ライフサイエンスコーパス: L1CAM

1 L1CAM knock-out mice show hypoplasia of the corticospina

2 L1CAM regulates expression of NBS1, a critical component

3 L1CAM(+) and CD133(+) cells cosegregated in gliomas, and

4 ically downstream of the MNR-1/Menorin-SAX-7/L1CAM adhesion complex and upstream of the DMA-1 recepto

5 part of the skin-derived MNR-1/Menorin-SAX-7/L1CAM adhesion complex.

6 The ligand complex SAX-7/L1CAM and MNR-1 function at defined locations in the sur

7 two transmembrane ligands on the skin, SAX-7/L1CAM and MNR-1, and the neuronal transmembrane receptor

8 n [7], and the conserved MNR-1/Menorin-SAX-7/L1CAM cell adhesion complex [8, 9].

9 OA binds to CASY-1/calsyntenin in AVG; SAX-7/L1CAM in sensory neuron PHC binds to RIG-6/contactin in

10 with the neural cell adhesion molecule SAX-7/L1CAM in the skin and through the neuronal leucine-rich

11 LECT-2 localization is dependent on SAX-7/L1CAM, but not on MNR-1/Menorin or DMA-1/LRR-TM, suggest

12 ions between MAGI-1, AFD-1/afadin, and SAX-7/L1CAM, which are part of a functional interactome that i

13 lation of MAGI-1 at junctions requires SAX-7/L1CAM, which can bind MAGI-1 via its C terminus.

14 rn was instructed by adhesion molecule SAX-7/L1CAM, which formed regularly spaced stripes on the hypo

15 similar to the cell adhesion molecule SAX-7/L1CAM.

16 e function of either HMR-1/cadherin or SAX-7/L1CAM.

17 rtem material from a 2-week-old male with an L1CAM mutation revealed normal corticospinal decussation

18 Thus, the cadherin and L1CAM adhesion systems are redundantly required for loca

19 Both cadherin complex components and L1CAM are localized at all sites of cell-cell contact du

20 ons among proteins of the APP, contactin and L1CAM families, with general implications for mechanisms

21 and produced precisely matching control and L1CAM-deficient neurons from these ES cells.

22 ression resulted in upregulation of GAS6 and L1CAM and downregulation of HMGA2.

23 TWIST1, in part via GAS6 and L1CAM, led to higher expression and activation of Akt up

24 Performance for SILV, GDF15, and L1CAM normalized to TYR in unequivocal melanoma versus b

25 etabolic reprogramming, as well as LOXL2 and L1CAM, which encode proteins that are required for lung

26 ession of GLUT1, LDHA, PDK1, LOX, LOXL2, and L1CAM mRNA in human breast cancer biopsies.

27 een identified for duplications of MECP2 and L1CAM.

28 o the outgrowth responses induced by NGF and L1CAM.

29 glioma cells both in vitro and in vivo, and L1CAM may represent a cancer stem cell-specific therapeu

30 ex by combining the roles of neuropilins and L1CAMs.

31 ion molecule, L1CAM, in glioma stem cells as L1CAM regulates brain development and is expressed in gl

32 ism for L1CAM regulation of cell survival as L1CAM knockdown decreased expression of the basic helix-

33 e MMP16 substrate MMP14 (MT1-MMP) as well as L1CAM cell adhesion molecule, identified here as a novel

34 bjects we found that the association between L1CAM interactions and memory maintenance revealed large

35 havior, consistent with interactions between L1CAM and two populations of cytoskeleton proteins.

36 n inhomogeneous surface distribution of both L1CAM and TrkA in various neural cells including neurons

37 int activation and radioresistance caused by L1CAM knockdown, demonstrating that L1CAM signals throug

38 through influencing the p-GSK3/beta-Catenin/L1CAM expression.

39 tastasis by regulating the GSK3/beta-Catenin/L1CAM signaling pathway.

40 yonic stem (ES) cells carrying a conditional L1CAM loss-of-function mutation and produced precisely m

41 e Sema3A receptor, Npn1, and its coreceptor, L1CAM, while the ERM C-terminal domain binds and caps F-

42 usly, we identified a role of the C. elegans L1CAM homolog, SAX-7, in maintaining neuronal and axonal

43 ion gene 2 (LAD-2), a Caenorhabditis elegans L1CAM, functions in axon pathfinding.

44 the spastic diplegia of males hemizygous for L1CAM mutations.

45 We identified a novel mechanism for L1CAM regulation of cell survival as L1CAM knockdown dec

46 ales, but do not support a critical role for L1CAM in corticospinal axonal guidance.

47 These data support a role for L1CAM in corticospinal tract development in hemizygous m

48 Nine genes, MET, PTN, SMO, FZD1, L1CAM, MMP2, NETO2, CTGF, and EDG2, were down-regulated

49 Consequentially, REST-targeted neural genes (L1CAM, beta3-tubulin, synaptophysin, and others) are der

50 on chromosome X in two known disease genes, L1CAM and PAK3, and in two novel candidate CP genes, CD9

51 Mutations in the human L1CAM gene cause X-linked hydrocephalus and MASA (Mental

52 Mutations in one of the human L1CAM genes, L1, can result in several neurological synd

53 uirement for the cell surface targets IGF2R, L1CAM and SLC31A1 in tumor cell growth in vitro, and sug

54 Core fucosylation impacted L1CAM cleavage and the ability of L1CAM to support melan

55 condary to neural cell adhesion molecule L1 (L1CAM) gene mutations includes the distinct finding of b

56 e gene for neural cell adhesion molecule L1 (L1CAM) result in a debilitating X-linked congenital diso

57 e main or sole clinical feature, 2 X-linked (L1CAM and AP1S2) and 2 autosomal recessive (CCDC88C and

58 demonstrate that the Drosophila melanogaster L1CAM homologue Neuroglian mediates adhesion between fun

59 ion proteins including the adhesion molecule L1CAM.

