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1                                              PDGFR alpha hyperphosphorylation and enhanced proliferat
2                                              PDGFR alpha-positive cells in optic nerve and spinal cor
3                                              PDGFR-alpha activation led to BBB impairment and this wa
4                                              PDGFR-alpha and -beta immunoreactivity was observed in r
5                                              PDGFR-alpha and -beta proteins are expressed in native a
6                                              PDGFR-alpha and -beta were expressed on all melanoma cel
7                                              PDGFR-alpha signaling may contribute to BBB impairment v
8                                              PDGFR-alpha suppression prevented neurological deficits,
9                                              PDGFR-alpha(+)Sca-1(+) (PalphaS) MSCs have augmented gro
10 ial growth factor receptor (VEGFR)-2 and -3, PDGFR-alpha and-beta, and c-Kit, was tested for efficacy
11                                           Ab-PDGFR-alpha decreased significantly the overall smooth m
12 eived a blocking antibody to PDGFR-alpha (Ab-PDGFR-alpha; 10 mg/kg; n=5) or PDGFR-beta (Ab-PDGFR-beta
13 PDGFR-beta (1.2+/-0.2, P<0.01) but not in Ab-PDGFR-alpha (2.2+/-0.4).
14                                     Serum Ab-PDGFR-alpha concentrations fell rapidly after day 7 to 0
15                                 In addition, PDGFR-alpha and -beta protein expression was observed in
16              These data demonstrate that all PDGFR alpha-positive cells in the embryonic rat spinal c
17 lial cells that express PDGF receptor alpha (PDGFR alpha) [1] and divide in response to PDGF [2-5], s
18 atelet-derived growth factor receptor alpha (PDGFR alpha) as one target of mutant Cbl-induced deregul
19 atelet-derived growth factor receptor alpha (PDGFR alpha)-positive.
20 atelet-derived growth factor receptor-alpha (PDGFR alpha) expression in vivo and in isolated mammary
21 atelet-derived growth factor receptor-alpha (PDGFR alpha), suggesting that negative selection using c
22 atelet-derived growth factor receptor alpha (PDGFR-alpha) and stem cell antigen 1 (Sca-1) have recent
23 atelet-derived growth factor receptor alpha (PDGFR-alpha) signaling, resulting in increased apoptosis
24 atelet-derived growth factor receptor alpha (PDGFR-alpha), a tyrosine kinase receptor, was found in p
25 atelet-derived growth factor receptor-alpha (PDGFR-alpha) activation caused an increase of IKDR in NG
26 atelet-derived growth factor receptor-alpha (PDGFR-alpha)(+)Sca-1(+)CD45(-)Ter119(-) (PalphaS) cells.
27 growth factor receptor beta (PDGFR beta) and PDGFR alpha, but not insulin-like growth factor-1R and e
28  from fusion of the Fip1-like 1 (FIP1L1) and PDGFR alpha (PDGFRA) genes has been identified as a ther
29                         Both PDGFR-beta- and PDGFR-alpha-mediated pathways promote collagen depositio
30                              Because KIT and PDGFR-alpha remain drivers of GIST after resistance to i
31 and indicate an oncogenic role for c-Kit and PDGFR-alpha tyrosine kinases in the context of Int3 sign
32 ing anti-PDGFR-beta antibody (APB5), an anti-PDGFR-alpha antibody (APA5), or control immunoglobulin G
33                                  The PDGF-B, PDGFR-alpha, and PDGFR-beta mRNA expression was induced
34 ived growth factor receptor-alpha and -beta (PDGFR-alpha and -beta), we designed this study to test t
35 nstrated that imatinib mesylate blocked both PDGFR-alpha and PDGFR-beta in vivo.
36 antibodies: allophycocyanin (APC)-conjugated PDGFR-alpha, FITC-conjugated Sca-1, phycoerythrin (PE)-c
37                                 By contrast, PDGFR-alpha+ cells exhibiting the morphology of ICC gut
38                                 In contrast, PDGFR-alpha inhibition did not affect vascular maturatio
39  oligodendrocytes develops from a different, PDGFR alpha-negative lineage(s).
40 o test the hypothesis that inhibiting either PDGFR-alpha or PDGFR-beta with a specific mouse/human ch
41   Viral entry in cells harbouring endogenous PDGFR-alpha was competitively inhibited by pretreatment
42 R-1, -3, c-Kit and RET, most cells expressed PDGFR-alpha and -beta.
43              PDGF-A null mice had many fewer PDGFR alpha-progenitors than either wild-type or PDGF-B
44                Consistent with this finding, PDGFR-alpha immunoreactivity was confined to NG2+ cells
45 mouse, a deletion that includes the gene for PDGFR alpha, is a recessive lethal that exhibits a domin
46 ed function for PDGFR-beta in CDR formation, PDGFR-alpha is also clearly capable of eliciting CDRs.
47 like Nanog(low)Sox2(low)Lin28(high)CD24(high)PDGFR-alpha(high) population.
48                               Targeted human PDGFR-alpha activation in mouse beta-cells stimulated Er
49 ockade of receptor function with a humanized PDGFR-alpha blocking antibody (IMC-3G3) or targeted inhi
50 otype in Pdgfr-alpha(-/-) embryos identified PDGFR-alpha as a critical mediator of signaling in the e
51 a activation and exogenous PDGF-AA increased PDGFR-alpha activation, regardless of thrombin inhibitio
52 neutralizing antibodies inhibit HCMV-induced PDGFR-alpha phosphorylation.
