Project description:Sca1+/cKit– hematopoietic BMCs of hosts bearing instigating tumors (BPLER) promote the growth of responding (HMLER-HR) tumors that form with a myofibroblast-rich, desmoplastic stroma. BMCs from mice bearing Non-instigating tumors lack this ability Sca1+/cKit- BMCs were isolated from mice bearing Matrigel control or size-matched instigating or non-instigating tumors by FACS directly into Trizol reagent (Invitrogen).
Project description:Sca1+/cKitâ hematopoietic BMCs of hosts bearing primary tumors promote the growth of distant tumors that form with a myofibroblast-rich, desmoplastic stroma. BMCs from old mice bearing primary tumors lack this ability Sca1+/cKit- BMCs were isolated from young and old mice bearing Matrigel control or size-matched primary tumors by FACS directly into RLT Plus Buffer (Qiagen Rneasy Plus Micro Kit)
Project description:Sca1+/cKit– hematopoietic BMCs of hosts bearing instigating tumors (BPLER) promote the growth of responding (HMLER-HR) tumors that form with a myofibroblast-rich, desmoplastic stroma. BMCs from mice bearing Non-instigating tumors lack this ability
Project description:Sca1+/cKit– hematopoietic BMCs of hosts bearing primary tumors promote the growth of distant tumors that form with a myofibroblast-rich, desmoplastic stroma. BMCs from old mice bearing primary tumors lack this ability
Project description:To study the effect of miR-221/222-deficiency on early hematopoietic lineage differentiation pathways on sorted multipotent progenitor (MPP), common lymphoid progenitor (CLP), lineage-ckit+Sca1- and lineage-ckit-Sca1- populations of miRNA-proficient and deficient mice.
Project description:WT GMPs (Lin- IL7R- Sca1- ckit+ FcgRhiCD34+) and inv(16)/KITD816Y GMPs (Lin- Sca1- ckit+ CD41- FcgR+ CD150-) were FACS sorted as described in material and methods from supplementary data (Estruch M et al 2020)
Project description:Gene expression analyses of hematopoietic stem cells (HSCs), progenitor cells (HPCs), and differentiated cell. Gene expressions of long-term HSCs (CD34-ckit+Sca1+Lineage-), short term HSCs (CD34+ckit+Sca1+Lineage-), Progenitor cells (ckit+Sca1- Lineage-), and differentiated cels (Lineage+) were examined by microarray. Results provide insight into the mechanism of hematopoietic cell differentiation. Long-term HSCs (CD34-ckit+Sca1+Lineage-), Short term-HSCs (CD34+ckit+Sca1+Lineage-), Progenitor cells (ckit+Sca1- Lineage-, and Lineage+), and differentiated cell (Lineage+) were sorted from mouse bone marraw and were examined by microarray. Results provide insight into the mechanism of hematopoietic cell differentiation.
Project description:Gene Expression profiling of HSCs isolated at different stages of ontogeny to address correlation between gene expression and changes in DNA methylation Gene expression profiling of hematopoietic stem cells isolated from e14.5 fetal liver (lineage- ckit+ sca1+CD150+ CD48- Mac1+), 3 month old mice (lineage- ckit+ sca1+ CD34- Flk2-) and 25 month old mice (lineage- ckit+ sca1+ CD34- Flk2-)
Project description:The study profiled the effect of Phf6 deletion on gene expression in hematopoietic stem cells (HSCs), multipotent progenitor cells (MPPs) and hematopoietic progenitor cells (HPC-1). Phf6lox/Y;Tie2-creTg/+ mice were prepared on a C57BL/6 background so that Phf6 deletion could be selectively mediated by Tie2-cre. Cell populations were sorted from bone marrow samples using standard surface markers (Lin–SCA1+cKIT+(LSK) CD150+ CD48– for HSCs, Lin–SCA1+cKIT+(LSK) CD150– CD48– for MPPs and Lin–SCA1+cKIT+(LSK) CD150- CD48+ for HPC-1 cells). Phf6 intact and Phf6-delected cells of all three types were profiled by paired-end RNA-seq using an Illumina NextSeq 500 sequencer. RNA-seq libraries were prepared from the HPC-1 samples used a standard Illumina TruSeq library protocol whereas the libraries for the HSC and MPP samples used a SMART-seq ultra low input kit for cDNA synthesis and amplification. Statistical analysis of the TruSeq and SMART-seq samples was undertaken separately.
