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The SRC-family kinase LYN acts as a tumour suppressor gene in an in vivo BRCA1 loss-of-function-associated mammary tumourigenesis model

ABSTRACT: The SRC-family kinase LYN acts as a tumour suppressor gene in an in vivo BRCA1 loss-of-function-associated mammary tumourigenesis model

PROVIDER: PRJNA917599 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22956700_1.fastq.gz	Fastqsanger.gz
	SRR22956700_2.fastq.gz	Fastqsanger.gz
	SRR22956701_1.fastq.gz	Fastqsanger.gz
	SRR22956701_2.fastq.gz	Fastqsanger.gz
	SRR22956702_1.fastq.gz	Fastqsanger.gz

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The SRC-family kinase LYN acts as a tumour suppressor gene in an in vivo BRCA1 loss-of-function-associated mammary tumourigenesis model

Project description:To examine the interaction between LYN kinase and BRCA1 loss-of-function in an in vivo mouse mammary tumour model, we have used conditional knockout Brca1 and Lyn alleles targeted to the mammary epithelium, on a p53 heterozygote background. Comparison of tumour cohorts demonstrated that homozygous conditional Lyn cohorts developed tumours significantly faster than the other genotypes. Transcriptomic analysis to identify and compare tumours with the highest and lowest Lyn levels from across the cohorts showed that ‘Lyn high’ tumours had a significantly slower doubling time and were enriched in inflammatory pathways and canonical NfkB signalling. ‘Lyn low’ tumours had a faster doubling time and were enriched in PI3K, WNT and NOTCH pathways. Therefore, these results suggest that, in this model at least, LYN acts as a tumour suppressor in the context of Brca1 loss.

2023-01-23 | GSE222075 | GEO

Tyrosine Phosphorylation of NLRP3 by Src Family Protein Tyrosine Kinase Lyn Suppresses NLRP3 Inflammasome Activation

Project description:The NLRP3 inflammasome is a multi-protein complex that triggers the activation of the inflammatory protein caspase-1 and the maturation of the cytokine IL-1 in response to microbes and other danger signals in host cells. Here, we sought a deeper understanding of how the NLRP3 inflammasome is regulated. We found that inflammasome activation induced the Src family kinase Lyn to phosphorylate NLRP3 at Tyr918, and that this phosphorylation of NLRP3 correlated with a subsequent increase in its ubiquitination, which facilitated its proteasome-mediated degradation. NLRP3 tyrosine phosphorylation and ubiquitination was abrogated in Lyn-deficient macrophages, which produced increased amounts of IL-1. Furthermore, mice lacking Lyn were highly susceptible to LPS-induced septic shock in an NLRP3-dependent manner. Our data demonstrate that Lyn-mediated tyrosine phosphorylation of NLRP3 is a prerequisite for its ubiquitination, thus dampening NLRP3 inflammasome activity.

2022-05-19 | PXD028582 | Pride

Src heterodimerically activates Lyn or Fyn to serve as targets for esophageal squamous cell carcinoma (ESCC) diagnosis and treatment

Project description:we combined phosphoproteomics and several cellular and molecular biologic strategies to identify that Src specifically interacted with the members of Src-family kinases (SFKs), such as Fyn or Lyn to form heterodimers, and subsequently phosphorylate the tyrosine sites in SH2 and kinase domains, which critically contributed to the ESCC malignancy.

2022-03-15 | PXD032306 |

Macrophage Lyn kinase is a Sex-Specific Regulator of Post-SAH Neuroinflammation

Project description:Lyn kinase is a member of the Src family of tyrosine kinases, primarily known for its role in regulating immune cell signaling. It can phosphorylate and modulate the activity of various proteins involved in immune responses, including TLR4. In our study, we investigated the sex-specific involvement of Lyn kinase in regulating TLR4 signaling to understand the TLR4 mediated inflammatory response after SAH. Our results highlight sex-specific modulation of Lyn kinase activity in TLR4 signaling after hemorrhagic stroke and indicate that successful treatment of neuroinflammation may require sex-specific treatments.

2026-01-21 | GSE287635 | GEO

Lyn expression in macrophages promotes TLR activation and restricts proliferation in an isoform-independent manner

Project description:Toll-like receptor (TLR) signaling is vital to macrophage function, and dysregulation is associated with many disease states. The Src-family kinase (SFK) Lyn serves activating and inhibitory roles downstream of TLRs, yet distinct functions of the isoforms LynA and LynB in TLR signaling have not been investigated. We used isoform-specific knockout mice (LynAKO and LynBKO) to interrogate the contribution of each isoform to TLR signaling in bone marrow-derived macrophages (BMDMs). Bulk RNA sequencing and cytokine analyses revealed that complete Lyn deficiency (LynKO) dampens TLR4- and TLR7-induced inflammatory gene expression and TNF production, but enhances extracellular matrix (ECM) gene expression and promotes cell-cycle progression and macrophage proliferation. In contrast, expression of either LynA or LynB was sufficient to preserve wild-type (WT) transcriptional responses and TNF production, despite moderately reduced total Lyn levels. These data suggest that Lyn promotes macrophage activation downstream of TLRs and restrains aberrant proliferation and matrix deposition in a largely dose-dependent rather than isoform-specific manner. Our findings provide new insight into the roles of LynA and LynB in TLR signaling and can inform future studies of macrophage-driven pa-thology in autoimmune disease, fibrosis, and cancer.

