ライフサイエンスコーパス: CD150

1 CD150 (signaling lymphocyte activation molecule [SLAM])

2 CD150 cell surface expression is up-regulated with rapid

3 CD150 exhibits lateral mobility, segregating into interc

4 CD150 signaling lymphocytic activation molecule (SLAM),

5 CD150+ CD48- Sca-1+ Lineage- c-kit+ cells from old, reco

6 CD150-induced signal transduction is controlled by SAP/S

7 D48(-)CD41(-) cells and 1 (37%) of every 2.7 CD150(+)CD48(-)Sca-1(+)lineage(-)Mac-1(+) fetal liver ce

8 ion in irradiated mice, 1 (18%) of every 5.7 CD150(+)CD48(-)CD41(-) cells and 1 (37%) of every 2.7 CD

9 l-characterized ephrinB2/B3, sialic acid and CD150-mediated entry pathways.

10 rthermore, we observe that both CD150(+) and CD150(-) cells can be found within the SP population and

11 (-), Kit(+/-), Flt3(+), Sca(+), CD34(+), and CD150(-), was identified.

12 s all HSC populations, CD41, CD45, CD34, and CD150 were developmentally regulated: the earliest embry

13 ESC-HSCs express CD41 and CD150, lack CD34, and are heterogeneous for CD45.

14 HSCs express CD41 and CD34 and lack CD45 and CD150, whereas more mature HSCs lack CD41 and CD34 and e

15 HSCs lack CD41 and CD34 and express CD45 and CD150.

16 by 2 homophilic adhesion molecules, CD84 and CD150 (SLAM [signaling lymphocyte activation molecule]),

17 ntial erythroid-megakaryocyte progenitor and CD150(+)CD9(hi)endoglin(lo) cells are TPO-responsive and

18 Anti-CD150 antibodies also synergize with interleukin 12 (IL-

19 Anti-CD150 triggering induces strong costimulation of T cells

20 sociated protein (SAP, SH2D1A), because anti-CD150 induces similar levels of DNA synthesis in SAP(-/-

21 synthesis of murine T cells induced by anti-CD150 is not dependent on SLAM-associated protein (SAP,

22 g we have generated a panel of rat antimouse CD150 monoclonal antibodies.

23 g it possible to highly purify adult HSCs as CD150(+)CD48(-)CD244(-) cells.

24 e and microbial sensor SLAMF1 (also known as CD150) is lost in a subset of patients with an aggressiv

25 HSCs were highly purified as CD150(+)CD244(-)CD48(-) cells while MPPs were CD244(+)CD

26 Furthermore, we observe that both CD150(+) and CD150(-) cells can be found within the SP p

27 Here, we identify a CCR2(+)CD150(+)CD48(-) LSK hematopoietic subset as the most ups

28 -fold higher proliferation rates than CCR2(-)CD150(+)CD48(-) LSK cells, displays a myeloid differenti

29 Both murine LSKCD48(-)CD166(+)CD150(+) and LSKCD48(-)CD166(+)CD150(+)CD9(+) cells, as

30 D48(-)CD166(+)CD150(+) and LSKCD48(-)CD166(+)CD150(+)CD9(+) cells, as well as human Lin(-)CD34(+)CD38

31 re CD48(+)CD244(-)CD150(-) or CD48(+)CD244(+)CD150(-), just as in adult bone marrow.

32 t restricted progenitors were CD48(+)CD244(+)CD150(-).

33 D244(-)CD48(-) cells while MPPs were CD244(+)CD150(-)CD48(-) and most restricted progenitors were CD4

34 lony-forming progenitors were CD48(+)CD244(-)CD150(-) or CD48(+)CD244(+)CD150(-), just as in adult bo

35 Tet2(-/-);Flt3(ITD) progenitors (LSK CD48(+)CD150(-)) propagate disease in secondary recipients and

36 HSCs defined as Lin(-)Sca1(+)c-kit(Hi)CD48(-)CD150(+).

37 and there was no recovery of the LSK-CD48(-)CD150(+) and LSK-CD34(-)Flt3(-) populations 15 to 18 mon

38 accompanied by a reduction of the LSK-CD48(-)CD150(+) and LSK-CD34(-)Flt3(-) populations in the bone

39 ngent marker combination (L(-)K(+)S(+)CD48(-)CD150(+)), revealed unexpected heterogeneity in their pr

40 compartments [Lin-, LSK, and SLAM (LSK/CD48-/CD150+)] increased with the age.

