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 iring survival and self-renewal in BCR-ABL1+ CD150+ lineage-negative Sca-1+ c-Kit+ leukemic cells.

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

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

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

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

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

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

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

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

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

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

20 Anti-CD150 triggering induces strong costimulation of T cells

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

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

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

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

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

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

27 BaMV that infected Vero cells expressing bat CD150.

28 In vitro assays using bat CD150 for cell entry and partial cross-neutralization of

29 eceptor binding protein of MBaMV utilize bat CD150 and not human CD150, as an entry receptor in a mam

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

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

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

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

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

35 ong-term expanding clones within the CD201(+)CD150(+)CD48(-)c-Kit(+)Sca-1(+)Lin(-) population of prec

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

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

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

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

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

41 quired within the Lin(-)Sca(+)Kit(+)-CD48(-) CD150(+) fraction for canonical and noncanonical TGF-bet

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

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

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

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

46 nally characterize MPP5 (LSK CD34+CD135-CD48-CD150-).

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

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

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

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

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

52 Importantly, reducing the dysfunctional CD150(high) HSCs can alleviate aging phenotypes in old r

53 subset of monocyte-derived cells expressing CD150 induced a disease-specific fibroblast population,

54 divergence, FeMV H glycoprotein uses feline CD150 as a receptor and cannot use human CD150.

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

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

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

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

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

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

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

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

63 -2-CD34-KSL cells and indistinguishable from CD150+CD34-KSL cells.

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

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

66 ein of MBaMV utilize bat CD150 and not human CD150, as an entry receptor in a mammalian cell line.

67 ine CD150 as a receptor and cannot use human CD150.

68 t bat-associated morbilliviruses, used human CD150 and nectin-4 cellular receptors, suggesting differ

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

70 ndecan-2 expression was increased 10-fold in CD150+CD48-CD34-c-Kit+Sca-1+Lineage- cells (long-term HS

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

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

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

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

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

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

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

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

79 Mechanistically, CD150(low) HSCs from old mice but not their CD150(high)

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

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

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

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

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

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

86 files and functions, marked by low levels of CD150 expression.

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

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

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

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

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

92 tyrosine residues in the cytoplasmic tail of CD150.

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

94 lizes nonphospho binding of SAP to Tyr281 of CD150.

95 Notably, transplantation of old CD150(low) HSCs attenuates aging phenotypes and prolongs

96 pread without the need to engage nectin-4 or CD150, known receptors for MeV that are not present on n

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

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

99 ling lymphocyte activation molecule (SLAM or CD150).

100 red to those transplanted with unselected or CD150(high) HSCs.

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

102 cted the binding of SH2D1A to phosphorylated CD150.

103 e marrow and the production of proreparatory CD150(+)CD48(-)CCR2(+) hematopoietic stem cells.

104 the interaction of the cell surface protein CD150 with the bacterial outer membrane protein Omp25, i

105 fusion activation with the cellular receptor CD150 (signaling lymphocyte activation molecule [SLAM]/F

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

122 Here, we show that SLAMF1/CD150 is highly and uniquely induced in macrophages by a

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

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

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

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

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

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

129 fied nearly all repopulating HSCs within the CD150+CD34-KSL population.

130 CD150(low) HSCs from old mice but not their CD150(high) counterparts can effectively differentiate i

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

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

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

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

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

136 ct recognition of a live pathogen by HSC via CD150, which attests to a very early contribution of HSC

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

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

139 in vivo repopulating capacity compared with CD150+ cells.