ライフサイエンスコーパス: L1CAM

1 L1CAM expressing TLS are most common in mismatch-repair

2 L1CAM is a transmembrane protein expressed on neurons th

3 L1CAM knock-out mice show hypoplasia of the corticospina

4 L1CAM regulates expression of NBS1, a critical component

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

6 L1CAM-positive extracellular vesicles (L1EV) are an emer

7 L1CAM-positive extracellular vesicles (L1EV) were immuno

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

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

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

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

12 elopment requires the adhesion protein SAX-7/L1CAM and the cytoplasmic protein GRDN-1/CCDC88C to anch

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

14 We found that the SAX-7/L1CAM cell adhesion molecule engages in distinct molecul

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

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

17 SAX-7/L1CAM, a hypodermal component of this complex, shows a m

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

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

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

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

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

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

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

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

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

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

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

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

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

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

32 state in neuroblastoma as well as GSK3B and L1CAM that are involved in neuronal cell adhesion and mi

33 Overexpression of IGF2 and L1CAM was associated with decreased response to neoadjuv

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

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

36 een identified for duplications of MECP2 and L1CAM.

37 son with the presumed NDEV markers NCAM1 and L1CAM by using super-resolution microscopy and biochemic

38 o the outgrowth responses induced by NGF and L1CAM.

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

40 ex by combining the roles of neuropilins and L1CAMs.

41 r prevention mouse model, (161)Tb-based anti-L1CAM radioimmunotherapy as a new therapeutic modality a

42 e clinics by establishing (161)Tb-based anti-L1CAM radioimmunotherapy as a novel therapeutic modality

43 We found that (161)Tb-based anti-L1CAM radioimmunotherapy eliminated ovarian CSCs more ef

44 SCs more efficiently than (177)Lu-based anti-L1CAM radioimmunotherapy, emphasizing its promising ther

45 gainst CSCs compared with (177)Lu-based anti-L1CAM radioimmunotherapy.

46 erived exosomes (NDEs) were enriched by anti-L1CAM antibody immunoabsorption from plasmas of subjects

47 After radiolabeling anti-L1CAM DOTA-chCE7 with (177)Lu or (161)Tb and purificatio

48 We demonstrate that treatment with the anti-L1CAM antibody Ab417 decreases L1CAM overexpression and

49 mmunocapture of neuronal exosomes using anti-L1CAM antibodies, prior to the array-based assaying of a

50 ently extracted from patient sera using anti-L1CAM conjugated zwitterionic polymer-modified magnetic

51 Furthermore, pathways regulated by APP, L1CAM, and genes of the caspase family may represent pro

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

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

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

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

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

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

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

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

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

61 y plasmin, and increased shedding of cleaved L1CAM in the cerebrospinal fluid.

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

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

64 CWH43 deletion also decreased L1CAM nuclear translocation, suggesting decreased L1CAM

65 nuclear translocation, suggesting decreased L1CAM intracellular signaling.

66 with the anti-L1CAM antibody Ab417 decreases L1CAM overexpression and nuclear translocation and persi

67 ult-onset iNPH by selectively downregulating L1CAM in the ventricular and subventricular zone.

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

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

70 S in outcome of EC patients, and establishes L1CAM as a simple biomarker.

71 Thus, our findings identify PyN-expressed L1CAM as a critical CAM required for innervation of neoc

72 an increased number of exosomes enriched for L1CAM, a marker predominantly expressed in the brain, in

73 the spastic diplegia of males hemizygous for L1CAM mutations.

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

75 tennary N-glycans with select preference for L1CAM and other N-glycoproteins with multiple N-glycans

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

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

78 expression analyses demonstrate that AR-FUT4-L1CAM-AJs signaling correlates with pathological staging

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

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

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

82 analysis of CUT&Tag with RNA-seq highlighted L1CAM (L1 cell adhesion molecule), a known endothelial-t

83 g CRISPR/Cas9 gene editing, we modeled human L1CAM and CRB2 mediated aqueductal stenosis.

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

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

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

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

88 relationship between expression of IRS-1 in L1CAM(+) exosomes and systemic IR as assessed by homeost

89 es in serine-312 phosphorylation of IRS-1 in L1CAM(+) exosomes in subjects with MDD.

