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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
11 eived a blocking antibody to PDGFR-alpha (Ab-PDGFR-alpha; 10 mg/kg; n=5) or PDGFR-beta (Ab-PDGFR-beta
16 lial cells that express PDGF receptor alpha (PDGFR alpha) [1] and divide in response to PDGF [2-5], s
17 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) expression in vivo and in isolated mammary
20 atelet-derived growth factor receptor-alpha (PDGFR alpha), suggesting that negative selection using c
21 atelet-derived growth factor receptor alpha (PDGFR-alpha) and stem cell antigen 1 (Sca-1) have recent
22 atelet-derived growth factor receptor alpha (PDGFR-alpha) signaling, resulting in increased apoptosis
23 atelet-derived growth factor receptor alpha (PDGFR-alpha), a tyrosine kinase receptor, was found in p
24 atelet-derived growth factor receptor-alpha (PDGFR-alpha) activation caused an increase of IKDR in NG
25 atelet-derived growth factor receptor-alpha (PDGFR-alpha)(+)Sca-1(+)CD45(-)Ter119(-) (PalphaS) cells.
26 growth factor receptor beta (PDGFR beta) and PDGFR alpha, but not insulin-like growth factor-1R and e
27 from fusion of the Fip1-like 1 (FIP1L1) and PDGFR alpha (PDGFRA) genes has been identified as a ther
30 and indicate an oncogenic role for c-Kit and PDGFR-alpha tyrosine kinases in the context of Int3 sign
31 ing anti-PDGFR-beta antibody (APB5), an anti-PDGFR-alpha antibody (APA5), or control immunoglobulin G
33 ived growth factor receptor-alpha and -beta (PDGFR-alpha and -beta), we designed this study to test t
35 antibodies: allophycocyanin (APC)-conjugated PDGFR-alpha, FITC-conjugated Sca-1, phycoerythrin (PE)-c
38 o test the hypothesis that inhibiting either PDGFR-alpha or PDGFR-beta with a specific mouse/human ch
39 Viral entry in cells harbouring endogenous PDGFR-alpha was competitively inhibited by pretreatment
43 mouse, a deletion that includes the gene for PDGFR alpha, is a recessive lethal that exhibits a domin
46 ockade of receptor function with a humanized PDGFR-alpha blocking antibody (IMC-3G3) or targeted inhi
47 otype in Pdgfr-alpha(-/-) embryos identified PDGFR-alpha as a critical mediator of signaling in the e
48 a activation and exogenous PDGF-AA increased PDGFR-alpha activation, regardless of thrombin inhibitio
51 pathway with lithium treatment rescued NG2(+)PDGFR-alpha(+) progenitor cell proliferation in BBS muta
53 responds to activation of PDGFR-beta but not PDGFR-alpha, was not phosphorylated on tyrosine in mutan
54 after E16, coinciding with the appearance of PDGFR alpha-immunoreactive cells in the starting populat
56 spinal cord cells that had been depleted of PDGFR alpha-expressing cells by antibody-mediated comple
58 othesis that TGF-beta mediates the levels of PDGFR alpha protein via regulation of c-Cbl was tested.
59 e were profound reductions in the numbers of PDGFR alpha-progenitors and oligodendrocytes in the spin
62 IFN-gamma treatment led to downregulation of PDGFR-alpha (platelet-derived growth factor receptor-alp
63 Both RA and D3 decreased the expression of PDGFR-alpha and PDGFR-beta throughout differentiation.
66 tial of the melanoma cells: higher levels of PDGFR-alpha were expressed on cells with higher metastat
67 in expression, activity, and localization of PDGFR-alpha and -beta were analyzed by Western blot and
70 e present study, we investigated the role of PDGFR-alpha following ICH-induced brain injury in mice,
71 ker profile of infected cells, NG2+, olig2+, PDGFR-alpha+, nestin+, GFAP-, and CC1-, indicated a clos
72 We found that FAP was robustly expressed on PDGFR-alpha(+), Sca-1(+) multipotent bone marrow stromal
74 d demonstrated that disrupting the paracrine PDGFR alpha signaling between tumor cells and stromal fi
75 stimulation by HCMV, tyrosine-phosphorylated PDGFR-alpha associated with the p85 regulatory subunit o
77 atelet-derived growth factor-alpha receptor (PDGFR-alpha) is specifically phosphorylated by both labo
79 telet-derived growth factor alpha-receptors (PDGFR alpha) are expressed by a subset of neuroepithelia
80 through activation of PDGF-alpha receptors (PDGFR-alpha) on perivascular astrocytes, and treatment o
86 Taken together, these data indicate that PDGFR-alpha is a critical receptor required for HCMV inf
88 The therapeutic interventions targeting the PDGFR-alpha signaling may be a novel strategy to prevent
89 r astrocytes, and treatment of mice with the PDGFR-alpha antagonist imatinib after ischemic stroke re
92 ental groups received a blocking antibody to PDGFR-alpha (Ab-PDGFR-alpha; 10 mg/kg; n=5) or PDGFR-bet
95 +) progenitor cells, as well as in human WAT-PDGFR-alpha(+) adipocytes, supporting the physiological
96 beige phenotype in differentiated mouse WAT-PDGFR-alpha(+) progenitor cells, as well as in human WAT
100 HCMV glycoprotein B directly interacts with PDGFR-alpha, resulting in receptor tyrosine phosphorylat
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