Project description:Gene expression analysis has revealed that Interleukin-6 signalling in murine erythroid progenitors is altered during ageing. Here we study the impact of inhibition of IL6 on the transcription profile of progenitors from bone marrow in aged mice
Project description:Rapid expansion of stress erythroid progenitors is a key response to acute anemia during stress erythropoiesis. Besides the rapidly amplifying progenitors, a small population of stem-cell like erythroid progenitors undergoes limited number of cell divisions and maintains their stemness. In this study, we addressed the differences in expression profiles of regulatory genes between two stress erythroid progenitor populations that were identified by proliferation capacity and physiological status. We used microarrays to detail the gene expression profiles of stem-cell like stress erythroid progenitors and rapidly amplifying stress erythroid progenitors during stress erythropoiesis.
Project description:Functional study has revealed that the erythroid differentiation capacity is compromised during ageing. Here we report the transcriptome profiles of erythroid progenitors in the bone marrow of young and aged mice
Project description:KRAS mutation is widely presumed to confer independence from upstream RTK signalling, however emerging evidence from mouse models of lung cancer suggests that ERBB RTKs may amplify signalling through RAS isoforms and participate in mutant RAS-driven lung cancer. This is one of 3 datasets where we examined the transcriptional impact of treatment of KRAS mutant human lung cancer cell lines with the multi-ERBB inhibitor Neratinib
Project description:This SuperSeries is composed of the following subset Series: GSE35379: Genome-wide occupancy map of GATA-1 in proliferating and differentiating murine ES cell derived erythroid progenitors (ES-EP) GSE35384: Transcriptome analysis of differentiating normal and leukemic erythroid progenitors Refer to individual Series
Project description:KRAS mutation is widely presumed to confer independence from upstream RTK signalling, however emerging evidence from mouse models of lung cancer suggests that ERBB RTKs may amplify signalling through RAS isoforms and participate in mutant RAS-driven lung cancer. This is one of 3 datasets where we examined the transcriptional impact of treatment of KRAS mutant human lung cancer cell lines with the multi-ERBB inhibitor Neratinib