2025-11-18 | GSE300925 | GEO

Disease Associated Microglial TLR4-Lyn kinase is a critical regulator of neuroinflammation, Aβ phagocytosis, neuronal damage and cell survival in a 5XFAD mouse model.

Project description:Disease-Associated Microglia (DAM) are a focus in Alzheimer's disease (AD) research due to their central involvement in the response to amyloid-beta plaques. Microglial Toll-like receptor 4 (TLR4) is instrumental in the binding of fibrillary amyloid proteins, while Lyn kinase (Lyn) is a member of the Src family of non-receptor tyrosine kinases involved in immune signaling. Increased expression of protective Syk kinase was observed, enhanced microglial Aβ phagocytosis, decreased neuronal dystrophy, and a further increase in the cell survival signaling and protective DAM population was noted. Lyn can be activated in response to TLR4 stimulation, leading to phosphorylation of various substrates and modulation of inflammatory and phagocytosis signaling pathways.

2026-01-17 | GSE287470 | GEO

Gene expression profiling in wild-type, Irf5-KO, Lyn-KO and Lyn/Irf5-DKO BMDCs unstimulated or stimulated with CpG-B ODN

Project description:To characterize the relationship between IRF5 and Lyn in innate immune responses at a genome-wide scale, we performed gene expression microarray analysis for wild-type (WT), Irf5-KO, Lyn-KO and Lyn/Irf5-DKO bone marrow-derived dendritic cells (BMDCs) with or without 6 h-stimulation with 150 nM CpG-B ODN. We extracted the transcripts that were upregulated by CpG-B ODN in WT BMDCs, further upregulated in Lyn-KO BMDCs and then downregulated in Lyn/Irf5-DKO BMDCs (fold change ≥ 2, false discovery rate < 0.05). When these 79 transcripts were sorted by their expression levels in Lyn-KO BMDCs, most of the top 20 genes (13 out of 20) were those encoding type I interferons (IFNs), indicating that Lyn particularly suppresses IRF5 induction of type I IFNs.

2016-07-25 | GSE63014 | GEO

Gene expression profiling in wild-type, Irf5-KO, Lyn-KO and Lyn/Irf5-DKO BMDCs unstimulated or stimulated with CpG-B ODN

Project description:To characterize the relationship between IRF5 and Lyn in innate immune responses at a genome-wide scale, we performed gene expression microarray analysis for wild-type (WT), Irf5-KO, Lyn-KO and Lyn/Irf5-DKO bone marrow-derived dendritic cells (BMDCs) with or without 6 h-stimulation with 150 nM CpG-B ODN. We extracted the transcripts that were upregulated by CpG-B ODN in WT BMDCs, further upregulated in Lyn-KO BMDCs and then downregulated in Lyn/Irf5-DKO BMDCs (fold change â?¥ 2, false discovery rate < 0.05). When these 79 transcripts were sorted by their expression levels in Lyn-KO BMDCs, most of the top 20 genes (13 out of 20) were those encoding type I interferons (IFNs), indicating that Lyn particularly suppresses IRF5 induction of type I IFNs. BMDCs from WT, Irf5-KO, Lyn-KO and Lyn/Irf5-DKO mice in a C57BL/6 background were unstimulated or stimulated with CpG-B ODN. Biological triplicate for each genotype were analyzed (24 samples in total).

2016-07-25 | E-GEOD-63014 | biostudies-arrayexpress

Transcriptome of LYN deficient HS-5 stroma cells

Project description:LYN kinase is a tyrosine kinase, that regulates cellular homeostasis in a context-specific manner. Our group could show, that its expression in the leukemic microenvironment of chronic lymphocytic leukemia contributes to disease progression (Nguyen PH et al.; Cancer Cell; 2016). To analyze the effect of LYN kinase on the leukemia supportive phenotype of the bone marrow stromal cell line HS-5, we generated single cell clones of LYN deficient stroma cells. These cells were analyzed in a Multi-Omic approach, including microarray based analysis of the transcriptome.

2023-01-01 | E-MTAB-10980 | biostudies-arrayexpress

RNA-Seq analysis of LYN deficient stromal cells sorted from murine spleens

Project description:LYN kinase is a tyrosine kinase, that regulates cellular homeostasis in a context-specific manner. Our group could show, that its expression in the leukemic microenvironment of chronic lymphocytic leukemia contributes to disease progression (Nguyen PH et al.; Cancer Cell; 2016). We analyzed the effect of LYN deficiency on murine splenic stromal cells by FACS-sorting stroma cells from Lyn(wt/wt) and Lyn(-/-) spleen (7AAD-Cd45-Cd71-Cd31-Cd26+Cd54+).

2023-02-10 | E-MTAB-12630 | biostudies-arrayexpress

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