deep human proteome atlas (PXD010154) - IP-MS of AARS1, a client of the CTAP reader FBXO31 (MFM-X208) - In vitro fragmentation of purified hemoglobin (MFM-X294, MFM-X298) and tRNA ligase complex (MFM-X314) Experiments are labeled with experiment IDs (MFM-X...). PSM tables contain Experiment IDs and interpretable sample aliases.

2024-11-05 | PXD055814 | Pride

C-terminal amides mark proteins for degradation via SCF/FBXO31

Project description:FBXO31 is a substrate adapter for the SCF-type ubiquitin ligase complex SCF/FBXO31 which ubiquitylates C-terminal amide-bearing proteins (CTAPs), thereby triggering their proteasomal degradation in human cells. Profiling of active cullin-RING ubiquitin E3 ligases was performed in naive or FBXO31 knockdown cell lines treated with hydrogen peroxide.

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C-terminal amides mark proteins for degradation via SCF/FBXO31 – Expression Proteomics

Project description:FBXO31 is a substrate adapter for the SCF-type ubiquitin ligase complex SCF/FBXO31 which ubiquitylates C-terminal amide-bearing proteins (CTAPs), thereby triggering their proteasomal degradation in human cells. FBXO31(D334N) is a dominant de novo mutation found among patients with cerebral palsy. To identify proteins affected by FBXO31(D334N) expression, we engineered HEK293T cells to carry a FBXO31 knockout and rapidly inducible FBXO31 expression using the Shield-1 degron system. WT or D334N variants of FBXO31 were induced for 12h and proteomic changes captured by whole cell proteomics using TMT-based quantification. Deposited files include raw MS spectra, protein-, peptide- and psm-level identification results, and differential gene expression results.

2024-11-05 | PXD055818 | Pride

FBXO31-mediated Ubiquitination of OGT Maintains O-GlcNAcylation Homeostasis to Restrain Endometrial Malignancy

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Project description:Targeted protein degradation (TPD) is a powerful strategy for controlling protein abundance. Here, we establish FBXO31 as a TPD-competent E3 ligase by exploiting its recognition of C-terminal amide-bearing degrons. Using an amidated Ala-Phe motif as a chemical recruiter, multiple small-molecule binders can be transformed into FBXO31-dependent degraders that induce rapid and potent target degradation. Mechanistic studies confirm FBXO31-mediated ternary complex formation and identify key residues in FBXO31 required for recruiter engagement and target degradation. We further show that an FBXO31-based multi-kinase degrader exhibits a distinct and broader degradation profile than a CRBN-based degrader, highlighting a potentially expanded degradable target space beyond CRBN.

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2015-08-01 | E-GEOD-71288 | biostudies-arrayexpress

FBXO31-mediated Ubiquitination of OGT Maintains O-GlcNAcylation Homeostasis to Restrain Endometrial Malignancy

Project description:FBXO31-mediated Ubiquitination of OGT Maintains O-GlcNAcylation Homeostasis to Restrain Endometrial Malignancy

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Oxygen-dependent regulation of E3(SCF)ubiquitin ligases and a Skp1-associated JmjD6 homolog in Dictyostelium

Project description:The SCF (Skp1/cullin-1/F-box protein) class of E3 polyubiquitin ligases generates a signal for proteasomal degradation of thousands of proteins in animals. The evolutionary diversification of the F-box protein (FBP) family of substrate receptor subunits has challenged elucidation of these complexes in protists. Using bioinformatics and orthogonal Skp1 interactome methods, we expand the list of putative FBPs in the social amoeba Dictyostelium and show that Skp1 interactions are highly remodeled between growth and development. In addition, a subset of FBPs was less represented when the posttranslational hydroxylation and glycosylation of the Skp1 subunit was abrogated by deletion of the O2-dependent Skp1 prolyl hydroxylase PhyA. The significance of Skp1 modification for SCF activity was indicated by partial rescue of phyA-KO cell development with proteasomal inhibitors.

2022-07-22 | PXD033864 | Pride

Nicotinic acetylcholine receptors and EGF induce c-Kit ligand/Stem Cell Factor (SCF) in a M-NM-2-arrestin-1 and E2F1 dependent manner in NSCLC

Project description:Lung cancer remains the leading cause of cancer-related deaths worldwide. M-NM-2-arrestin-1 (ARRB1), a scaffolding protein involved in the termination or desensitization of signals arising from activated G-protein-coupled receptors (GPCRs) has been shown to play a role in invasion and proliferation of many cancers, including nicotine-induced proliferation of human nonM-bM-^@M-^Ssmall cell lung cancers (NSCLCs). In this study, we analyzed nicotine induced and M-NM-2-arrestin-1 dependent genes from the microarray data. Our analysis show that SCF (Stem cell factor) strongly differentiated smokers from non-smokers implying an important role of this gene in NSCLCs. SCF, a major cytokine is the ligand for the c-Kit proto-oncogene. Here we elucidate the molecular mechanisms by which nicotine as well as EGF induces the expression of SCF in lung adenocarcinoma cell lines A549 and H1650. ChIP assays and transient transfection experiments showed that transcription factor E2F1 can positively regulate SCF expression at the transcriptional level; depletion of E2F1 or M-NM-2-arrestin-1 prevented the nicotine-mediated induction of SCF. Given that the binding of SCF to c-Kit leads to activation of multiple downstream signaling pathways including Src, PI3K, MEK and EGFR pathways, our data suggest that the SCF plays a central role in lung carcinogenesis, and may be a potential therapeutic target for combating NSCLC. Studies presented here also provide evidence that SCF along with nicotine promotes self-renewal and proliferation of lung cancer stem cells (CSCs). Our findings reveal an important role and prognostic significance of SCF that can serve as a novel prognostic and predictive biomarker for NSCLC. Transfection of A549 cell line with control siRNA, Beta arrestin siRNA and then stimulation of nicotine

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