53  observed after other types of liver injury, PDGFR-alpha loss in HSCs led to a significant albeit tra
54        At least one target of imatinib (KIT, PDGFR-alpha, or PDGFR-beta) was expressed in all tumors,
55 pathway with lithium treatment rescued NG2(+)PDGFR-alpha(+) progenitor cell proliferation in BBS muta
56 so known as neuron-glial antigen 2 or NG2)(+)PDGFR-alpha(+) neural progenitors.
57 responds to activation of PDGFR-beta but not PDGFR-alpha, was not phosphorylated on tyrosine in mutan
58 after E16, coinciding with the appearance of PDGFR alpha-immunoreactive cells in the starting populat
59     Our findings highlight a novel aspect of PDGFR alpha signaling in tumorigenesis.
60  spinal cord cells that had been depleted of PDGFR alpha-expressing cells by antibody-mediated comple
61 lso failed to induce hyperphosphorylation of PDGFR alpha.
62 othesis that TGF-beta mediates the levels of PDGFR alpha protein via regulation of c-Cbl was tested.
63 e were profound reductions in the numbers of PDGFR alpha-progenitors and oligodendrocytes in the spin
64  > G mutation in exon 12 (amino acid 567) of PDGFR-alpha.
65 e Pdgf-c gene or pharmacological blockade of PDGFR-alpha impair the WAT-beige transition.
66 IFN-gamma treatment led to downregulation of PDGFR-alpha (platelet-derived growth factor receptor-alp
67   Both RA and D3 decreased the expression of PDGFR-alpha and PDGFR-beta throughout differentiation.
68 are downregulated by increased expression of PDGFR-alpha or PDGFR-beta in NSCLC cells.
69 king a functional Shp-2, while the levels of PDGFR-alpha EGFR and IGFIR were not changed.
70 tial of the melanoma cells: higher levels of PDGFR-alpha were expressed on cells with higher metastat
71 in expression, activity, and localization of PDGFR-alpha and -beta were analyzed by Western blot and
72 so correlated with the expression pattern of PDGFR-alpha.
73 Subsequent experiments confirmed the role of PDGFR-alpha and PDGFR-beta as receptors for AAV-5.
74 e present study, we investigated the role of PDGFR-alpha following ICH-induced brain injury in mice,
75 r our findings support a profibrotic role of PDGFR-alpha in HSCs during chronic liver injury in vivo
76                       To examine the role of PDGFR-alpha in HSCs, Lrat-Cre recombinase and Pdgfra-flo
77 ker profile of infected cells, NG2+, olig2+, PDGFR-alpha+, nestin+, GFAP-, and CC1-, indicated a clos
78  We found that FAP was robustly expressed on PDGFR-alpha(+), Sca-1(+) multipotent bone marrow stromal
79       Only siRNA constructs for c-Kit and/or PDGFR-alpha were able to inhibit HC11-Int3 colony format
80 d demonstrated that disrupting the paracrine PDGFR alpha signaling between tumor cells and stromal fi
81 stimulation by HCMV, tyrosine-phosphorylated PDGFR-alpha associated with the p85 regulatory subunit o
82 vimentin+), and oligodendrocyte progenitors (PDGFR-alpha+) were proliferating.
83 atelet-derived growth factor-alpha receptor (PDGFR-alpha) is specifically phosphorylated by both labo
84 the platelet-derived growth factor receptor (PDGFR-alpha-polypeptide) and AAV-5 transduction.
85 telet-derived growth factor alpha-receptors (PDGFR alpha) are expressed by a subset of neuroepithelia
86  through activation of PDGF-alpha receptors (PDGFR-alpha) on perivascular astrocytes, and treatment o
87          We conclude that TGF-beta regulates PDGFR alpha in the mammary stroma via a c-Cbl-independen
88              Furthermore, RGC-5 cells showed PDGFR-alpha/beta tyrosine phosphorylation that induced t
89 mor cells and stromal fibroblasts by soluble PDGFR alpha-IgG significantly reduced tumor growth.
90               Thrombin inhibition suppressed PDGFR-alpha activation and exogenous PDGF-AA increased P
91           Together, these data indicate that PDGFR-alpha and tyrosine kinase activity act via a commo
92     Taken together, these data indicate that PDGFR-alpha is a critical receptor required for HCMV inf
93 ectable levels in O4+ cells, suggesting that PDGFR-alpha signaling is absent in pre-OLs in situ.
94  The therapeutic interventions targeting the PDGFR-alpha signaling may be a novel strategy to prevent
95 r astrocytes, and treatment of mice with the PDGFR-alpha antagonist imatinib after ischemic stroke re
96 dation for the future testing of therapeutic PDGFR-alpha inhibition in hepatic fibrosis, especially i
97                                        Thus, PDGFR alpha signaling is required for the recruitment of
98            In vitro, Cbl-N directly bound to PDGFR alpha derived from PDGF-AA-stimulated cells but no
99 ental groups received a blocking antibody to PDGFR-alpha (Ab-PDGFR-alpha; 10 mg/kg; n=5) or PDGFR-bet
100 -mediated induction was primarily limited to PDGFR-alpha.
101                 In mutant Cbl transfectants, PDGFR alpha was hyperphosphorylated and constitutively c
102 +) progenitor cells, as well as in human WAT-PDGFR-alpha(+) adipocytes, supporting the physiological
103  beige phenotype in differentiated mouse WAT-PDGFR-alpha(+) progenitor cells, as well as in human WAT
104                                         When PDGFR alpha-positive cells were purified from embryonic
105                               Cells in which PDGFR-alpha was genetically deleted or functionally bloc
106 association of transfected Cbl proteins with PDGFR alpha.
107  HCMV glycoprotein B directly interacts with PDGFR-alpha, resulting in receptor tyrosine phosphorylat

 
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