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RNA sequencing to determine gene expression changes in Siglec-15 knockdown oteosarcoma cells

ABSTRACT: RNA sequencing to determine gene expression changes in Siglec-15 knockdown oteosarcoma cells

PROVIDER: PRJNA732360 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14631584_1.fastq.gz	Fastqsanger.gz
	SRR14631584_2.fastq.gz	Fastqsanger.gz
	SRR14631585_1.fastq.gz	Fastqsanger.gz
	SRR14631585_2.fastq.gz	Fastqsanger.gz
	SRR14631586_1.fastq.gz	Fastqsanger.gz

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RNA sequencing to determine gene expression changes in Siglec-15 knockdown oteosarcoma cells

Project description:In our study, we found that Siglec-15 was critical to osteosarcoma characteristics. To identify the downstream target genes of Siglec-15 in osteosarcoma, we conducted the RNA-seq analysis of Siglec-15 knockdown in osteosarcoma cell line 143B cells.

2021-05-25 | GSE175414 | GEO

Structural insights into Siglec-15 reveal glycosylation dependency for its interaction with T cells through integrin CD11b

Project description:Sialic acid-binding Ig-like lectin 15 (Siglec-15) is emerging as an immune modulator and target for cancer immunotherapy. However, limited knowledge regarding its mechanism of action and structure, or its binding partners with T cells, restrains the development of drug candidates that could unleash its full therapeutic potential. Here, we determine the crystal structure of Siglec-15 and delineate its binding epitope by co-crystallization with an anti-Siglec-15 blocking antibody. Saturation transfer-difference nuclear magnetic resonance (STD-NMR) spectroscopy assisted with molecular dynamics simulations reveals the binding mode of Siglec-15 to (2,3)- and 2,6)- linked sialic acids and to the cancer-associated sialyl-Tn (STn) glycoform. Binding of Siglec-15 to T cells, which lack STn expression, depends on the presence of (2,3)- and 2,6)- linked sialoglycans. We identify the leukocyte integrin CD11b as a binding partner of Siglec-15 on human T cells. Collectively, these data provide an integrative understanding of the structural features of Siglec-15 and underscore glycosylation as an additional layer of control of T cell responses.

2023-07-20 | PXD042009 | Pride

Effect of deficiency of Siglec-15 during osteoclast differentiation of murine bone marrow macrophages

Project description:To investigate the function of Siglec-15 in the regulation of osteoclast differentiation, Siglec-15 deficient mice was established. Then gene expression profiling analysis using data obtained from RNA-seq of bone marrow macrophages with M-CSF and RANKL at two different time points was performed.

2023-12-01 | GSE218768 | GEO

Determine anti-Siglec-F and IL-33 costimulation induced transcriptional changes on murine eosinophils

Project description:Determine anti-Siglec-F and IL-33 costimulation induced transcriptional changes on murine eosinophils

| PRJNA702493 | ENA

Determine anti-Siglec-F and IL-33 costimulation induced transcriptional changes on murine eosinophils

Project description:Eosinophils costimulation with anti-Siglec-F and IL-33 synergistically increases their IL-4 and IL-13 release (Willebrand et al. PLoS One 2016). Here we analyze costimulation induced transcriptional changes involved that potentially enhance effector release.

2021-11-23 | GSE166968 | GEO

Tumor-derived kynurenine induces Siglec-15 expression and promotes CD8+T cell exhaustion in oral squamous cell carcinoma

Project description:Metabolic deregulation and immune escape are pivotal hallmarks of cancer; however, the profile of metabolic reprogramming in oral squamous cell carcinoma (OSCC) and how it drives immune escape remain unclear. We identified significant metabolic disorders in OSCC. Amino acid metabolism, especially tryptophan/kynurenine metabolism, was altered. Here, we found that kynurenine promotes migration, invasion, and proliferation in vitro and in vivo. In addition, most immune checkpoints were upregulated in patients with high kynurenine levels. We then identified that kynurenine can promote Siglec-15 expression via AhR activation. Furthermore, tumor-derived kynurenine can directly exhaust CD8+ T cells, whereas blocking of kynurenine transporters reversed this effect. Moreover, we found that ectopic expression of Siglec-15 can promote immune escape in tumor microenvironment (TME) by suppressing T cell infiltration and inducing CD8+ T cell exhaustion in vivo, while targeting AhR reduces kynurenine-mediated immune escape. Finally, we design NH2-MSNs nanoparticles to deliver Siglec-15 small interfering RNA, which successfully remodels the TME and enhances anti-PD-1 efficacy in tumor-bearing immunocompetent mice. Clinically, Siglec-15 expression is correlated with AhR expression and high infiltration of exhausted CD8+ T cells. These findings reveal that the Kyn/AhR/Siglec-15 signaling pathway is a novel immunometabolism mechanism in OSCC, thus opening a new therapeutic avenue for metabolic immunotherapy.

2024-07-03 | GSE222673 | GEO

RNA sequencing to determine gene expression changes in SQLE knockdown osteosarcoma cells

Project description:RNA sequencing to determine gene expression changes in SQLE knockdown osteosarcoma cells

| PRJNA1028999 | ENA

The inhibitory receptor Siglec-G controls the severity of chronic lymphocytic leukemia

Project description:Chronic Lymphocytic Leukaemia (CLL) is the most common leukemia in adults in the Western world. B cell receptor (BCR) signalling is known to be crucial for the pathogenesis and maintenance of CLL cells develop from mature CD5+ B cells. BCR signalling is regulated by the inhibitory co-receptor Siglec-G and Siglec-G-deficient mice have an enlarged CD5+ B1a cell population. Here, we determine how Siglec-G expression influences the severity of CLL.

2023-05-03 | GSE227678 | GEO

Type-I interferon inducible genes 26 weeks after mCMV infection in Siglec-H wt and Siglec-H ko mice and their non infected controls

Project description:Type I interferons are critical anti-viral cytokines during virus infections and have also been implicated in the pathogenesis of systemic lupus erythematosus (SLE). The secretion of type I interferon of pDCs is modulated by Siglec-H, a DAP12 associated receptor on pDCs. We showed that Siglec-H deficient pDCs produce more of the type I interferon IFN-Î± in vitro and that Siglec-H ko mice produce more IFN-Î± after murine cytomegalovirus (mCMV) infection in vivo, leading to efficient clearance of the virus. Furthermore, ageing Siglec-H ko mice showed a mild form of systemic autoimmunity. In contrast, Siglec-H ko mice developed a severe form of systemic lupus-like autoimmune disease with strong kidney nephritis several weeks after a single mCMV infection. This induction of systemic autoimmune disease after virus infection in Siglec-H ko mice was accompanied by a type I interferon signature and fully dependent on type I interferon signaling. These results show that Siglec-H normally serves as modulator of type I interferon responses after infection with a persistent virus and thereby prevents induction of autoimmune disease. For microarray experiments gene expression profiles of total splenic cells from two wt and Siglec-H ko mice 26 weeks after infection with luciferase expressing murine Cytomegalovirus (5x105 pfu) or from two uninfected wt and Siglec-H ko control mice were analyzed

2016-03-16 | E-GEOD-79248 | biostudies-arrayexpress

Effect of deficiency of Siglec-15 during osteoclast differentiation of murine bone marrow macrophages

Project description:Effect of deficiency of Siglec-15 during osteoclast differentiation of murine bone marrow macrophages

| PRJNA905426 | ENA