戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (left1)

通し番号をクリックするとPubMedの該当ページを表示します
1                                              PDGFB can mediate the development of mouse spinal tumors
2 sk in a joint model in FARIVE (VWF P < .001; PDGFB P = .002).
3 creased expression of EMP-1, NOTCH-1, FLT-1, PDGFB, and several other genes that may contribute to th
4 e actin and fibrosis-associated genes) via a PDGFB-dependent mechanism.
5  a high-affinity monoclonal antibody against PDGFB (MOR8457) in mouse models of biliary fibrosis.
6 n were positive for fusion of the COL1A1 and PDGFB loci in 7 patients; and RT-PCR showed the COL1A1-P
7 of three genes (coding for CXCR7, ITGB2, and PDGFB) significantly inhibits C. pneumoniae entry, but t
8 omoters of target genes like LOXL2, LCN2 and PDGFB.
9  CTTNBP2, MYC (alias c-myc), PTEN, MEN1, and PDGFB] in six nonrecurrent and seven recurrent radical p
10 alysis of the array data identified NFIB and PDGFB as the 2 major candidate target oncogenes that may
11 on and prolonging survival in both PDGFA and PDGFB-driven tumours.
12                            CD31, PDGFRB, and PDGFB all strongly correlate with IBA1+ TAM infiltration
13  past 2 years, 3 genes (SLC20A2, PDGFRB, and PDGFB) were identified as causative of primary familial
14       While expression of both PDGFRbeta and PDGFB has been noted in patient breast tumors for decade
15 s and growth factors, for example, TGFB2 and PDGFB.
16 bits the endothelial Pdgfb transcription and PDGFB growth signaling to the non-coronary leaflet mesen
17                                    TREM2 and PDGFB mRNA levels were positively correlated in human ca
18                     The levels of Twist1 and PDGFB are higher in PAE cells isolated from idiopathic p
19 Hypoxia upregulates the levels of Twist1 and PDGFB in HPAE cells.
20            Although plasma levels of VWF and PDGFB correlated modestly (rho approximately 0.30) with
21 results confirmed the association of VWF and PDGFB with VTE after correction for multiple testing, wh
22            However, unlike oncogenes such as PDGFB or ras, Wnt-1 and -2 failed to induce detectable t
23 e (MYORG), platelet-derived growth factor B (PDGFB) and platelet-derived growth factor receptor beta
24 cell genes platelet-derived growth factor B (PDGFB) and vascular endothelial cell growth factor recep
25            Platelet-derived growth factor B (PDGFB) plays a crucial role in recruitment of PDGF recep
26 f a 1.5 kb platelet derived growth factor B (PDGFB) promoter.
27 ion of the platelet-derived growth factor B (PDGFB) receptor, a transmembrane tyrosine kinase.
28 naling via platelet-derived growth factor B (PDGFB), expressed by endothelial cells, and its receptor
29 11 (IL11), platelet-derived growth factor-B (PDGFB), and hyaluronan synthase 2 (HAS2), as well as the
30 ioma in platelet-derived growth factor beta (PDGFB)-driven tumors.
31 3), and platelet-derived growth factor beta (PDGFB).
32         Platelet-derived growth factor-beta (PDGFB) is a mitogen for hepatic stellate cells (HSCs).
33 on with platelet-derived growth factor-beta (PDGFB).
34 e COL1A1-platelet-derived growth factor beta(PDGFB) fusion gene.
35                            Tumours driven by PDGFB have a significantly lower median survival compare
36  in 7 patients; and RT-PCR showed the COL1A1-PDGFB fusion transcript in 6 patients.
37 ell lymphoma, MPB-BRAF in glioma, and COL3A1-PDGFB in dermatofibrosarcoma protuberans-like.
38 ing neutrophils in HCC or monocyte-deficient PDGFB-driven and Nf1-silenced GBM models extend the surv
39 previously unknown role for platelet-derived PDGFB, whereby it promotes and maintains vascular integr
40 s and MDM creates an interdependence driving PDGFB-driven GBM progression.
