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Expression data from RAD21 knockdown in MCF7 cells

ABSTRACT: RAD21 plays multi-functional roles in cell. We explored which genes are target of RAD21 in the cell. We used microarray to find out the target of RAD21 comparing between shGFP(control) and shRAD21 expressing MCF7 cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE82049 | GEO | 2016/06/01

SECONDARY ACCESSION(S): PRJNA323814

REPOSITORIES: GEO

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Expression data from RAD21 knockdown in MCF7 cells

Project description:RAD21 plays multi-functional roles in cell. We explored which genes are target of RAD21 in the cell. We used microarray to find out the target of RAD21 comparing between shGFP(control) and shRAD21 expressing MCF7 cells. we stably expressed shGFP or shRAD21 in each MCF7 cell and selected single cells having high transfection efficiency of shRNAs. And then we had cultured the single cells for 30 days to harvest sufficient cells.

2016-06-01 | E-GEOD-82049 | biostudies-arrayexpress

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Project description:MTD project_description Inflammation and decreased stem cell function characterize organism aging, yet the relationship between these factors remains incompletely understood. This study shows that aged hematopoietic stem and progenitor cells exhibit increased ground-stage NF-κB activity, which enhances their responsiveness to undergo differentiation and loss of self-renewal in response to inflammation. The study identifies Rad21/cohesin as a critical mediator of NF-κB signals, by increasing chromatin accessibility of inter-/intra-genic and enhancer regions. Rad21/NF-κB are required for normal differentiation, but limit self-renewal of hematopoietic stem cells (HSCs) during aging and inflammation in an NF-κB dependent manner. HSCs from aged mice fail to downregulate Rad21/cohesin and inflammation/differentiation inducing signals in the resolution phase after acute inflammation. and The inhibition of cohesin/NF-κB is sufficient to revert the hypersensitivity of aged HSPCs to inflammation-induced differentiation. During aging, myeloid-biased HSCs with disrupted and naturally occurring reduced expression of Rad21/cohesin are increasingly selected over lymphoid-biased HSCs. Together, Rad21/cohesin mediated NF-κB signaling limits HSPC function during aging and selects for cohesin deficient HSCs with myeloid skewed differentiation.

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