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Expression data of mouse calvarial stem cells from p75 floxed mice (p75fl/fl) stimulated with Adenovirus encoding Cre recombinase (Ad-Cre) or control (Ad-GFP) [RNA-seq]

ABSTRACT: Expression data of mouse calvarial stem cells from p75 floxed mice (p75fl/fl) stimulated with Adenovirus encoding Cre recombinase (Ad-Cre) or control (Ad-GFP) [RNA-seq]

PROVIDER: PRJNA745468 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15097819_1.fastq.gz	Fastqsanger.gz
	SRR15097819_2.fastq.gz	Fastqsanger.gz
	SRR15097820_1.fastq.gz	Fastqsanger.gz
	SRR15097820_2.fastq.gz	Fastqsanger.gz
	SRR15097821_1.fastq.gz	Fastqsanger.gz

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Expression data of mouse calvarial stem cells from p75 floxed mice (p75fl/fl) stimulated with Adenovirus encoding Cre recombinase (Ad-Cre) or control (Ad-GFP) [RNA-seq]

Project description:The cranial sutures are fibrous joints containing skeletal progenitor cells, which maintain homeostasis of the uninjured skull or participate in healing the skull after injury. Nerve growth factor (NGF) via its high-affinity receptor tropomyosin receptor kinase A (TrkA) regulates skeletal re-innervation, which is essential for later elements of bone repair, including revascularization and bone matrix deposition. However, emerging evidence suggests that NGF signaling may have more pleiotropic effects in bone repair than previously considered. In addition to induction of nerve ingrowth and promotion of nerve survival, pro-NGF may bind to its low-affinity receptor Ngfr (p75, Cd271), which is present in a variety of mesenchymal cells. p75 expression has been correlated to cell migration and invasion in multiple cell types. NGF binding to the p75 receptor stimulates migration and initiates recruitment of various adaptors, which activate NF-κB, RhoA, and c-Jun N-terminal kinase (JNK) signaling. In this study, changes in the transcriptome of calvarial stem cells after p75 knockout were evaluated by RNA sequencing.

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Project description:Comparative gene expression profiling of olfactory enshealting cells : p75 High vs p75 Low cells population Two-color experiment, p75 high(Cy5)/p75Low (Cy3). Biological replicates: 4 . Paired samples.

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Myh6 promoter-driven Cre recombinase excises floxed DNA fragments in a subset of male germline cells.

Project description:Myh6-Cre transgenic mouse line was known to express Cre recombinase only in the heart. Nevertheless, during breeding Myh6-Cre to Rosa26fstdTom reporter (tdTom) mouse line, we observed that a significant part of their F2 tdTom/+ offspring had tdTom reporter gene universally activated. Our results show that Myh6-Cre transgenic mice have Cre recombinase activity in a subpopulation of the male germline cells, and that Myh6 gene transcripts are enriched in the interstitial Leydig cells and the undifferentiated spermatogonia stem cells. In summary, the current study confirms that the previously known "heart-specific" Myh6 promoter drives Cre expression in the testis.

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Role of LEDGF/p75 in MLL chemoresistance

Project description:The study has been focused on the characterization of the role of LEDGF/p75 in chemiresistance in pediatric leukemia Abstract: MLL is an aggressive subtype of leukemia with a poor prognosis that mostly affects pediatric patients. MLL-rearranged fusion proteins (MLLr) induce aberrant target gene expression resulting in leukemogenesis. MLL and its fusions are tethered to chromatin by LEDGF/p75, a transcriptional co-activator that specifically recognizes H3K36me2/3. LEDGF/p75 is ubiquitously expressed and associated with regulation of gene expression, autoimmune responses and HIV replication. LEDGF/p75 was proven to be essential for leukemogenesis in MLL. Apart from MLL, LEDGF/p75 has been linked to lung, breast and prostate cancer. Intriguingly, LEDGF/p75 interacts with Med-1, which co-localizes with BRD4. Both are known as co-activators of super-enhancers. Here, we describe LEDGF/p75-dependent chemoresistance of MLLr cell lines. Investigation of the underlying mechanism revealed a role of LEDGF/p75 in the cell cycle and in survival pathways and showed that LEDGF/p75 protects against apoptosis during chemotherapy. Remarkably, LEDGF/p75 levels also affected expression of BRD4 and Med1. Altogether, our data suggest a role of LEDGF/p75 in cancer survival, stem cell renewal, and activation of nuclear super enhancers.

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