Dataset Information

Proteome of Control versus shKDM2B in MDA-MB-231 Cells

ABSTRACT: Project comparing the proteome between control and knockdown of KDM2B in MDA-MB-231 cell lines. Previous data demonstrated that knockdown of KDM2B induced transcriptional changes in ribosomal and metabolic gene targets and thus TMT proteomics was pursued to compare the protein level changes that occur after knockdown of KDM2B.

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Epithelial Cell, Cell Culture

DISEASE(S): Breast Cancer

SUBMITTER: Vollter Anastas

LAB HEAD: Philip N.

PROVIDER: PXD046970 | Pride | 2023-11-22

REPOSITORIES: Pride

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	Control_Versus_shKDM2B_proteomics.xlsx	Xlsx
	S22030-fraction-1-Aug03.raw	Raw
	S22030-fraction-1-July25.raw	Raw
	S22030-fraction-10-Aug03.raw	Raw
	S22030-fraction-10-July25.raw	Raw

Items per page:

1 - 5 of 23

Publications

Transcriptional regulation of amino acid metabolism by KDM2B, in the context of ncPRC1.1 and in concert with MYC and ATF4.

Chavdoula Evangelia E Anastas Vollter V La Ferlita Alessandro A Aldana Julian J Carota Giuseppe G Spampinato Mariarita M Soysal Burak B Cosentini Ilaria I Parashar Sameer S Sircar Anuvrat A Nigita Giovanni G Sehgal Lalit L Freitas Michael A MA Tsichlis Philip N PN

Metabolism: clinical and experimental 20231106

<h4>Introduction</h4>KDM2B encodes a JmjC domain-containing histone lysine demethylase, which functions as an oncogene in several types of tumors, including TNBC. This study was initiated to address the cancer relevance of the results of our earlier work, which had shown that overexpression of KDM2B renders mouse embryonic fibroblasts (MEFs) resistant to oxidative stress by regulating antioxidant mechanisms.<h4>Methods</h4>We mainly employed a multi-omics strategy consisting of RNA-Seq, quantita ...[more]

PMID: 37935302

Similar Datasets

Project description:Background: Hypertensive nephrosclerosis is one of the most frequent causes of chronic kidney failure. Proteome analysis potentially improves the pathophysiological understanding and diagnostic precision of this disorder. In the present exploratory study, we investigated experimental nephrosclerosis in the two-kidney, one-clip (2K1C) hypertensive rat model. Methods: The renal cortex proteome from juxtamedullary cortex and outer cortex of 2K1C male Wistar–Hannover rats (n¼4) was compared with the sham-operated controls (n¼6), using mass spectrometry-based quantitative proteomics. We combined a high abundant plasma protein depletion strategy with an extended liquid chromatographic gradient to improve peptide and protein identification. Immunohistology was used for independent confirmation of abundance. Results: We identified 1724 proteins, of which 1434 were quantified with at least two unique peptides. Comparative proteomics revealed 608 proteins, including the platelet-derived growth factor receptor-b signalling pathway, with different abundances between the non-clipped kidney of hypertensive 2K1C rats and the corresponding kidney of the normotensive controls (P<0.05, absolute fold change 1.5). Among the most significantly altered proteins in the whole cortex were periostin, transgelin, and creatine kinase B-type. Relative abundance of periostin alone allowed clear classification of 2K1C and controls. Enrichment of periostin in 2K1C rats was verified by immunohistology, showing positivity especially around the fibrotic vessels. Conclusion: The proteome is altered in hypertensioninduced kidney damage. We propose periostin, especially in combination with transgelin and creatine kinase B-type, as possible proteomic classifier to distinguish hypertensive nephrosclerosis from the normal tissue. This classifier needs to be further validated with respect to early diagnosis of fibrosis, prognosis, and its potential as a novel molecular target for pharmacological interventions.