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Consequences of SF3B1 mutation on the proteome

ABSTRACT: In this study, we evaluated the differential proteome of SF3B1-mutated and SF3B1-Wild-Type uveal melanoma cells (isogenic Mel202 cells). We performed a quantitative label-free tandem liquid chromatography mass spectrometry (LC-MS/MS) analysis of SF3B1WT and SF3B1mut Mel202 cells.

INSTRUMENT(S): Q Exactive HF-X

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Uveal Melanoma Cell

SUBMITTER: Valentin SABATET

LAB HEAD: Damarys Loew

PROVIDER: PXD022726 | Pride | 2022-03-15

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	Design.xls	Xls
	H0540BL.msf	Msf
	H0540BL.raw	Raw
	H0541BL.msf	Msf
	H0541BL.raw	Raw

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Transcriptomic analyses of primary uveal melanomas

Project description:SF3B1 is coding an essential splicing factor. This gene was found recurrently mutated in uveal melanoma. To understand the consequences of these hotspot SF3B1 mutations, we performed high coverage RNA-seq on 74 primary uveal melanomas, which were treated by primary enucleation. We analyzed data for aberrant splicing in relation with SF3B1 status.

2016-07-03 | E-MTAB-4097 | biostudies-arrayexpress

SF3B1 Degron knockdown RNA-seq

Project description:Knockdown of mutant and/or wild-type SF3B1 in MEL202 cell line by Degron knock-in, followed by RNA-seq, to identify splicing events governed by mutant SF3B1. Control: parental MEL202 cell line. Experiments: mutant-SF3B1 knockdown; wildtype-SF3B1 knockdown; mutant SF3B1 knockout. Treatments: each of these four conditions plus and minus shld.

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SF3B1 association with chromatin determines splicing outcomes

Project description:Much remains unknown concerning the mechanism by which the splicing machinery pinpoints short exons within intronic sequences and how splicing factors are directed to their pre-mRNA targets. Part of the explanation probably lies in differences in chromatin organization between exons and introns. Proteomic, co-immunoprecipitation, and sedimentation analyses described here indicated that SF3B1, an essential splicing component of the U2 snRNP complex, is strongly associated with nucleosomes. ChIP-seq and RNA-seq analyses revealed that SF3B1 is specifically bound to nucleosomes located at exonic positions. SF3B1 binding is enriched at nucleosomes positioned over short exons flanked by long introns that are also characterized by differential GC content between exons and introns. Disruption of SF3B1 binding to such nucleosomes affected the splicing of these exons similarly to inhibition of SF3B1 expression. Our findings suggest that the association of SF3B1 with nucleosomes is functionally important for splice site recognition and that SF3B1 conveys splicing-relevant information embedded in chromatin structure. MNase-seq on Input and SF3B1 pull-down, mRNA-seq on control and SF3B1 si-RNA treated cells as well as on TSA (Trichostatin A) treated and untreated cells.

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Splicing patterns in SF3B1 mutated uveal melanoma generate shared immunogenic tumor-specific neo-epitopes [scRNA-seq]

Project description:Purpose: In this study, we show that mutations of the splicing factor SF3B1 in uveal melanoma (UM) generate immunogenic neo-antigens.

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Splicing patterns in SF3B1 mutated uveal melanoma generate shared immunogenic tumor-specific neo-epitopes [scADT-seq]

Project description:Purpose: In this study, we show that mutations of the splicing factor SF3B1 in uveal melanoma (UM) generate immunogenic neo-antigens.

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Splicing patterns in SF3B1 mutated uveal melanoma generate shared immunogenic tumor-specific neo-epitopes [scTCR-seq]

Project description:Purpose: In this study, we show that mutations of the splicing factor SF3B1 in uveal melanoma (UM) generate immunogenic neo-antigens.

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Splicing patterns in SF3B1 mutated uveal melanoma generate shared immunogenic tumor-specific neo-epitopes [bulk TCR-seq]

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Transcriptome analysis of chronic lymphoid leukemia reveals isoform regulation associated with mutations in SF3B1

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