ライフサイエンスコーパス: CADM1

1 ll factor (SCF) or cell adhesion molecule 1 (CADM1).

2 ed, and was inhibited by neutralizing SCF or CADM1.

3 with hair follicle keratinocytes expressing Cadm1.

4 helial layer was unaltered in the absence of Cadm1.

5 ree cell surface antigens: PTPRG, ICAM1, and CADM1.

6 mutations in the neuronal cell adhesion gene CADM1.

7 additional four susceptibility loci: 11q23.3 CADM1, a metastasis suppressor gene involved in modifyin

8 C adhesion; linear regression indicated that CADM1 accounts for up to 67% and 32% of adhesion to HLFs

9 m3(-/-)/Cadm1(-/-)), but not in mice lacking Cadm1 and Cadm2 (i.e., Cadm1(-/-)/Cadm2(-/-)).

10 ctive risk variants associate with increased CADM1 and CADM2 expression in the hypothalamus of human

11 bind heterophilically and preferentially to cadm1 and cadm4, respectively.

12 HLMC interactions with HASMCs via CADM1 and Kit inhibit the potentially beneficial effects

13 ter-receptor expression, HLFs expressed both CADM1 and nectin-3, whereas HASMCs expressed only nectin

14 and two loci near cell adhesion molecule 1 (CADM1) and cell adhesion molecule 2 (CADM2), which encod

15 xpress C-type lectin-like receptor 9A, XCR1, CADM1, and TLR3 but lack TLR4 and TLR9.

16 ysis of mouse lens cell membranes identified Cadm1 as a major constituent of the fiber cell membrane

17 e polymorphisms in cell adhesion molecule 1 (CADM1) associated with VT.

18 Downregulation of CADM1 attenuated both HLMC and HMC-1 adhesion to both pr

19 2(-/-)) or Cadm3 and Cadm1 (i.e., Cadm3(-/-)/Cadm1(-/-)), but not in mice lacking Cadm1 and Cadm2 (i.

20 hesion mediated by cell adhesion molecule-1 (CADM1), but the adhesion mechanism through which HLMCs i

21 t not in mice lacking Cadm1 and Cadm2 (i.e., Cadm1(-/-)/Cadm2(-/-)).

22 f four neuronal specific adhesion molecules (CADM1, CADM2, CADM3 and CADM4) that mediate the direct c

23 that in contrast to mice lacking the single Cadm1, Cadm2, or Cadm3 genes, genetic ablation of all th

24 acking Cadm4 (PGK-Cre/Cadm4(fl/fl)), but not Cadm1, Cadm2, or Cadm3, develop focal hypermyelination c

25 with mice lacking different combinations of Cadm1-Cadm3 genes.

26 Somatic mutations of CADM1 cause reversible hypertension and reveal a role fo

27 1(+) cells, cDC2 are CD135(+)CD14(-)CD172a(+)CADM1(+)CD115(+)wCD11R1(+)CD1(+) cells and pDCs are CD4(

28 nerve bundles to eosinophils, mast cells and CADM1(+) cells was also quantified.

29 Eosinophils, mast cells and CADM1(+) cells were observed in close contact or touchin

30 rs from the discovery for suicidal ideation (CADM1, CLIP4, DTNA, KIF2C), prioritization with CFG for

31 With respect to CADM1 counter-receptor expression, HLFs expressed both C

32 The differential expression of CADM1 counter-receptors on HLFs compared to HASMCs may a

33 estless legs syndrome loci, whereas 5 (BBS7, CADM1, CREB5, NRG3, SUN1) have not previously been assoc

34 ed HLMC proliferation and survival through a CADM1-dependent mechanism.

35 Systematic deletion of CADM1 domains indicates that the transmembrane region is

36 Our findings reveal that Cadm1 expression in the hair follicle plays a role in au

37 Reducing Cadm1 expression in the hypothalamus and hippocampus pro

38 Cadm1 expression was analyzed by Western blotting and im

39 suggests that screening tumours for loss of CADM1 expression will help identify those patients most

40 ncluding MACROD2, A2BP1, MCPH1, MAST4, CDH8, CADM1, FOXP1, AUTS2, MBD5, 7q21, 20p, USH2A, KIRREL3, DB

41 CADM1 gene expression analyzed in blood outgrowth endoth

42 th the JAK/STAT inhibitor ruxolitinib mimics CADM1 gene restoration in preventing SqCC growth and met

43 ausative variant to the coding region of the CADM1 gene.