41 binds to the phosphorylated receptors CD84, CD150, CD229 and CD244, and acts as a natural inhibitor,

42 those animals, and we now show that CD86(-) CD150(+) CD48(-) HSCs from normal adult mice are particu

43 f Hoxa(-/-) and WT hematopoietic stem cells (CD150(+)/CD48(-)/Lineage(-)/c-kit(+)/Sca-1(+)) identifie

44 In contrast, CD150(-) MPP enriched for lymphoid potential were synerg

45 Interestingly, both Flt3(+)CD150(-) and Flt3(-)CD150(-) myeloid progenitors are sus

46 that this is exclusively found in the Flt3(+)CD150(-) subset of CMPs at the clonal level.

47 Therefore, these Flt3(+)CD150(-) myeloid progenitors were T/myeloid potent.

48 Yet, Flt3(+)CD150(-) myeloid progenitors are not likely to efficient

49 terestingly, both Flt3(+)CD150(-) and Flt3(-)CD150(-) myeloid progenitors are susceptible to Notch1-m

50 ulted in increase in cells with a LSK Flt3(-)CD150(+)CD48(-) long-term HSC (LTHSC) phenotype but redu

51 y by cells of the phenotype c-kit+Sca-1+Flt3+CD150-CD48-Lin-, which defines multipotent progenitors i

52 We show that megakaryocytes arise from CD150(+) bipotential progenitors that display both plate

53 ing HSC (LT-HSC) pool (Lin(-)Sca1(+)c-Kit(hi)CD150(+)CD48(-)) are quiescent, with only a small percen

54 Accumulation of splenic HSCs (CD150+CD48-Lin(-/low)Sca1+cKit+) was diminished in TLR4-

55 in(-)Sca-1(-)c-Kit(+)CD41(-)FcgammaRII/III(-)CD150(-)CD105(-)).

56 , that also inhibited syncytium formation in CD150(+) B95-8 cells.

57 face receptors of the SLAM family, including CD150, CD244, and CD48, were differentially expressed am

58 AM family of cell-surface markers, including CD150 (SlamF1), to offer potential advantages over estab

59 tin-4 receptor than when H is engaged to its CD150 receptor.

60 Cross-linking CD150 on CD4 T cells induces rapid serine phosphorylatio

61 am locus have profound alterations in Ly108, CD150, and Ly9 expression that is associated with iNKT c

62 ontexts, we examined the SLAM family markers CD150 and CD48.

63 Here we show that four SLAM family markers, CD150, CD48, CD229, and CD244, can distinguish HSCs and

64 For example, minor CD150(Hi)CD48(-) populations lacking CD86 or CD18 expand

65 Nonetheless, CD150, CD244, and CD48 are not pan-stem cell markers, as

66 ted SLAM (CD150(+)CD48(-)) and non-SLAM (not CD150(+)CD48(-)) cells from human umbilical cord blood C

67 A three-pronged interaction with Tyr(281) of CD150 can occur in absence of phosphorylation.

68 Real-time PCR analysis of CD150(-)Flt3(+) cells from wild-type control, Hoxa9(-/-)

69 ateral mobility and homophilic clustering of CD150 between neighboring cells is not dependent on SAP/

70 Simultaneous loss of CD150(Lo/-)CD48(-) HSC and gain of the normally rare sub

71 tor compartment revealed elevated numbers of CD150(+hi)CD34(-)CD41(+) myeloid-biased stem cells in Ho

72 To further explore the role of CD150 signaling in costimulation and T(H)1 priming we ha

73 or the pTyr motif in the cytoplasmic tail of CD150 but, unlike SH2D1A, EAT-2 does not bind to non-pho

74 motif with Tyr281 of the cytoplasmic tail of CD150 is very similar to the structure of SH2D1A complex

75 tyrosine residues in the cytoplasmic tail of CD150.

