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Cancer arises through reprogramming-like processes in mice

ABSTRACT: Gene expression data from CD22+B220+ FACS-purified splenocytes of adult wild-type, Sca1-Bcl6(floxed) and Sca1-Bcl6(Δ) knock-in CBAxC57BL/6J mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE36503 | GEO | 2014/03/01

SECONDARY ACCESSION(S): PRJNA153449

REPOSITORIES: GEO

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Cancer arises through reprogramming-like processes in mice

Project description:Gene expression data from CD22+B220+ FACS-purified splenocytes of adult wild-type, Sca1-Bcl6(floxed) and Sca1-Bcl6(Δ) knock-in CBAxC57BL/6J mice. The Bcl6 floxed vector was generated by inserting the mouse Bcl6–IRES-eGFP cassette flanked by loxP sites into the ClaI site of the pLy6 vector. The transgene fragment was excised from its vector by restriction digestion with NotI, purified and injected into CBAxC57BL/6J fertilized eggs. Two independent transgenic lines were generated and analyzed. Sca1-Bcl6(floxed) mice were bred to mb1-Cre mice to generate Sca1-Bcl6(Δ) mice. Splenic B220+CD22+ cells were FACS purified from wild-type, Sca1-Bcl6(floxed) and Sca1-Bcl6(Δ) mice and arrayed using Affymetrix Mouse Gene 1.0 ST arrays.

2014-03-01 | E-GEOD-36503 | biostudies-arrayexpress

HGAL Enhances BCR-mediated Syk Activation, Leading to Lymphoid Hyperplasia and Amyloidosis

Project description:Gene expression data from CD22+B220+ FACS-purified splenocytes of adult Sca1-HGAL knock-in CBAxC57BL/6J mice or wild-type littermates.

2013-05-22 | GSE35400 | GEO

HGAL Enhances BCR-mediated Syk Activation, Leading to Lymphoid Hyperplasia and Amyloidosis

Project description:Gene expression data from CD22+B220+ FACS-purified splenocytes of adult Sca1-HGAL knock-in CBAxC57BL/6J mice or wild-type littermates. Transgenic mice expressing HGAL (GCET2) under control of the Sca1 (Ly-6E.1) promoter were generated. CD22 and B220 dual-positive B-cells were FACS purified from spleens of adult transgenic mice and wildtype littermates, total-RNA was isolated, and transcriptional profiling performed using GeneChip® Mouse Gene 1.0 ST Arrays.

2013-05-22 | E-GEOD-35400 | biostudies-arrayexpress

Transient expression of Bcl6 is sufficient for oncogenic function and induction of mature B-cell lymphoma

Project description:Reduced representation bisulfite sequencing (RRBS) of hematopoeitic stem/progenitor cells and mature B-cells from wild-type mice and mice transiently expressing Bcl6 under control of the Sca1 promoter. CBAxC57BL/6J mice were engineered to transiently express a Bcl6 cDNA in hematopoeitic stem/progenitor cells under control of the Sca1 promoter and then delete the transgene by cre-mediated recombination upon expression of Cd79a (Sca1-BCL6?). Hematopoeitic stem/progentior cells (HSPC, Sca1+Lin-) from the bone marrow and mature B-cells (B220+) from the peripheral blood were isolated from these mice and wild-type CBAxC57BL/6J mice by fluorescence activated cell sorting. Cells from 6-9 mice were pooled, for a total of 4 experimental conditions. DNA was extracted for each condition and analyzed by reduced representation bisulfite sequencing.

2014-03-28 | E-GEOD-56310 | biostudies-arrayexpress

Transient expression of Bcl6 is sufficient for oncogenic function and induction of mature B-cell lymphoma

2014-03-28 | GSE56310 | GEO

HDAC1 and 2 repress lineage inappropriate expression of Flt3 and Ptprf in B cells via Pax5 and Grg4

Project description:Total RNA was isolated from pre BI (early lymphcytes) cells sorted by FACS with the following markers: B220+, CD25-, C-kit+,IgM-, CD19+. The animals used carried floxed Hdac1 & 2 either in combination with mb1-cre (refered to as DKO) or not (WT).

