The skin interfollicular epidermis (IFE) is the first barrier against the external environment and its maintenance is critical for survival. Two seemingly opposite theories have been proposed to explain IFE homeostasis. One posits that IFE is maintained by a long-lived slow-cycling stem cell (SC) population that give rise to short-lived transit-amplifying (TA) cell progeny, while the other suggests that homeostasis is achieved by a single committed progenitor (CP) that balances stochastic fate. Here, we probed the cellular heterogeneity within the IFE using two different inducible CREER targeting IFE progenitors. Quantitative analysis of clonal fate data and proliferation dynamics demonstrate the existence of two distinct proliferative cell compartments composed of slow-cycling SC and CP, both of which undergo population asymmetric self-renewal. However, following wounding, only SCs contribute substantially to the repair and long-term regeneration of the tissue, while CP cells make a minimal and transient contribution.
Distinct contribution of stem and progenitor cells to epidermal maintenance.
Specimen part
View SamplesTranscriptional profile of control and VEGF overexpressing FACS-isolated CD34+ Cancer stem cells from DMBA/TPA induced skin tumours
A vascular niche and a VEGF-Nrp1 loop regulate the initiation and stemness of skin tumours.
No sample metadata fields
View SamplesBasal cell carcinoma initiating cells undergo profound and rapid reprogramming into embryonic hair follicle progenitor like fate upon SmoM2 expression. Activation of Wnt/-catenin signaling pathways is required in a cell autonomous manner for the reprogramming of adult IFE progenitors into EHFP-like fate as well as for tumor initiation.
Adult interfollicular tumour-initiating cells are reprogrammed into an embryonic hair follicle progenitor-like fate during basal cell carcinoma initiation.
Specimen part
View SamplesPurpose: There is growing evidence that interaction between stromal and tumor cells is pivotal in breast cancer progression and response to therapy. Since the pioneer work of Allinen et al. suggested that during breast cancer progression striking changes occur in CD10+ stromal cells, we aimed to better characterize this cell population and its clinical relevance.
Characterization and clinical evaluation of CD10+ stroma cells in the breast cancer microenvironment.
Specimen part, Disease stage
View SamplesA doxycycline-inducible system was used to induce PU.1 expression in cultured myeloid cell lines. The parent cell line used was BN (Kamath et al., Leukemia 22:1214-1225, 2008).
PU.1 promotes cell cycle exit in the murine myeloid lineage associated with downregulation of E2F1.
Specimen part, Treatment
View SamplesWe examined the patterns of gene expression of mouse thymic leukemias extracted from Mb1-CreDPB mice by RNA sequencing (RNA-seq). Our goal was to integrate RNA-seq data with whole-exome sequencing (WES) to determined secondary driver mutations of leukemogenesis in the absence of Spi-B and PU.1, Overall design: Thymic leukemias were isolated from diseased Mb1-CreDPB mice. In summary, thymuses were homogenized and red blood cells were removed with ACK buffer, washed with PBS and counted. The amount of 8 million cells were pelleted an RNA was extracted using Rneasy RNA Isolation Kit (Qiagen). RNA was quantified and the purity was checked by spectophotrometer. RNA was sent to subsequently sequencing procedures.
Driver mutations in Janus kinases in a mouse model of B-cell leukemia induced by deletion of PU.1 and Spi-B.
Disease, Disease stage, Cell line, Subject
View SamplesWe demonstrate that the G protein Gi3 is the cellular target of the adenosine A3 receptor (A3R). By using a cell permeable peptide comprising the C-terminal end of Gi3 fused to an importation sequence (ALL1) as a selective inhibitor of Gi3 signaling, we show that by coupling to Gi3, the A3R stimulates multiple signaling pathways in human mast cells, leading to upregulation of cytokines, chemokines and growth factors.Following contact with activated T cell membranes, endogenous adenosine binds to and activates the A3R, resulting in Gi3-mediated signaling. Specifically, the majority of ERK1/2 signaling initiated by contact with activated T cell membranes, is mediated by Gi3, giving rise to ALL1-inhibitable cellular responses. These results unveil the physiological GPCR that couples to Gi3 and establish the important role played by this G-protein in inflammatory conditions that involve adenosine-activated mast cells.
Activation of mast cells by trimeric G protein Gi3; coupling to the A3 adenosine receptor directly and upon T cell contact.
Cell line
View SamplesWe analyzed the transcriptome of dormant and after-ripened imbibed seeds of the Arabidopsis accession Cape verde Islands.
Dormant and after-Ripened Arabidopsis thaliana Seeds are Distinguished by Early Transcriptional Differences in the Imbibed State.
Specimen part, Time
View SamplesFoxp1/4 transcription factors are conserved transcriptional repressors expressed in overlapping patterns during lung development as well as in the adult lung. However, the role of Foxp1/4 in development and homeostasis of the pseudostratified epithelium of the proximal airways and trachea is unknown.
Foxp1/4 control epithelial cell fate during lung development and regeneration through regulation of anterior gradient 2.
Specimen part
View SamplesSON is a large Ser/Arg (SR)-related protein localized in nuclear speckles. SON siRNA causes defects in mitotic progression and genome instability. We used microarrays to detail the pattern of gene expression after SON knockdown.
SON controls cell-cycle progression by coordinated regulation of RNA splicing.
Specimen part
View Samples