76 sphatase SHP-2 occurs primarily on Tyr281 of CD150 because SHP-2 requires both Tyr281 and Tyr327 for

77 lizes nonphospho binding of SAP to Tyr281 of CD150.

78 mobilized mice included mainly CD48+ and/or CD150- cells that lacked reconstituting ability.

79 ling lymphocyte activation molecule (SLAM or CD150), we asked whether and how its tropism is altered.

80 ling lymphocyte activation molecule (SLAM or CD150).

81 A, EAT-2 does not bind to non-phosphorylated CD150.

82 cted the binding of SH2D1A to phosphorylated CD150.

83 differential role of the cellular receptors CD150 and PVRL4 in disease progression.

84 een enhanced using the SLAM family receptors CD150, CD244, and CD48.

85 toplasmic tail of the cell-surface receptors CD150/SLAM, CD84, CD229/Ly-9, and CD244/2B4.

86 ences in CD229 and CD244 expression resolved CD150(-)CD48(-/low)Lineage(-/low)Sca-1(+)c-Kit(+) cells

87 en neighboring cells is not dependent on SAP/CD150 interaction.

88 We isolated SLAM (CD150(+)CD48(-)) and non-SLAM (not CD150(+)CD48(-)) cell

89 gnaling lymphocyte activation molecule SLAM (CD150) expressed only in immune cells or through the ubi

90 osine motif in the cytoplasmic tail of SLAM (CD150) and related cell surface proteins.

91 rough the immune cell-specific protein SLAM (CD150) or other receptors, including the ubiquitous prot

92 aling lymphocytic activation molecule (SLAM [CD150]) that is expressed in lymphocytes and other immun

93 aling lymphocytic activation molecule (SLAM)/CD150 family includes a family of chromosome 1-encoded c

94 aling lymphocytic activation molecule (SLAM, CD150) is the universal morbillivirus receptor.

95 naling lymphocyte activation molecule (SLAM, CD150) with human-like tissue specificity.

96 aling lymphocytic activation molecule (SLAM; CD150) and the adherens junction protein nectin-4 (polio

97 aling lymphocytic activation molecule (SLAM; CD150) is the immune cell receptor for measles virus (MV

98 We further demonstrate that SLAM (Slamf1, CD150), a surface receptor that uses SAP signaling, is s

99 This report shows that CD150 colocalizes with the T-cell receptor (TCR) followi

100 increased megakaryocytic maturation, and the CD150(+)CD9(lo)endoglin(hi) fraction, which contains ery

101 This fraction is distinct from the CD150(+)CD9(hi)endoglin(lo) fraction, which contains bip

102 SH2D1A able to interfere with Thr -2 of the CD150 binding motif (mutant T53I) severely impaired non-

103 immune responses, implicating members of the CD150-SH2D1A family as targets in the pathogenesis and t

104 oid-megakaryocyte progenitor population, the CD150(+)CD9(lo)endoglin(lo) fraction of Lin(-)cKit(+)IL7

105 Antibodies to CD150 also enhance IFN-gamma production both in wild-typ

106 quires both Tyr281 and Tyr327 for binding to CD150, and SAP binds to nonphosphorylated Tyr281.

107 at the SAP protein has 2 modes of binding to CD150.

108 this is an important pathway contributing to CD150-mediated T-cell proliferation.

109 ratio of Flt3(hi) multipotent progenitors to CD150(+) stem cells in the mouse BM, suggesting defectiv

110 Fetal liver HSCs were CD150(+)CD48(-)CD244(-), and the vast majority of colony

111 d cyclophosphamide/G-CSF-mobilized mice were CD150+ CD48-, just as in normal young bone marrow.