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Label-free quantification of proteins in wild type and CLPP-null mouse embryonic fibroblasts

ABSTRACT: We studied consequences of genetic deletion of mitochondrial peptidase CLPP for global proteome profile in unstressed cells.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Cell Culture, Fibroblast

SUBMITTER: Ilka Wittig

LAB HEAD: Georg Auburger

PROVIDER: PXD023677 | Pride | 2022-02-16

REPOSITORIES: Pride

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			Action	DRS
	160504_GU_Auburger_MEFs_Sample10_B.raw	Raw
	160504_GU_Auburger_MEFs_Sample10_SCX1.raw	Raw
	160504_GU_Auburger_MEFs_Sample10_SCX2.raw	Raw
	160504_GU_Auburger_MEFs_Sample10_SCX3.raw	Raw
	160504_GU_Auburger_MEFs_Sample10_SCX4.raw	Raw

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Publications

Inactivity of Peptidase ClpP Causes Primary Accumulation of Mitochondrial Disaggregase ClpX with Its Interacting Nucleoid Proteins, and of mtDNA.

Key Jana J Torres-Odio Sylvia S Bach Nina C NC Gispert Suzana S Koepf Gabriele G Reichlmeir Marina M West A Phillip AP Prokisch Holger H Freisinger Peter P Newman William G WG Shalev Stavit S Sieber Stephan A SA Wittig Ilka I Auburger Georg G

Cells 20211129 12

Biallelic pathogenic variants in <i>CLPP</i>, encoding mitochondrial matrix peptidase ClpP, cause a rare autosomal recessive condition, Perrault syndrome type 3 (PRLTS3). It is characterized by primary ovarian insufficiency and early sensorineural hearing loss, often associated with progressive neurological deficits. Mouse models showed that accumulations of (i) its main protein interactor, the substrate-selecting AAA+ ATPase ClpX, (ii) mitoribosomes, and (iii) mtDNA nucleoids are the main cellu ...[more]

PMID: 34943861

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Project description:We investigated brain tissue from N471D WASH complex subunit strumpellin knock-in mice as a genetic model for hereditary spastic paraplegia type 8. While WASHC5-related protein interaction partners and complexes showed no change in abundancies, the proteomic analysis depicted consistent upregulation of BPTF and downregulation of KLHL11 in heterozygous and homozygous knock-in mice. This finding suggests mechanistic links for hereditary spastic paraplegia type 8 through the roles of BPTF and KLHL11 in neurodegeneration and protein quality control, respectively.

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Cancer-associated fibroblasts produce matrix-bound vesicles that influence endothelial cell function (part 6: Mammary Fibroblasts Proteome)

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Cancer-associated fibroblasts produce matrix-bound vesicles that influence endothelial cell function (part 2: THP-1 proteome )

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Cancer-associated fibroblasts produce matrix-bound vesicles that influence endothelial cell function (part 1: Proteins transferred from cancer-associated fibroblasts to endothelial cells : trans-SILAC)

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Cancer-associated fibroblasts produce matrix-bound vesicles that influence endothelial cell function (part 4: Proteomic analysis of pCAFs expressing high and low α-SMA protein levels)

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Cancer-associated fibroblasts produce matrix-bound vesicles that influence endothelial cell function (part 3: Proteomic analysis of CM-EVs and MBVs secreted by pCAFs)

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Transcription start site identification in Bacillus subtilis

Project description:Cappable-seq was used to map transcription start sites globally in wild type Bacillus subtilis. Total RNA was isolated from cells grown in LB media until exponential phase. RNA corresponding to transcription start sites was capped with a 5' biotin tag, which was used for enrichment via a pull down with streptavidin beads. Enriched RNA was converted to cDNA and then subjected to illumina sequencing.

2021-04-16 | E-MTAB-8582 | biostudies-arrayexpress

Transcription start site identification in wild type Escherichia coli

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Protein turnover rates within mitochondrial complexes in mitochondrial disease patients and in a DNAJC30 knock-out cell line

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