Description
Key facts
Cell type:U-87 MG,
Species or organism:Human,
Tissue:Brain,
Form:LiquidSee storage information,
Knockout validation:Sanger Sequencing,Western blot,
Mutation description:Knockout achieved by using CRISPR/Cas9, Homozygous: 67 bp deletion in exon 4.,
Disease:Glioblastoma
Product details:
We will provide viable cells that proliferate on revival.
This product is subject to limited use licenses from The Broad Institute and ERS Genomics Limited, and is developed with patented technology. For full details of the limited use licenses and relevant patents please refer to our
limited use license
patent pages
Properties and Storage Information:
Gene name-CSF1, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Western blot, Zygosity-Homozygous, Shipped at conditions-Dry Ice, Appropriate short-term storage conditions--196°C, Appropriate long-term storage conditions--196°C
Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
M-CSF or macrophage colony-stimulating factor is a cytokine involved in the regulation of macrophage production. Alternative names for M-CSF include CSF-1 and colony-stimulating factor 1. The M-CSF protein has a molecular mass of approximately 18 to 22 kDa. M-CSF is mainly expressed in various tissues including the placenta kidney and bone marrow. It functions as a homodimer important for the survival proliferation and differentiation of mononuclear phagocyte lineage cells.
Biological function summary
M-CSF influences the production differentiation and function of macrophages and osteoclasts. It is not part of a large complex but interacts with its receptor the CSF1R (colony-stimulating factor 1 receptor) on the surface of target cells. This interaction promotes the survival and proliferation of the target cells playing significant roles in immune response and bone homeostasis by regulating osteoclast development.
Pathways
The interaction of M-CSF with its receptor is central to several biological pathways notably the immune system pathway and bone resorption pathway. Within these pathways the binding of M-CSF to CSF1R activates downstream signaling cascades such as the PI3K/AKT and MAPK pathways importantly affecting cell survival and differentiation. The M-CSF pathway intersects with other cytokines and factors like GM-CSF (granulocyte-macrophage colony-stimulating factor) which also regulate immune cell dynamics.
Dysregulation of M-CSF levels is implicated in conditions such as osteoporosis and certain cancers. In osteoporosis M-CSF's role in osteoclast development links to increased bone resorption leading to bone loss. In cancers M-CSF overexpression may facilitate tumor-associated macrophage infiltration therefore supporting tumor progression. The interaction with CSF1R is significant as it serves as a potential target for therapeutic strategies aimed at modulating macrophage activity in these diseases.
