Up-regulation of ras-GAP genes is reversed by a MEK inhibitor and doxorubicin in v-Ki-ras-transformed NIH/3T3 fibroblasts

Hashii, Minako; Fukuda, Mitsunori; Nomura, Hideki; Ito, Naoko; Takahashi, Hiroto; Hattori, Satoshi; Mikoshiba, Katsuhiko; Noda, Makoto; Higuchi, Yoshinori

doi:10.1016/j.bbrc.2007.02.133

Cited by 1 publication

(2 citation statements)

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“…We have also isolated two key regulators of the Ras/MAPK signaling pathway. GAP1 m is up-regulated in oncogenic rastransformed fibroblasts [48]. GAP1 m transcript expression is induced by growth factors and is dependent on MEK activity in transformed NIH 3T3 cells [48], which is consistent with our results.…”

Section: Discussionsupporting

confidence: 92%

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Macrophage differentiation of myeloid progenitor cells in response to M-CSF is regulated by the dual-specificity phosphatase DUSP5

Grasset

Gobert-Gosse

Mouchiroud

et al. 2009

Journal of Leukocyte Biology

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M-CSF regulates the production, survival, and function of monocytes and macrophages. The MAPKs ERK1/2 are key elements for signal integration downstream of the M-CSFR, and their sustained activation is essential for macrophage differentiation. In this study, we sought to isolate genes whose induction by M-CSF is dependent on persistent MAPK activation, thereby being possibly involved in the commitment of myeloid progenitors to macrophage differentiation. Following SSH between cDNA libraries from FD-Fms cells stimulated by M-CSF for 8 h in the presence or the absence of the MEK inhibitor U0126, we isolated DUSP5. DUSP5 expression is induced by M-CSF in various myeloid cells and acts as a specific negative-feedback regulator of ERK1/2. In FD-Fms cells that proliferate and differentiate toward macrophages in response to M-CSF, overexpression of DUSP5 increased M-CSF-dependent proliferation and strongly decreased differentiation. Similarly, overexpression of DUSP5 in the multipotent EGER-Fms cells not only significantly increased M-CSF-induced proliferation and prevented macrophage differentiation but also favored granulocytic differentiation. Altogether, experiments demonstrated that DUSP5 is implicated in M-CSF signaling and suggested that it may influence myeloid cell fate.

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Section: Discussionsupporting

confidence: 92%

“…GAP1 m is up-regulated in oncogenic rastransformed fibroblasts [48]. GAP1 m transcript expression is induced by growth factors and is dependent on MEK activity in transformed NIH 3T3 cells [48], which is consistent with our results. However, neither GAP1 m expression nor its role during hematopoiesis has been documented so far.…”

Section: Discussionsupporting

confidence: 92%