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Extracellular vesicles shed by follicular lymphoma B cells promote the polarization of bone marrow stromal cell niche

ABSTRACT: Characterisation of the extracellular vesicles shed by follicular lymphoma B cells that induce the polarization of bone marrow stroma cell toward a pro-tumoral niche.

INSTRUMENT(S): Orbitrap Eclipse

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Valentin SABATET

LAB HEAD: Damarys Loew

PROVIDER: PXD023749 | Pride | 2021-02-08

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	Design.xls	Xls
	X1805FD.msf	Msf
	X1805FD.raw	Raw
	X1806FD.msf	Msf
	X1806FD.raw	Raw

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GFP-CYYR1 interactome vs. GFP in HEK293 cells

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Fibroblast-tracks are topographical cues that direct cancer cell migration

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Identification of RNF111 substrates by integrative ubiquitome and proteome analysis

Project description:In the present work, we sought to identify exhaustively the endogenous substrates ubiquitinated and degraded by the E3 ubiquitin ligase RNF111 in presence of TGF-β signaling by performing label free quantitative proteomics after enrichment of ubiquitinated proteins (ubiquitome) in parental U2OS cell line compared to U2OS CRISPR engineered clones expressing a truncated form of RNF111 devoid of C-terminal Ring domain. We compare two methods of enrichment for ubiquitinated proteins prior to mass spectrometry proteomics analysis, the diGly remnant peptide immunoprecipitation with a K-e-GG antibody and a novel approach using protein immunoprecipitation with an ubiquitin pan (Pan UB) nanobody that recognizes all ubiquitin chains and mono-ubiquitination. These ubiquitomes were compared to the corresponding proteome to identify proteins ubiquitinated and degraded by RNF111 upon TGF-β signaling pathway.

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NeonGreen-POLQ knock-in in Human embryonic kidney 293 cells VS Human embryonic kidney 293 cells

Project description:Replication stress (RS) can lead to the formation of DNA double strand breaks (DSBs) and threatens genomic stability. Homologous recombination (HR) pathway is essential to prevent RS and repairs associated DSBs. Upon excessive RS or HR deficiency, DSBs can persist in mitosis, wherein DNA damage response and DSB repair are inhibited. Thus, the fate of DSBs remaining or arising in mitosis remains poorly understood. Here we unwind two distinct roles of the polymerase theta (Polθ) in the maintenance of genomic stability. First, by mass spectrometry and foci screening we show that, in interphase, Polθ interacts with HR proteins and its recruitment to IR-induced DSBs is highly dependent of HR pathway. Secondly, we identify a novel role of the Polθ in counteracting the deleterious effect of DSBs in mitosis. Contrariwise to its interphase recruitment, Polθ recruitment to mitotic DSBs is HR-independent and triggered by mitotic kinases activities. In response to RS or HR deficiency, Polθ localizes to DSBs throughout mitosis and forms nuclear bodies in the G1 daughter cells. In addition, Polθ localizes to centromeres and acentric fragments and activates the mitotic checkpoint. Conversely, Polθ deficiency leads to premature anaphase onset, resulting in an accumulation of mitotic abnormalities. Strikingly, the specific inhibition of Polθ in mitosis kills HR-deficient cells, identifying mitotic Polθ function as its key role in maintaining genome integrity. Our results pinpoint to the mitotic Polθ-mediated replication stress response pathway as a unique vulnerability of cancer cells, with great potential for further investigation.

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