ライフサイエンスコーパス: deleted in colorectal cancer

1 ssural axons by activating its receptor DCC (Deleted in Colorectal Cancer).

2 It mapped close to Dcc (deleted in colorectal cancer).

3 RGC axons express the netrin receptor, DCC (deleted in colorectal cancer).

4 of UNC5B but not UNC5C, UNC5D, neogenin, or deleted in colorectal cancer.

5 cking antibody against the netrin-1 receptor Deleted in Colorectal Cancer.

6 DCC (deleted in colorectal cancer), a candidate tumor suppres

7 at netrin-1 via its transmembrane receptors, deleted in colorectal cancer and uncoordinated-5 homolog

8 naptic cell-adhesion molecules neurexins or 'deleted-in-colorectal-cancer', and the postsynaptic glut

9 transmembrane receptors, represented by DCC (deleted in colorectal cancer) and UNC5.

10 n of the Netrin-1 guidance cue receptor DCC (deleted in colorectal cancer) appear to confer resilienc

11 n of the Netrin-1 guidance cue receptor DCC (deleted in colorectal cancer) appear to confer resilienc

12 idance molecule Netrin and its receptor DCC (deleted in colorectal cancer) attract commissural axons

13 vation of its main attractive receptor, DCC (deleted in colorectal cancer), axons cross the ventral m

14 This event appears to be mediated by DCC (deleted in colorectal cancer), but not neogenin or Unc5h

15 Slit-roundabout repulsion and netrin-deleted in colorectal cancer (DCC) (frazzled) attraction

16 rin-1, a bifunctional guidance cue, binds to deleted in colorectal cancer (DCC) and DSCAM mediating a

17 rowth of axons in vitro through the receptor Deleted in Colorectal Cancer (DCC) and elicits turning o

18 st-derived cells express the netrin receptor deleted in colorectal cancer (DCC) and migrate toward ne

19 Attraction occurs through the receptor Deleted in Colorectal Cancer (DCC) and repulsion occurs

20 Netrin-1 binds its receptors deleted in colorectal cancer (DCC) and the UNC5 homologs

21 In vertebrates, the receptor families deleted in colorectal cancer (DCC) and UNC5 mediate resp

22 Netrin-1 and its receptor Deleted in Colorectal Cancer (DCC) are proteins enriched

23 report in the developing mouse cochlea that deleted in colorectal cancer (Dcc) contributes to the pr

24 elective accumulation of a membrane-tethered deleted in colorectal cancer (DCC) derivative (DCC-alpha

25 The receptor deleted in colorectal cancer (DCC) directs dynamic polar

26 Netrin receptors of the Deleted in Colorectal Cancer (DCC) family are implicated

27 Neogenin, a deleted in colorectal cancer (DCC) family member, has be

28 e have identified a Drosophila member of the deleted in colorectal cancer (DCC) gene family.

29 The deleted in colorectal cancer (DCC) gene, a candidate tum

30 The deleted in colorectal cancer (DCC) homolog neogenin func

31 Deleted in colorectal cancer (DCC) is a well-established

32 We now show that deleted in colorectal cancer (DCC) is subject to proteol

33 The receptor deleted in colorectal cancer (DCC) mediates the attracti

34 lyzed the Probst bundles in both Netrin1 and deleted in colorectal cancer (DCC) mutant mice.

35 ot JNK2 or JNK3, activity in the presence of deleted in colorectal cancer (DCC) or Down syndrome cell

36 Extracellular netrin-1 and its receptor deleted in colorectal cancer (DCC) promote axon branchin

37 of chromosome 18q and lack of expression of deleted in colorectal cancer (DCC) protein has been repo

38 In filopodia, Netrin-1-dependent Deleted in Colorectal Cancer (DCC) receptor activation i

39 of Drosophila, the conserved Frazzled (Fra)/Deleted in Colorectal Cancer (DCC) receptor promotes mid

40 al structure of netrin-1 in complex with the Deleted in Colorectal Cancer (DCC) receptor.

41 Deleted in colorectal cancer (DCC), a large transmembran

42 We show that Deleted in Colorectal Cancer (DCC), a transmembrane prot

43 on techniques, we examined the expression of Deleted in colorectal cancer (DCC), a vertebrate recepto

44 e of APP, CTFs derived from Notch1, Jagged2, deleted in colorectal cancer (DCC), and N-cadherin remai

45 ctant netrin-1, functioning via its receptor Deleted in Colorectal Cancer (DCC), in attracting the le

46 f pioneer neurons and pioneer axons, such as deleted in colorectal cancer (DCC), in most fiber tracts

47 de evidence that in humans, Netrin receptor, Deleted in Colorectal Cancer (DCC), is a master regulato

48 nd netrin-2 in chicks) and netrin receptors [deleted in colorectal cancer (DCC), neogenin, and the ad

49 e interaction of netrin-1 with its receptor, deleted in colorectal cancer (DCC), on sympathetic growt

50 duplications, and they are highly similar to Deleted in Colorectal Cancer (DCC), which functions as a

51 rom midline-expressed Slits and potentiating deleted in colorectal cancer (DCC)-mediated midline attr

52 intact Xenopus brain demonstrated a role for deleted in colorectal cancer (DCC)-mediated netrin signa

53 its attractive function through the receptor Deleted in Colorectal Cancer (DCC).

54 s polyposis coli [APC] gene region) and 18q (deleted in colorectal cancer [DCC] gene region) were rar

55 We propose a model in which the UNC-40 (Deleted in Colorectal Cancer; DCC) receptor captures UNC

56 es with those of Netrin-1-deficient and DCC (deleted in colorectal cancer)-deficient mice.

57 he optic disk and the netrin-1 receptor DCC (deleted in colorectal cancer) expressed on retinal gangl

58 rotein binds to netrin receptors of the DCC (deleted in colorectal cancer) family [DCC and neogenin]

59 The Deleted in Colorectal Cancer gene (DCC) encodes a cell s

60 lelic loss has not been elucidated, the DCC (deleted in colorectal cancer) gene is a candidate.

61 The DCC (Deleted in colorectal cancer) gene was first identified

62 pair, Netrin (Net) and Frazzled (Fra) (DCC, Deleted in Colorectal Cancer, in vertebrates), is recogn

63 Here we report that the netrin receptor DCC (deleted in colorectal cancer) interacts with the focal a

64 DCC (deleted in colorectal cancer) is a candidate tumor suppr

65 DCC (deleted in colorectal cancer) is a functional receptor f

66 DCC (deleted in colorectal cancer) is postulated to function

67 One of these, DCC (deleted in colorectal cancer), is a candidate tumour-sup

68 e Netrins, and their putative receptors DCC (deleted in colorectal cancer), Neogenin, and Unc-5.

69 Inactivating netrin-1, deleted in colorectal cancer, or uncoordinated-5 homolog

70 neuron RIA, the netrin receptor UNC-40 (DCC, deleted in colorectal cancer) plays a conventional guida

71 In neuronal cells, MAZ interacts with DCC (Deleted in Colorectal Cancer product), the receptor for

72 as well as to guidance receptors such as the Deleted in Colorectal Cancer protein and Neogenin.

73 In Caenorhabditis elegans, the UNC-40/DCC (deleted in colorectal cancer) receptor mediates response

74 , acting through its principal receptor DCC (deleted in colorectal cancer), serves as an axon guidanc

75 Inhibiting Netrin/DCC (deleted in colorectal cancer) signaling perturbs the abi

76 Here, we report that in mice lacking Dcc (deleted in colorectal cancer), some early-born neurons c