Dataset Information

Identification of the RNF12/RLIM proximal proteome

ABSTRACT: RNF12/RLIM is an E3 ubiquitin ligase that plays key developmental roles and is genetically disrupted in the neurodevelopmental disorder Tonne-Kalscheuer syndrome. RNF12/RLIM regulates X-chromosome inactivation and controls the expression of neural and gametogenesis related genes. To better understand how RNF12/RLIM performs these transcription-related functions, we performed a TurboID proximity ligation experiment to identify RNF12/RLIM proximal proteins in mouse embryonic stem cells treated with DMSO or MG132. This knowledge will increase our understanding of how this protein controls developmental gene expression and how disruption of these pathways drives disease.

INSTRUMENT(S): Orbitrap Fusion

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Cell Culture, Embryonic Stem Cell

DISEASE(S): Tonne-kalscheuer Syndrome

SUBMITTER: Renata Soares

LAB HEAD: Greg Findlay

PROVIDER: PXD046733 | Pride | 2024-01-09

REPOSITORIES: Pride

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			Action	DRS
	Experiment_MaxQuant_01_from_MayD_113022_01.mzid.gz	Mzid
	Experiment_MaxQuant_01_from_MayD_113022_01.mzid.gz_Experiment_MaxQuant_01_from_MayD_113022_01.MGF	Mzid
	Experiment_MaxQuant_02_from_MayD_113022_02.mzid.gz	Mzid
	Experiment_MaxQuant_02_from_MayD_113022_02.mzid.gz_Experiment_MaxQuant_02_from_MayD_113022_02.MGF	Mzid
	Experiment_MaxQuant_03_from_MayD_113022_03.mzid.gz	Mzid

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Project description:Developmental checkpoints in stem/progenitor cells are critical to the determination, commitment and differentiation into distinct lineages. Cancer cells often retain expression of lineage-specific checkpoint proteins, but their potential impact in cancer remains elusive. T lymphocytes mature in the thymus following a highly orchestrated developmental process that entails the successive rearrangements and expression of T-cell receptor (TCR) genes. Low affinity recognition of self-peptide/MHC complexes (self-pMHC) presented by thymic epithelial cells by the TCR of CD4+CD8+ (DP) cortical thymocytes transduces positive selection signals that ultimately shape the developing T cell repertoire. DP thymocytes not receiving these signals die by lack of stimulation whereas those that recognize self-pMHC with high affinity undergo TCR-mediated apoptosis and negative selection. In T-cell acute lymphoblastic leukaemia (T-ALL), leukaemic transformation of maturating thymocytes results from the acquisition of multiple genetic and epigenetic alterations in oncogenes and tumour suppressor genes, that disrupt the normal regulatory circuits and drive clonal expansion of differentiation-arrested lymphoblasts. We show here that TCR triggering by negatively-selecting self-pMHC prevented T-ALL development and leukaemia maintenance in mice. Induction of TCR signalling by high affinity self-pMHC or treatment with monoclonal antibodies to the CD3 signalling chain (anti-CD3) caused massive leukaemic cell death and a gene expression program resembling that of thymocyte negative selection. Importantly, anti-CD3 treatment hampered leukaemogenesis in mice transplanted with either mouse or patient-derived T-ALLs. These data provide a rationale for targeted therapy based on anti-CD3 treatment of T-ALL patients and demonstrate that endogenous developmental checkpoint proteins are amenable to therapeutic intervention in cancer cells. Gene expression data from four culture conditions was performed for the following cells: ALL-SIL-TCRÎ±/Î²-GFP co-cultured on OP9-DL1 for 48 h, ALL-SIL-TCRÎ±/Î²-GFP without co-culture, ALL-SIL cells transduced with TLX shRNA (sh-TLX), and ALL-SIL transduced with sh-control vectors. All conditions are performed in two replicates.

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Identification of the RNF12/RLIM proximal proteome

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