60 y inactivating the axon pathfinding molecule L1CAM, which metastatic cells express for spreading alon

61 tations involving L1 cell adhesion molecule (L1CAM) and integrin signaling pathways; and (iv) APOBEC-

62 ish the L1 family of cell adhesion molecule (L1CAM) binding to ankyrin in cultured cells.

63 L1 cell adhesion molecule (L1CAM) gene mutations are associated with X-linked 'rece

64 ousal, and of the L1 cell adhesion molecule (L1CAM) interactions gene set with the repetition-based m

65 The L1 cell adhesion molecule (L1CAM) participates in neuronal development.

66 sion, among which L1 cell adhesion molecule (L1CAM) was significantly higher upon a reduction of C1QB

67 The L1 cell adhesion molecule (L1CAM), a member of the Ig superfamily, plays a crucial

68 amily immunoglobulin cell adhesion molecule (L1CAM), along the Purkinje AIS-soma axis.

69 e 4 (ANGPTL4) and L1 cell adhesion molecule (L1CAM).

70 e role of a neuronal cell adhesion molecule, L1CAM, in glioma stem cells as L1CAM regulates brain dev

71 -pass transmembrane cell adhesion molecules (L1CAMs) is conserved from Caenorhabditis elegans and Dro

72 The L1 family of cell adhesion molecules (L1CAMs) is important for neural development.

73 n impacted L1CAM cleavage and the ability of L1CAM to support melanoma invasion.

74 To understand the basis of L1CAM function in adhesion and migration, we quantified

75 ed directly the diffusion characteristics of L1CAM on the upper surface of ND-7 neuroblastoma hybrid

76 nt ES cell clones, we found that deletion of L1CAM dramatically impaired axonal elongation and, to a

77 Hundreds of L1CAM gene mutations have been shown to be associated wi

78 Moreover, inhibitors of L1CAM-ankyrin interactions promote L1CAM-mediated axon g

79 tive ADF/cofilin and reduced by knockdown of L1CAM.Together, these data suggest that ERM proteins org

80 cells cosegregated in gliomas, and levels of L1CAM were higher in CD133(+) glioma cells than normal n

81 g the actin-dependent retrograde movement of L1CAM.

82 ls that regulate tyrosine phosphorylation of L1CAM members and modulate their binding to ankyrin.

83 s suggest that the clinical presentations of L1CAM mutations in human patients could be accounted for

84 al role in the anti-coordinate regulation of L1CAM-mediated adhesion and migration.

85 h glioma xenograft model, shRNA targeting of L1CAM expression in vivo suppressed tumor growth and inc

86 ity of GSCs through nuclear translocation of L1CAM intracellular domain (L1-ICD).

87 ults implicate ankyrin-based localization of L1CAMs in subcellular organization of GABAergic synapses

88 These results reveal a recruitment of L1CAMs to the DPC to ensure neural integrity is maintain

89 The extracellular region of L1CAMs mediates cell adhesion via interactions with dive

90 Interference with HIF, ANGPTL4 or L1CAM expression inhibits vascular metastasis of BrCa ce

91 hese genes demonstrated that loss of GAS6 or L1CAM sensitized cells to cisplatin, but that loss of HM

92 ut not on those binding exclusively Itgb1 or L1CAM, DS GCs were significantly enlarged (2.0-fold), fo

93 bitors of L1CAM-ankyrin interactions promote L1CAM-mediated axon growth.

94 by NGF, but also by the L1 adhesion protein, L1CAM, whose soluble construct binds the receptor with s

95 We find that cell surface L1CAM engages in diffusion, retrograde movement, and sta

96 stem cell tumor growth in vivo, we targeted L1CAM in glioma cells before injection into immunocompro

97 Targeting L1CAM by RNA interference attenuated DNA damage checkpoi

98 Targeting L1CAM using lentiviral-mediated short hairpin RNA (shRNA

99 To determine if targeting L1CAM was sufficient to reduce glioma stem cell tumor gr

100 These data demonstrate that L1CAM augments DNA damage checkpoint activation and radi

101 aused by L1CAM knockdown, demonstrating that L1CAM signals through NBS1 to regulate DNA damage checkp

102 Here, we show that L1CAM (CD171) regulates DNA damage checkpoint responses

103 Together, these data show that L1CAM is required for maintaining the growth and surviva

104 Taken together, these results indicate that L1CAMs constitute a family of ubiquitous adhesion molecu

105 ofascin, which is highly conserved among the L1CAM family of cell adhesion molecules, and describes s

106 tis elegans animals genetically null for the L1CAM homologue LAD-1, exhibit variably penetrant pleiot

107 function of the intracellular domains in the L1CAM cytoplasmic tail.

108 Neurofascin, a member of the L1CAM family of ankyrin-binding cell adhesion molecules,

109 yrin binding to neurofascin, a member of the L1CAM family of nervous system cell adhesion molecules.

110 xpression of wild-type L1CAM, but not of the L1CAM point mutants R1166X and S1224L, rescued the decre

111 Importantly, we found that the L1CAM mutation selectively decreased activity-dependent

112 In the intact wtPC12, the L1CAM construct induced autophosphorylation and internal

113 Overexpression of wild-type L1CAM, but not of the L1CAM point mutants R1166X and S12

114 tor that inhibits EC-EC interaction, whereas L1CAM increases the adherence of BrCa cells to ECs.

115 e a useful technique to screen for boys with L1CAM mutations.

116 of the basis pontis in 4 affected boys with L1CAM mutations.

117 A with high REST PC12 cells transfected with L1CAM documented the transactivation of the receptor by