41 evidence for the potent inflammatory effects PDGFB has in paediatric HGGs.
42 odels incorporating human-relevant EGFRvIII, PDGFB and NF1 driver mutations to characterize the genot
43 gand that antagonizes ANG2, or AAVs encoding PDGFB, a chemoattractant for pericytes.
44 onocyte chemoattraction in monocyte enriched PDGFB-driven GBM invokes a compensatory neutrophil influ
45 xpression of platelet-derived growth factor (PDGFB) in human pulmonary arterial endothelial (HPAE) ce
46 sed higher ISGs together with elevated FGF2, PDGFB, and XIAP, compared with CL derived from day 18 cy
47 mulated proangiogenic genes, including FGF2, PDGFB, and PDGFAR.
48 celiac disease are immune response eQTLs for PDGFB and IL18R1.
49 rain calcification, and mice hypomorphic for PDGFB (Pdgfbret/ret) present with brain vessel calcifica
50 studies reveal a previously unknown role for PDGFB-to-PDGFRbeta paracrine signaling in the promotion
51 ng, with potential key mechanistic roles for PDGFB, MMP12, and SPARCL1 in orchestrating fibrosis.
52         HRMPs and HRECs expressed functional PDGFB-R and VEGFR-2, respectively.
53 tases of mammary tumor cells expressing high PDGFB when injected intravenously.
54 sed of 363 primary human breast tumors, high PDGFB protein expression was prognostic for brain metast
55 ed in patient breast tumors for decades, how PDGFB-to-PDGFRbeta tumor-stroma signaling mediates breas
56 senchymal transition and increase hypoxia in PDGFB-driven GBM.
57 eviously, we have reported that mutations in PDGFB in humans are associated with primary familial bra
58 -a directly drives mesenchymal transition in PDGFB-driven primary GBM cells.
59 th clinical phenotypes of ADCA-DN, including PDGFB and PRDM8 for cerebellar ataxia, psychosis and dem
60 ring and quantitative PCR analysis indicates PDGFB-driven tumours have a highly inflammatory microenv
61 cy worsens pathology and memory in male J20 (PDGFB-APP(SwInd)) mice.
62 e ligand induction, and its preferred ligand PDGFB is released by neighboring epithelial and endothel
63 ) resulted in upregulation of PDGFA, but not PDGFB nor VEGF.
64 nd our study suggests a novel association of PDGFB plasma levels with VTE.
65                                Expression of PDGFB is thought to be important in the pathogenesis of
66  transcription factor to drive expression of PDGFB, leading to resistance to palbociclib by enhancing
67 abolism genes and promotes the expression of PDGFB, which activates mTOR signalling and the downstrea
68         To further examine the importance of PDGFB in mouse primary intramedullary spinal cord tumors
69 iplatelet therapy or selective inhibition of PDGFB might reduce biliary fibrosis in patients with liv
70 this patient demonstrates that inhibition of PDGFB receptor tyrosine kinase activity can significantl
71                      Conditional knockout of PDGFB in platelets demonstrates its previously unknown r
72 mpaired in mice with conditional knockout of PDGFB in platelets.
73                                    A lack of PDGFB in platelets led to enhanced hypoxia and epithelia
74                           Elevated levels of PDGFB accelerated orthotopic tumor growth and intracrani
75 uced circulating serum and hepatic levels of PDGFB and significantly reduced progression of fibrosis
76                                    Levels of PDGFB protein, but not messenger RNA, were increased in
77  MDR2-null mice normalized hepatic levels of PDGFB within 48 hours, reducing levels of a marker of HS
78 well-characterized RCAS/Ntv-a mouse model of PDGFB-driven low grade glioma.
79 ion that results in dermal overexpression of PDGFB and favors the development of fibrotic tumors migh
80       We found that modest overexpression of PDGFB using a relatively weak phosphoglycerate kinase (P
81  reveals that it is not just the presence of PDGFB, but how it is presented to pericytes, that determ
82 background on IGFBP2-mediated progression of PDGFB-initiated oligodendroglioma.
