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

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

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

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

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

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

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

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

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

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

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

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

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

18 1(+) cells, cDC2 are CD135(+)CD14(-)CD172a(+)CADM1(+)CD115(+)wCD11R1(+)CD1(+) cells and pDCs are CD4(

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

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

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

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

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

24 Reducing Cadm1 expression in the hypothalamus and hippocampus pro

25 Cadm1 expression was analyzed by Western blotting and im

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

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

28 CADM1 gene expression analyzed in blood outgrowth endoth

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

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

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

32 Cadm1 has been implicated in tumor formation and synapto

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

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

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

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

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

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

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

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

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

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

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

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

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

46 Cadm1 is expressed by epidermal cells and mediates heter

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

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

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

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

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

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

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

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

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

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

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

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

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

60 CADM1 overexpression or downregulation was achieved usin

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

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

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

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

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

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

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

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

69 12 genes and of multiple pathways, including CADM1, SPHK1, and YAP/TAZ, whose expression independentl

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

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

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

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

74 Cadm1 was present in epithelial and superficial fiber ce

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