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Mass spectrometry and phosphorylation analysis of ORC1 protein, wild type or RNA-binding mutant (R441A, R444A and R465A), in GAA-RNA (RNA interactors of ORC1 identified by RIP-seq and iCLIP) knockdown or control conditions.

ABSTRACT: Mass spectrometry of wild type or mutant (RNA-binding) ORC1. Experiments were done in cellstransfected with a control ASO or an anti-GAA ASO, to knockdown RNA interactors of ORC1.

INSTRUMENT(S): LTQ Orbitrap Velos Pro

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell, Cell Culture

DISEASE(S): Colon Cancer

SUBMITTER: Aina Maria Mas

LAB HEAD: Maite Huarte

PROVIDER: PXD043232 | Pride | 2023-10-24

REPOSITORIES: Pride

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			Action	DRS
	83600_98293.pep.xml	Pepxml
	83601_98294.pep.xml	Pepxml
	83670_98293.pep.xml	Pepxml
	83671_98294.pep.xml	Pepxml
	84832_99400.pep.xml	Pepxml

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Publications

ORC1 binds to cis-transcribed RNAs for efficient activation of replication origins.

Mas Aina Maria AM Goñi Enrique E Ruiz de Los Mozos Igor I Arcas Aida A Statello Luisa L González Jovanna J Blázquez Lorea L Lee Wei Ting Chelsea WTC Gupta Dipika D Sejas Álvaro Á Hoshina Shoko S Armaos Alexandros A Tartaglia Gian Gaetano GG Waga Shou S Ule Jernej J Rothenberg Eli E Gómez María M Huarte Maite M

Nature communications 20230724 1

Cells must coordinate the activation of thousands of replication origins dispersed throughout their genome. Active transcription is known to favor the formation of mammalian origins, although the role that RNA plays in this process remains unclear. We show that the ORC1 subunit of the human Origin Recognition Complex interacts with RNAs transcribed from genes with origins in their transcription start sites (TSSs), displaying a positive correlation between RNA binding and origin activity. RNA dep ...[more]

PMID: 37488096

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Project description:Currently available enzyme replacement therapies for lysosomal storage diseases are limited in their effectiveness due in part to short circulation times and suboptimal biodistribution of the therapeutic enzymes. We previously engineered Chinese hamster ovary (CHO) cells to produce -galactosidase A (GLA) with various N-glycan structures and demonstrated that elimination of mannose-6-phosphate (M6P) and conversion to homogeneous sialylated N-glycans prolonged circulation time and improved biodistribution of the enzyme following a single-dose infusion into Fabry mice. Here, we confirmed these findings using repeated infusions of the glycoengineered GLA into Fabry mice and further tested whether this glycoengineering approach, Long-Acting-GlycoDesign (LAGD), could be implemented on other lysosomal enzymes. LAGD-engineered CHO cells stably expressing a panel of lysosomal enzymes [aspartylglucosamine (AGA), beta-glucuronsidase (GUSB), catepsin D (CTSD), tripeptidyl peptidase (TPP1), alpha-glucosidase (GAA) or iduronate 2-sulfatase (IDS)] successfully converted all M6P-containing N-glycans to complex sialylated N-glycans. The resulting homogenous glycodesigns enabled glycoprotein profiling by native mass spectrometry. Notably, LAGD extended the plasma half-life of all three enzymes tested (GLA, GUSB, AGA) in wildtype mice. LAGD may be widely applicable to lysosomal replacement enzymes to improve their circulatory stability and therapeutic efficacy.

2023-02-13 | PXD038783 | Pride

Identification of phosphorylation sites in piggyBac transposase N-terminus

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Targeted degradation of sense and antisense C9orf72 RNA foci as therapy for amyotrophic lateral sclerosis and frontotemporal dementia (strand specific RNA-seq)

Project description:Purpose: The purpose of this experiment is to identify expression changes after ASO-dependent depletion of mouse C9orf72 in the spinal cord of wild-type C57Bl/6 female mice. Methods: Strand specific RNA-seq was performed using RNAs extracted from spinal cord of C57Bl/6 mice two weeks after intracerebroventricular stereotactic injection of saline (n=3), a control ASO (n=3) or an ASO targeting mouse C9orf72 (n=3). C9orf72 RNA levels were reduced to approximately 30% of control levels in spinal cords from mice treated with the C9orf72 ASO. Results: Statistical comparison of RPKM values between RNAs from C9orf72 and control ASO treated animals or C9orf72 and saline treated samples revealed that only 12 genes were consistently upregulated (defined by P<0.05 adjusted for multiple testing) and 12 genes including C9orf72 were downregulated (defined by P<0.05 adjusted for multiple testing). Conclusions: Only few RNA expression changes were identified in the spinal cord following reduction of C9orf72. Use of strand specific RNA-seq to test the consequences of C9orf72 loss of function in mouse spinal cord.

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Targeted degradation of sense and antisense C9orf72 RNA foci as therapy for amyotrophic lateral sclerosis and frontotemporal dementia (strand specific RNA-seq)

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