83    Platelets constitute a major reservoir of PDGFB and are continuously activated in the tumor microe
84                               Restoration of PDGFB in aortic root endothelium rescues the non-coronar
85    The endothelium is an essential source of PDGFB in this process.
86  to HSCs, and were identified as a source of PDGFB protein in MDR2-null mice.
87           We studied the cellular sources of PDGFB and the effects of a high-affinity monoclonal anti
88                          Cellular sources of PDGFB were identified using quantitative reverse-transcr
89 s associated with decreased survival time of PDGFB-driven tumor-bearing mice.
90 e clinical prognostic and therapeutic use of PDGFB-to-PDGFRbeta signaling in women with breast cancer
91 d in Nestin-positive brain cells by PDGFA or PDGFB overexpression with Cdkn2a or Tp53 co-mutations.
92 e Akt pathway and collaborates with K-Ras or PDGFB in the development and progression of two major ty
93 on decreased expression of oncogenes (PDGFA, PDGFB, and TGFB1) and increased expression of tumor supp
94 arkers near PDGFalpha (PDGFA) and PDGFbeta, (PDGFB) also failed to maintain significance after correc
95                       Transplantation of PGK-PDGFB-transduced Sca1(+) cells increased MSC proliferati
96 elet-derived growth factor beta polypeptide [PDGFB], vascular endothelial growth factor [VEGF], vascu
97                            Platelets produce PDGFB to activate HSC and promote fibrosis in MDR2-null
98  involving 9p23-p22.3 (NFIB) and 22q12-qter (PDGFB) may be of importance for disease progression in a
99 ied the RCAS/Tv-a model where RCAS-Cre, RCAS-PDGFB, and RCAS-H3.3K27M were used to drive tumourigenes
100 de gliomas are generated by introducing RCAS-PDGFB-RFP and RCAS-Cre in a Nestin/tv-a; TP53(fl/fl) PTE
101 d has thus far been associated with SLC20A2, PDGFB or PDGFRB mutations.
102                   These data support a SOX17-PDGFB axis underlying aortic root development that is cr
103                                    Adult SPC-PDGFB transgenic mice exhibited lung pathology character
104 ly among individual mice within the same SPC-PDGFB transgenic lineage.
105 n 1-year-old wild-type (WT) and J20 mice (Tg:PDGFB-APPSwInd), overexpressing human amyloid precursor
106                   Our analysis revealed that PDGFB-driven tumours were more proliferative and enriche
107                Mechanistically, we show that PDGFB-dependent SRF activation is mediated via MRTF (myo
108                           Here, we show that PDGFB-driven GBM cells induce the expression of the pote
109 moving inhibitory regulatory elements in the PDGFB mRNA, we are able to substantially elevate its exp
110                                Levels of the PDGFB were increased in serum samples from patients with
111  known as mural cells, are recruited through PDGFB (platelet-derived growth factor B)-PDGFRB (platele
112                                        Thus, PDGFB and IL18R1 represent plausible candidates for stud
113                               In contrast to PDGFB-driven GBM, Nf1-silenced tumors have a constitutiv
114 n injury model, with positive correlation to PDGFB (platelet-derived growth factor subunit B) and MMP
115       Here we switch the therapeutic gene to PDGFB, another potent mitogen for mesenchymal stem cells
116 n the tumour microenvironment in response to PDGFB stimulation.
117 se that induces SMC migration in response to PDGFB, mechanistically via modulation of contractile mar
118         Mechanistically, 4D9 increased TREM2+PDGFB+ macrophages and PDGF receptor-alpha+ fibroblast-l
119                           Endothelial Twist1-PDGFB signaling plays a key role in alphaSMA-positive ce
120 lar lumen structures and hypoxia upregulates PDGFB expression and stimulates accumulation of alphaSMA
121 iability of cells coexpressing IGFBP2 versus PDGFB expression alone.
122 ic beta-catenin, which was not observed with PDGFB, ras or erbB2 transfectants.
123     Mutations in seven genes (SLC20A2, XPR1, PDGFB, PDGFRB, MYORG, NAA60, and JAM2) are associated wi

 
Page Top