Accumulation of cells expressing macrophage colony-stimulating factor receptor gene in the ovary of a pregnant viviparous fish, Neoditrema ransonnetii (Perciformes, Embiotocidae)

2016 ◽  
Vol 50 ◽  
pp. 223-230 ◽  
Author(s):  
Kazuki Ueda ◽  
Erina Saito ◽  
Kaoru Iwasaki ◽  
Shigeyuki Tsutsui ◽  
Aoi Nozawa ◽  
...  
Keyword(s):  
Receptor Gene ◽  
Colony Stimulating Factor ◽  
Viviparous Fish ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

Induction of macrophage colony-stimulating factor-dependent growth and differentiation after introduction of the murine c-fms gene into FDC-P1 cells

1989 ◽  
Vol 9 (11) ◽  
pp. 5081-5092
Author(s):  
L R Rohrschneider ◽  
D Metcalf
Keyword(s):  
Gene Product ◽  
Morphological Changes ◽  
Receptor Gene ◽  
Myeloid Differentiation ◽  
Colony Stimulating Factor ◽  
Retroviral Infection ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Dependent Growth ◽  
Stimulating Factor

A system has been established for analyzing the functions of the c-fms/macrophage colony-stimulating factor (M-CSF) receptor gene product in hematopoietic growth and differentiation. The murine c-fms gene was introduced into the factor-dependent murine hematopoietic cell line FDC-P1 by retroviral infection, and conversion to M-CSF-dependent growth was assayed in agar cultures. Expression of the c-fms gene in FDC-P1 cells, which normally do not express this gene, resulted in the conversion of resultant FD(c-fms) cells to M-CSF-dependent growth. Stimulation of FD(c-fms) cells by M-CSF led to the formation of colonies of altered morphology and produced reversible morphological changes suggestive of myeloid differentiation. M-CSF also induced expression of mature myeloid surface marker proteins in the FD(c-fms) cells. Neither multi-CSF nor granulocyte-macrophage CSF induced similar phenotypic changes but remained able to stimulate the proliferation of undifferentiated FD(c-fms) cells. These results indicate that the c-fms gene was expressed functionally in FDC-P1 cells and transmitted signals for growth. Also, the interaction of M-CSF with the c-fms gene product generated an additional signal for myeloid differentiation but did not irreversibly commit FD(c-fms) cells to terminal differentiation. This system can be used for molecular analysis of the growth- and differentiation-promoting activities of the c-fms proto-oncogene.

Transcriptional Activation of the Granulocyte–Macrophage Colony-Stimulating Factor Receptor Gene in Cell Mutants

2000 ◽  
Vol 259 (1) ◽  
pp. 1-11
Author(s):  
Christine Laker ◽  
Jutta Friel ◽  
Marie-Josée Franz ◽  
Takahiko Hara ◽  
Panos Papadopoulos ◽  
...  
Keyword(s):  
Transcriptional Activation ◽  
Receptor Gene ◽  
Colony Stimulating Factor ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

scholarly journals Induction of macrophage colony-stimulating factor-dependent growth and differentiation after introduction of the murine c-fms gene into FDC-P1 cells.

1989 ◽  
Vol 9 (11) ◽  
pp. 5081-5092 ◽  
Author(s):  
L R Rohrschneider ◽  
D Metcalf
Keyword(s):  
Gene Product ◽  
Morphological Changes ◽  
Receptor Gene ◽  
Myeloid Differentiation ◽  
Colony Stimulating Factor ◽  
Retroviral Infection ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Dependent Growth ◽  
Stimulating Factor

A system has been established for analyzing the functions of the c-fms/macrophage colony-stimulating factor (M-CSF) receptor gene product in hematopoietic growth and differentiation. The murine c-fms gene was introduced into the factor-dependent murine hematopoietic cell line FDC-P1 by retroviral infection, and conversion to M-CSF-dependent growth was assayed in agar cultures. Expression of the c-fms gene in FDC-P1 cells, which normally do not express this gene, resulted in the conversion of resultant FD(c-fms) cells to M-CSF-dependent growth. Stimulation of FD(c-fms) cells by M-CSF led to the formation of colonies of altered morphology and produced reversible morphological changes suggestive of myeloid differentiation. M-CSF also induced expression of mature myeloid surface marker proteins in the FD(c-fms) cells. Neither multi-CSF nor granulocyte-macrophage CSF induced similar phenotypic changes but remained able to stimulate the proliferation of undifferentiated FD(c-fms) cells. These results indicate that the c-fms gene was expressed functionally in FDC-P1 cells and transmitted signals for growth. Also, the interaction of M-CSF with the c-fms gene product generated an additional signal for myeloid differentiation but did not irreversibly commit FD(c-fms) cells to terminal differentiation. This system can be used for molecular analysis of the growth- and differentiation-promoting activities of the c-fms proto-oncogene.

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