1              Messenger RNAs from resting and mitogenically activated fibroblasts were separated, acco

2 in (MAP) kinase activation by insulin in the mitogenically active 3T3-L1 fibroblasts with the metabol

3 he Epo-R, activated Jak2 and Jak3 and was as mitogenically active as the wild-type IL2beta-R (Jak1 an

4 f insulin signaling in the metabolically and mitogenically active cells.

5  that the truncated enzyme compensated for a mitogenically defective CSF-1R by interfering with this

6 roblast growth factor receptor 1 variant are mitogenically inactive and ligand binding to the recepto

7 1 is released in response to heat shock as a mitogenically inactive Cys-30 homodimer, we sought to de

8 184B5 and 32D/c-Met cells, while HGF/NK2 was mitogenically inactive, despite the ability of HGF/NK2 t

9 dent DNA synthesis in the cells expressing a mitogenically incompetent mutant betaPDGFR, but only whe

10 ant ligand-receptor pairs we have engineered mitogenically responsive cell lines expressing the major

11  but was detected only at low levels even in mitogenically stimulated adult SMCs.

12 as been proposed for oncogene-transformed or mitogenically stimulated cells, in differentiating kerat

13 s exhibit layers of regulation distinct from mitogenically stimulated cells.

14  of a Tat-associated CTD kinase derived from mitogenically stimulated human primary T lymphocytes (TT

15 ing power indicate increased cell cycling in mitogenically stimulated splenocytes, whereas these two

16 ion of IGF-IR and IRS-1 levels and responded mitogenically to both estrogen and IGF-I.

17 ng, we demonstrate that the Wnt pathway acts mitogenically to expand the populations of neuronal prog

18 ately express high levels of Met and respond mitogenically to HGF/SF.

19                             32D.E4 responded mitogenically to NRG1-beta and BTC.

20         Homozygous mutant cell lines respond mitogenically to TGFalpha, EGF, FGF1, and FGF2.