44 lthough not essential for lens transparency, Cadm1 has an indispensable role in establishing and main

45 Cadm1 has been implicated in tumor formation and synapto

46 2 (i.e., Cadm3(-/-)/Cadm2(-/-)) or Cadm3 and Cadm1 (i.e., Cadm3(-/-)/Cadm1(-/-)), but not in mice lac

47 te immunity (EXOC2), dendritic cell biology [CADM1 (IGSF4)], macrophage development (MMD2), TGF-beta

48 Overexpression of Cadm1 in cultured human keratinocytes did not promote cy

49 lly, we have for the first time demonstrated CADM1 in endothelial cells, where it appears to be selec

50 was elevated in obese mice, and induction of Cadm1 in excitatory neurons facilitated weight gain whil

51 hors examined the expression and function of Cadm1 in the mouse lens.

52 Epidermal overexpression of Cadm1 in transgenic mice led to increased autoimmune alo

53 tumour suppressor Cell adhesion molecule 1 (CADM1) inhibits SqCC proliferation and invasion, process

54 Thus, Crtam-Cadm1 interactions have a major impact on the residency

55 Lack of Crtam-Cadm1 interactions in Crtam(-/-) and Cadm1(-/-) mice res

56 During pathogenic infection, Crtam-Cadm1 interactions regulate the dynamic equilibrium betw

57 The immunoglobulin superfamily member Cadm1 is a single-pass, type 1 membrane protein that med

58 Cadm1 is an abundant component of the lens fiber cell me

59 CADM1 is expressed as several isoforms (SP4, SP1, SP6) i

60 Cadm1 is expressed by epidermal cells and mediates heter

61 e ligand of Crtam, cell adhesion molecule 1 (Cadm1), is expressed on gut CD103(+)DCs.

62 this study we have investigated the role of CADM1 isoforms in the adhesion of HLMCs and HMC-1 cells

63 Conversely, we found that CADM1 knockdown accelerates inactivation of endogenous P

64 CADM1 knockdown or mutation inhibited gap junction (GJ)-

65 Targeting SCF and CADM1 may enhance beta2-AR efficacy, particularly in cor

66 These data identify essential roles for Cadm1-mediated neuronal input in weight regulation and p

67 e determine that the extracellular domain of CADM1 mediates these effects by forming a complex with H

68 f Crtam-Cadm1 interactions in Crtam(-/-) and Cadm1(-/-) mice results in loss of CD4(+)CD8(+) T cells,

69 with pirfenidone, while five genes (CLINT1, CADM1, MTDH, SYDE1, and MCTS1) have been associated with

70 kade by Gap27 increased CYP11B2 similarly to CADM1 mutation.

71 ly consists of four members: Cadm4/Necl4 and Cadm1/Necl2 are found in both glia and axons, whereas Ca

72 igated the role of cell adhesion molecule 1 (Cadm1; Necl2) in this disease.

73 Synaptic Cell Adhesion Molecule 1 (SynCAM 1/CADM1/nectin-like 2 protein).

74 We subsequently show that treating CADM1 null tumours with the JAK/STAT inhibitor ruxolitin

75 , in contrast to wild-type lens fiber cells, Cadm1-null fiber cells had an irregular, highly undulati

76 The morphology of individual wild-type and Cadm1-null lens cells was visualized by confocal microsc

77 Lenses from Cadm1-null mice were of normal size and transparency.

78 CADM1 overexpression or downregulation was achieved usin

79 obesity, and tract-tracing analysis revealed Cadm1-positive innervation of POMC neurons via afferent

80 study identifies a novel mechanism by which CADM1 prevents SqCC progression and suggests that screen

81 Loss of Cadm1 protected mice from obesity, and tract-tracing ana

82 PTPRG and CADM1 remain largely unstudied in the context of multipl

83 on was achieved using adenoviral delivery of CADM1 short hairpin RNAs or isoform-specific cDNAs respe

84 pensated by the combined action of Cadm2 and Cadm1.SIGNIFICANCE STATEMENT Myelination by Schwann cell

85 Among the 8 CADM1 single nucleotide polymorphisms genotyped in the c

86 Collectively these data indicate that the CADM1 SP4 isoform is a key receptor mediating human MC a

87 The expression level of CADM1 SP4 strongly predicted the extent of MC adhesion;

88 investigations demonstrated causal roles for CADM1, SPHK1, and YAP/TAZ in mediating metastatic phenot

89 12 genes and of multiple pathways, including CADM1, SPHK1, and YAP/TAZ, whose expression independentl

90 sion system identified the adhesion molecule CADM1/SynCAM that slows the inactivation kinetics of PIE

91 Coculture with Cadm1-transduced MHC-matched APCs stimulated alopecic ly

92 IGSF4/CADM1/TSLC1, a pro-apoptotic cell adhesion molecule of t

93 om various strata of the lens indicated that Cadm1 was degraded during fiber cell differentiation, at

94 In epithelial cells, Cadm1 was enriched in basolateral membranes, whereas, in

95 Cadm1 was present in epithelial and superficial fiber ce

96 rate that cDC1 are CD135(+)CD14(-)CD172a(low)CADM1(+)wCD11R1(+) cells, cDC2 are CD135(+)CD14(-)CD172a