90 the insulin receptor substrate-1 (IRS-1) in L1CAM(+) exosomes in subjects with MDD as compared with

91 Importantly, the increase in L1CAM cleavage occurred primarily in the ventricular and

92 The increased IRS-1 levels in L1CAM(+) exosomes were greater in subjects with MDD and

93 Loss-of-function mutations in L1CAM are a common cause of severe neurodevelopmental de

94 cell membrane lipid microdomains, increased L1CAM cleavage by plasmin, and increased shedding of cle

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

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

97 The cell adhesion molecule L1 (L1CAM, L1 in short) plays crucial roles during neural de

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

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

100 Strikingly, we found the L1 family member L1CAM to be the only molecule required for ChC/PyN AIS i

101 Methods: L1CAM(+)/CD133(+) CSCs were examined in OC samples by im

102 (2019) identify the cell adhesion molecule L1CAM as integral to the mechanism by which chandelier c

103 soform of the cell-surface adhesion molecule L1CAM, termed L1-DeltaTM.

104 ion proteins including the adhesion molecule L1CAM.

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

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

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

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

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

110 L1 cell adhesion molecule (L1CAM) is a targetable CSC-associated biomarker aberrant

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

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

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

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

115 FUT4 fucosylates L1 cell adhesion molecule (L1CAM), which is required for FUT4-increased metastatic

116 beads to isolate L1 cell adhesion molecule (L1CAM)-positive extracellular vesicles with characterist

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

118 mutations in the L1 cell adhesion molecule (L1CAM, hereafter abbreviated L1) were identified in L1 s

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

120 se expression of the cell adhesion molecule, L1CAM, in the brains of CWH43 mutant mice and in human H

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

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

123 neral EV marker CD9 and markers for neurons (L1CAM, CD171), astrocytes (EAAT1), and oligodendrocytes

124 ng vascular DNA damage by inhibiting nuclear L1CAM translocation might effectively prevent anticancer

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

126 f PyN AISs by ChCs requires AIS anchoring of L1CAM by the cytoskeletal ankyrin-G/betaIV-spectrin comp

127 osylation of L1CAM, decreased association of L1CAM with cell membrane lipid microdomains, increased L

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

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

130 vascular fibrosis and the colocalization of L1CAM and DNA damage foci, while Ab417 attenuates these

131 ndMT) correlating with the colocalization of L1CAM and persistent DNA damage foci.

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

133 lls (CICs) identified by their expression of L1CAM/CD133 and highest telomerase activity.

134 letion leads to decreased N-glycosylation of L1CAM, decreased association of L1CAM with cell membrane

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

136 CAM expression in mature TLS, independent of L1CAM expression in the tumor.

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

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

139 We infer that low levels of L1CAM and CD81 (and other membrane proteins) are likely

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

141 g the actin-dependent retrograde movement of L1CAM.

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

143 of this study was to confirm the presence of L1CAM(+)/CD133(+) ovarian CSCs in patient samples and pr

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

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

146 Simultaneous silencing of L1CAM and REST in human aortic endothelial cells inhibit

147 necessary and sufficient for the skipping of L1CAM transmembrane domain in ECs, leading to the releas

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

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

150 molecule array assays to evaluate the use of L1CAM for NDEV isolation.

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

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

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

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

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

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

157 Like their vertebrate orthologs L1CAM and NCAM1/2, respectively, Nrg and Fas2 are cell a

158 Ovarian L1CAM(+)/CD133(+) CSCs were sorted via fluorescence-acti

159 tumor analysis confirmed that sorted ovarian L1CAM(+)/CD133(+) CSCs regenerated the tumor heterogenei

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

161 nd the levels of the neural adhesion protein L1CAM and the transferrin receptor (TFR1) are significan

162 by anti-human CD171 neural adhesion protein (L1CAM) antibody and extracted proteins quantified with E

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

164 Results: L1CAM(+)/CD133(+) CSCs (0.3%-21%) were confirmed in samp

165 istochemistry and co-immunofluorescence show L1CAM expression in mature TLS, independent of L1CAM exp

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

167 on of neural marker proteins, synaptophysin, L1CAM, NeuN, and GFAP was not significantly altered by E

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

169 Targeting L1CAM by RNA interference attenuated DNA damage checkpoi

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

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

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

173 We demonstrate that L1CAM is not associated with extracellular vesicles in h

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

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

176 Further, we show that L1CAM is required during both the establishment and main

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

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

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

180 in (HMP-1) and beta-catenin (HMP-2), and the L1CAM protein SAX-7.

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

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

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

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

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

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

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

188 licing factor NOVA2, which binds directly to L1CAM pre-mRNA, is necessary and sufficient for the skip

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

190 with persistent DNA damage show upregulated L1CAM and EndMT, indicating clinical applicability of Ab

191 Using L1CAM as a marker, 378 of the 411 molecularly classified

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

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

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

195 ssion analysis shows association of TLS with L1CAM overexpression.

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