ライフサイエンスコーパス: c-Fes

1 iated with and dephosphorylated Jak2 but not c-fes.

2 have previously shown that 151 base pairs of c-fes 5'-flanking sequences are sufficient for myeloid c

3 onstrated that plasmids containing 446 bp of c-fes 5'-flanking sequences linked to a luciferase repor

4 has established that BCR is a substrate for c-FES, a non-receptor tyrosine kinase linked to myeloid

5 nal transduction by transforming variants of c-Fes, a nonreceptor tyrosine kinase implicated in cytok

6 a retroviral homolog of c-Fes (v-Fps) and by c-Fes activated via N-terminal addition of the v-Src myr

7 nucleation assay, we observed that purified c-Fes also catalyzed extensive tubulin polymerization in

8 n-tyrosine kinase (Abl) distinct from c-Src, c-Fes, and other cytoplasmic tyrosine kinases.

9 Taken together, these results identify c-Fes as a regulator of the tubulin cytoskeleton that ma

10 osine kinome in colorectal cancer identified c-fes as one of only seven genes with consistent kinase

11 y stages of myeloid differentiation, such as c-fes, c-pim, granulocyte-macrophage colony-stimulating

12 Mutation or deletion of the more N-terminal c-Fes coiled-coil domain reversed negative regulation, l

13 hen this 2.5-kb DNA fragment was linked to a c-fes complementary DNA regulated by its own 446-base-pa

14 Structurally, c-Fes consists of a unique N-terminal region harboring a

15 We demonstrate that the c-fes(Delta c/Delta c) allele results in a truncated Fes

16 In vitro differentiation of c-fes(Delta c/Delta c) ES cells results in hyperprolifer

17 Generation of c-fes(Delta c/Delta c) mutant chimeric mice causes letha

18 sine kinase domains of c-fes (referred to as c-fes(Delta c/Delta c)).

19 To study the role of c-fes during myelopoiesis, we generated embryonic stem (

20 atopoietic transcription factor, termed FEF (c-fes expression factor), binds to a cis-acting element

21 that are derived from genes, such as c-Abl, c-Fes, Flt3, c-Fms, c-Kit and PDGFRbeta, that are normal

22 Previous studies have established that c-Fes forms high molecular weight oligomers in vitro, su

23 Here we show for the first time that c-Fes forms oligomers in live cells independently of its

24 We conclude that the human c-fes gene contains a strong myeloid-cell-specific promo

25 yeloid-cell-specific expression of the human c-fes gene have not been defined.

26 nscription regulatory sequences of the human c-fes gene.

27 A 13.2-kilobase (kb) human c-fes genomic fragment was previously shown to contain c

28 mRNA for c-fes has been detected exclusively in myeloid cells and

29 avian and feline transforming retroviruses, c-Fes has recently been implicated as a tumor suppressor

30 ransgene expression comparable to endogenous c-fes, independent of integration site.

31 These results establish that c-fes is an important regulator of myeloid cell prolifer

32 In living cells, c-Fes kinase activity is tightly regulated by a mechanis

33 No other DNA element within the 13-kb human c-fes locus contained positive cis-acting elements, with

34 The c-fes locus encodes a 93-kDa non-receptor protein tyrosi

35 The human c-fes locus encodes a non-receptor protein-tyrosine kina

36 (ES) cells with a targeted disruption of the c-fes locus.

37 we engineered a null mutation of the murine c-fes locus.

38 c-fes-/- mice are viable but not born in the expected Me

39 Live born c-fes-/- mice exhibit lymphoid/myeloid homeostasis defec

40 rminal coiled-coil regions are essential for c-Fes oligomerization in transfected COS-7 cells as well

41 phosphorylation of Jak2 and had no effect on c-fes phosphorylation.

42 s immediately 3' of the FEF site in both the c-fes promoter and the chicken lysozyme enhancer (CLE),

43 at is located at nucleotides -9 to -4 of the c-fes promoter between two Ets binding sites (at -19 to

44 t PU.1 (and not Elf-1) can transactivate the c-fes promoter in nonmyeloid cell lines.

45 els of transcription by both the CLE and the c-fes promoter in transient transfection experiments.

46 tion of the adjacent PU.1 site in either the c-fes promoter or the CLE, reduces activity by approxima

47 e 3' site (FP4-3') within the context of the c-fes promoter resulted in substantially reduced activit

48 e describe a functional PU.1 site within the c-FES promoter which SPI-B fails to bind efficiently and

49 site, analogous to their arrangement in the c-fes promoter, and allows the formation of a preliminar

50 The c-Fes protein-tyrosine kinase (Fes) has been implicated

51 ogether, our findings strongly implicate the c-Fes protein-tyrosine kinase as a tumor suppressor rath

52 The c-Fes protein-tyrosine kinase exhibits strong expression

53 The c-Fes protein-tyrosine kinase regulates the growth and d

54 The c-fes proto-oncogene encodes a 92-kd protein tyrosine ki

55 The human c-fes proto-oncogene encodes a cytoplasmic tyrosine kina

56 The c-fes proto-oncogene encodes a non-receptor tyrosine kin

57 The c-fes proto-oncogene encodes a unique nonreceptor protei

58 The protein product of the c-fes proto-oncogene has been implicated in the normal d

59 protein closely related or identical to the c-fes proto-oncogene product (FES) and association of th

60 The protein product of the c-fps/fes (c-fes) proto-oncogene has been implicated in the normal

61 The c-fes protooncogene encodes a nonreceptor tyrosine kinas

62 The c-fes protooncogene encodes a nonreceptor tyrosine kinas

63 -terminal SH2 and tyrosine kinase domains of c-fes (referred to as c-fes(Delta c/Delta c)).

64 The c-fes regulatory unit represents a novel reagent for tar

65 unique nonreceptor protein-tyrosine kinase (c-Fes) that contributes to the differentiation of myeloi

66 this report, we provide direct evidence that c-Fes, the normal human homolog of v-Fps, potently activ

67 c-Fes, thought to be involved in intracellular vesicle t

68 Although a 13-kilobase-pair (kb) human c-fes transgene exhibits high levels of expression in mi

69 To identify sequences required for this LCR, c-fes transgenes were analyzed in mice.

70 dence for coiled-coil-mediated regulation of c-Fes tyrosine kinase activity and signaling, a mechanis

71 , these data provide the first evidence that c-Fes, unlike c-Src, c-Abl, and other nonreceptor tyrosi

72 st transformation by a retroviral homolog of c-Fes (v-Fps) and by c-Fes activated via N-terminal addi

73 In this report, c-Fes was expressed in Saccharomyces cerevisiae to deter

74 oietic cells demonstrated that Jak2, but not c-fes, was present in anti-SHP-1 immunoprecipitates, sug