2016-03-16 | GSE36564 | GEO

miRNA expression profile of follicular (FO) and marginal zone (MZ) B cells

Project description:We have analyzed miRNA expression profile in FO and MZ B cells to identified differentially expressed miRNAs between this two subsets that could be potencially involved in the regulation of terminal B cell differentiation Spleens from CD19-Creki/+Dicerfl/+ and CD19-Creki/+Dicerfl/fl mice were collected and after erythrocyte lysis, splenocytes were stained with anti-B220, anti-CD21 and anti-CD23 antibodies. B220+CD21brightCD23+ (MZ) and B220+CD21+CD23bright (FO) B cell populations were sorted and total RNA of purified populations was extracted with TRIzol. miRNA microarray hybridations were performed on Mouse miRNA Microarray platform (Agilent Technologies).

2011-11-01 | E-GEOD-25139 | biostudies-arrayexpress

Facial bone fragmentation in blind cavefish arises through two unusual ossification processes.

Project description:The precise mechanisms underlying cranial bone development, evolution and patterning remain incompletely characterised. This poses a challenge to understanding the etiologies of craniofacial malformations evolving in nature. Capitalising on natural variation, "evolutionary model systems" provide unique opportunities to identify underlying causes of aberrant phenotypes as a complement to studies in traditional systems. Mexican blind cavefish are a prime evolutionary model for cranial disorders since they frequently exhibit extreme alterations to the skull and lateral asymmetries. These aberrations occur in stark contrast to the normal cranial architectures of closely related surface-dwelling fish, providing a powerful comparative paradigm for understanding cranial bone formation. Using a longitudinal and in vivo analytical approach, we discovered two unusual ossification processes in cavefish that underlie the development of 'fragmented' and asymmetric cranial bones. The first mechanism involves the sporadic appearance of independent bony elements that fail to fuse together later in development. The second mechanism involves the "carving" of channels in the mature bone, a novel form of post-ossification remodeling. In the extreme cave environment, these novel mechanisms may have evolved to augment sensory input, and may indirectly result in a trade-off between sensory expansion and cranial bone development.

| S-EPMC5934472 | biostudies-literature

TLR signaling in C57BL/6J TLR2,4,7-tolerant splenocytes over PBS-treated counterpart.

Project description:Murine splenocytes were isolated from the spleens of C57BL/6J mice and were pretreated in vitro for three days in the presence of Pam3CSK4 (1 μg/ml), high pure LPS from E.coli O111:B4 (100 ng/ml) and R848 (5 μg/ml). PBS-treated splenocytes served as negative control. We used Qiagen Toll-like Receptor RT2 Profiler PCR Array kit to quantitate gene expression profiling of the TLR signaling pathway.

2017-04-21 | GSE80572 | GEO

Tuberous sclerosis complex renal lesion pleiotropy arises from multiple aberrant developmental processes

Project description:Tuberous sclerosis complex (TSC) is a multisystem tumor-forming disorder caused by loss of TSC1 or TSC2. Renal manifestations predominately include cysts and angiomyolipomas. Despite a well-described monogenic etiology, the cellular pathogenesis has remained elusive. Here, we report a novel genetically-engineered human renal organoid model which recapitulates pleiotropic features of TSC kidney disease in vitro and upon orthotopic xenotransplantation. We find that loss of TSC1/2 affects multiple developmental processes in the renal epithelial, stromal, and glial compartments. First, loss of TSC1/2 leads to an expanded stroma by favouring stromal cell fate acquisition and alters terminal stromal cell identity. Second, epithelial cells in the TSC1/2-/- organoids exhibit a rapamycin-insensitive epithelial-to-mesenchymal transition. Third, a melanocytic population forms exclusively in TSC1/2-/- organoids, branching from MITF+ Schwann cell precursors of a bona fide neural crest-to-Schwann cell differentiation trajectory. Together, these results illustrate the pleiotropic developmental consequences of biallelic inactivation of TSC1/2 and offer insight into the pathogenesis of TSC kidney lesions.

2022-07-05 | GSE182632 | GEO

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