A Rank-based Semblance kernel over Probability Spaces
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA476369 | ENA |
REPOSITORIES: ENA
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Project description:CD45- sorted tumor cells from RANK+/+ and RANK-/- MMTV_PYMT late carcinomas
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Project description:Transcriptional profile of either RANK+/+ or RANK-/- MMTV-PyMT late carcinomas, orthotopically injected in syngeneic RANK+/+ mice. Once host mice developed tumors, CD45- tumor cells were sorted by flow cytometry in order to compare changes on tumor gene expression caused by the absence of RANK protein.
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Project description:MMTV-PyMT late carcinomas, orthotopically injected in syngeneic RANK+/+ mice were digested until single cells and cultured over Matrigel in the prescence or abscence of RANKL for 24 hours.
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Project description:RANK-positive and RANK-negative luminal progenitor cells were isolated by FACS from histologically normal human breast tissue from wild-type human donors. RNA-seq gene expression profiling was used to find differentially expressed genes between the RANK-positive and RANK-negative cell populations.
2016-06-20 | GSE71203 | GEO
Project description:The purpose of this study was to elucidate the molecular changes of the mammary epithelium induced by luminal cell specific RANK deletion. We have characterized the phenotypic consequences of RANK deletion in the luminal lineage of the mammary epithelium, and uncovered that Rank KO luminal cells have reduced long term renewal following sucessive pregnancies. Lineage tracing analysis has demonstrated that during pregnancy 2, Rank deleted luminal cells are repleace by a wt luminal cell population, derived from the basal epithelium. We therefore decided to perform RNA seq in resting mammary glands from virgin and parous (following pregnancy one) females, cells were FACS sorted based on the traditional markers CD24 and CD49f and in the case of luminal cells GFP (recombined cells). We have isolated luminal cells to identify the molecular pathways involved in reduced long term renewal oberved in the parous context; basal cells were isolated to adress the putative mechanims regulated the bipotency observed during second pregnancy
2023-09-01 | GSE199746 | GEO
Project description:Transcriptional profile of MMTV-PyMT late carcinomas after adjuvant or neoadjuvant treatment with RANK-Fc (receptor activator of NF-kB) cells isolated from one single MMTV-PyMT carcinoma were orthotopically injected in syngeneic WT mice, which were randomized 1:1 for neoadjuvant RANK-Fc or mock treatment (passage 1) for 4 weeks. Cells isolated from both treatment arms were pooled and injected into the fat pad of FvB recipients (passage 2) in limiting dilutions (mimicking occult disease) and again randomized 1:1 for additional RANK-Fc (adjuvant) or mock treatment
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Project description:Gene expression profiles of Ccl21a+ and Rank+ E17 thymic epithelial cells (TECs) were compared using Ccl21a-tdTomato-KI Rank-Venus-Tg mice
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Project description:By carrying out a systematic structure/function study of the RANK cytoplasmic domain, we previously identified a specific 4-a.a. RANK motif (IVVY535-538) which plays a critical role in osteoclastogenesis by mediating commitment of macrophages to the osteoclast lineage. We have recently validated the role of this IVVY motif in osteoclastogenesis in vivo by generating knockin (KI) mice bearing inactivating mutations in the RANK IVVY motif. This microarray experiment was performed to determine whether the IVVY motif is involved in regulating gene expression in osteoclastogenesis. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process.
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Project description:Joint destruction is the major clinic burden in patients with rheumatoid arthritis (RA). It is unclear, though, how this autoimmune disease progresses to the point of deterioration of the joint. Here, we report that in a mouse model of RA the upregulation of TLR2 expression and its a(2,3) sialylation in RANK+ myeloid monocytes mediate the transition from autoimmunity to osteoclast fusion and bone resorption, resulting in joint destruction. The expression of a(2,3) sialyltransferases were significantly increased in RANK+TLR2+ myeloid monocytes, and their inhibition or treatment with a TLR2 inhibitor blocked osteoclast fusion. Notably, analysis of our single-cell RNA-sequencing (scRNA-seq) libraries generated from RA mice revealed a novel RANK+TLR2- subset that negatively regulated osteoclast fusion. Importantly, the RANK+TLR2+ subset was significantly diminished with the treatments. Moreover, the RANK+TLR2- subset could differentiate into a TRAP+ osteoclast lineage, but the resulting cells did not fuse to form osteoclasts. Our scRNA-seq data showed that Maf is highly expressed in the RANK+TLR2- subset, and the a(2,3) sialyltransferase inhibitor induced Maf expression in the RANK+TLR2+ subset. The identification of a RANK+TLR2- subset provides a potential explanation for TRAP+ mononuclear cells in bone and their anabolic activity. Further, TLR2 expression and its a(2,3) sialylation in the RANK+ myeloid monocytes could be effective targets to prevent autoimmune-mediated joint destruction.
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Project description:Identification of genes regulated by RANK RVVY motif in macrophages by gene expression analysis of TNFR1-/-R2-/- BMMs expressing a chimeric receptor consisting of the external domain of mouse TNFR1 linked to the transmembrane and intracellular domain of mouse RANK (WT) and NFR1-/-R2-/- BMMs expressing a chimeric receptor consisting of the external domain of mouse TNFR1 linked to the transmembrane and intracellular domain of mouse RANK bearing inactivating mutations in the IVVY motif (Mu).
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