ライフサイエンスコーパス: v-Fos

1 e corresponding to the coiled-coil domain of v-Fos).

2 ells transformed by v-ras, v-src, v-raf, and v-fos.

3 tumorigenesis, that of myristoylation of FBR v-Fos.

4 Myristylation of FBR v-fos, a c-fos retroviral homologue that causes osteosar

5 Retroviral infections with FBR v-fos and G2A-R transform BALB/c-3T3 cells.

6 amination of the tumors reveals that the FBR v-fos bone tumors contain malignant cells with features

7 n the more progressed cell lines 16RH and 18 v-fos but not in the less progressed 16RL or 18 cell lin

8 A non-myristoylated mutant FBR v-Fos caused none of these effects.

9 inkel-Biskis-Reilly (FBR) osteosarcoma virus v-Fos causes tumors of mesenchymal origin, including ost

10 Further transformation by v-fos co-expression renders these keratinocytes tumorige

11 To determine whether myristylation of FBR v-fos contributes to in vivo tumorigenicity, we examined

12 ility in comparison to a nonmyristylated FBR v-fos (G2A-R).

13 e in vitro inhibition of adipogenesis by FBR v-Fos has in vivo significance as immunostaining of FBR

14 ransgenic mice expressing v-rasHa (HK1.ras), v-fos (HK1.fos), or human transforming growth factor alp

15 ety of tumors seen in mice which express FBR v-Fos implies that FBR v-Fos inhibits multiple different

16 n vivo significance as immunostaining of FBR v-Fos-induced tumors shows no CCAAT/enhancer binding pro

17 To study the mechanism of FBR v-Fos' inhibition of mesenchymal differentiation, we uti

18 teristic of terminal differentiation and FBR v-Fos' inhibition of the expression and activity of a ke

19 This inhibition is due to FBR v-Fos' inhibition of the growth arrest characteristic of

20 morphological and biochemical means that FBR v-Fos inhibits adipocyte differentiation in vitro.

21 In addition, FBR v-Fos inhibits DNA-dependent protein kinase, a kinase sp

22 ice which express FBR v-Fos implies that FBR v-Fos inhibits multiple differentiation pathways.

23 orage-independent (16RH) and tumorigenic (18 v-fos) keratinocyte lines compared to the less progresse

24 c to ionizing radiation, as no effect of FBR v-Fos on the UV light signaling pathway was seen.

25 in the increased transforming ability of the v-fos oncogene compared with the c-fos proto-oncogene an

26 We provide evidence that the v-Fos oncogene induces changes in gene expression that r

27 Transformation of fibroblasts with the v-fos oncogene produces a highly invasive phenotype that

28 growth promoting effects of the H-Ras or the v-Fos oncoproteins, since expression of B-ATF restricts

29 mice expressing either the myristylated FBR v-fos or the nonmyristylated G2A-R.

30 pressed genes in cells transformed by c-fos, v-fos, ras or Dnmt1.

31 Cells that express FBR v-Fos show a decreased ability to repair DNA damage caus

32 e two more progressed cell lines 16RH and 18 v-fos showed reduced AP-1 and NF-kappaB activation and r

33 Furthermore, v-Fos-stimulated invasion is independent of the pRb/p16(

34 Biskis-Reilly mouse osteosarcoma virus (FBR) v-fos, the retroviral homologue of the c-fos proto-oncog

35 ts with another non-C/EBP protein designated v-fos transformation effector (FTE), which is identical

36 c revertants, which show partial relief from v-fos transformation-induced alpha1(I) gene suppression.

37 eneChips, and the gene expression profile of v-Fos transformed cells supports its role in the regulat

38 onal silencing of the endogene in normal and v-fos-transformed cells but not in nontumorigenic revert

39 Therefore, we conclude that the ability of v-Fos-transformed cells to invade is dependent upon repr

40 of those genes that are downregulated in the v-Fos-transformed cells.

41 hat has a role in pseudopodial elongation in v-Fos-transformed rat fibroblast cells, forms a novel in

42 izing effects of 2DG were more pronounced in v-Fos-transformed versus nontransformed immortalized rat

43 11 of 26 FBR v-fos transgenic mice died as a result of gross tumor bu

44 ent on a lipid modification required for FBR v-Fos tumorigenesis, that of myristoylation of FBR v-Fos

45 ed by the observation that overexpression of v-Fos, which is highly proficient in transcriptional act