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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  past 2 years, 3 genes (SLC20A2, PDGFRB, and PDGFB) were identified as causative of primary familial
12            Although plasma levels of VWF and PDGFB correlated modestly (rho approximately 0.30) with
13 results confirmed the association of VWF and PDGFB with VTE after correction for multiple testing, wh
14            However, unlike oncogenes such as PDGFB or ras, Wnt-1 and -2 failed to induce detectable t
15 cell genes platelet-derived growth factor B (PDGFB) and vascular endothelial cell growth factor recep
16 ion of the platelet-derived growth factor B (PDGFB) receptor, a transmembrane tyrosine kinase.
17 naling via platelet-derived growth factor B (PDGFB), expressed by endothelial cells, and its receptor
18 ioma in platelet-derived growth factor beta (PDGFB)-driven tumors.
19 3), and platelet-derived growth factor beta (PDGFB).
20         Platelet-derived growth factor-beta (PDGFB) is a mitogen for hepatic stellate cells (HSCs).
21 on with platelet-derived growth factor-beta (PDGFB).
22 e COL1A1-platelet-derived growth factor beta(PDGFB) fusion gene.
23  in 7 patients; and RT-PCR showed the COL1A1-PDGFB fusion transcript in 6 patients.
24 ell lymphoma, MPB-BRAF in glioma, and COL3A1-PDGFB in dermatofibrosarcoma protuberans-like.
25 gand that antagonizes ANG2, or AAVs encoding PDGFB, a chemoattractant for pericytes.
26 celiac disease are immune response eQTLs for PDGFB and IL18R1.
27         HRMPs and HRECs expressed functional PDGFB-R and VEGFR-2, respectively.
28 ) resulted in upregulation of PDGFA, but not PDGFB nor VEGF.
29 nd our study suggests a novel association of PDGFB plasma levels with VTE.
30                                Expression of PDGFB is thought to be important in the pathogenesis of
31         To further examine the importance of PDGFB in mouse primary intramedullary spinal cord tumors
32 iplatelet therapy or selective inhibition of PDGFB might reduce biliary fibrosis in patients with liv
33 this patient demonstrates that inhibition of PDGFB receptor tyrosine kinase activity can significantl
34 uced circulating serum and hepatic levels of PDGFB and significantly reduced progression of fibrosis
35                                    Levels of PDGFB protein, but not messenger RNA, were increased in
36  MDR2-null mice normalized hepatic levels of PDGFB within 48 hours, reducing levels of a marker of HS
37 well-characterized RCAS/Ntv-a mouse model of PDGFB-driven low grade glioma.
38 ion that results in dermal overexpression of PDGFB and favors the development of fibrotic tumors migh
39       We found that modest overexpression of PDGFB using a relatively weak phosphoglycerate kinase (P
40  reveals that it is not just the presence of PDGFB, but how it is presented to pericytes, that determ
41 background on IGFBP2-mediated progression of PDGFB-initiated oligodendroglioma.
42  to HSCs, and were identified as a source of PDGFB protein in MDR2-null mice.
43           We studied the cellular sources of PDGFB and the effects of a high-affinity monoclonal anti
44                          Cellular sources of PDGFB were identified using quantitative reverse-transcr
45 e Akt pathway and collaborates with K-Ras or PDGFB in the development and progression of two major ty
46 on decreased expression of oncogenes (PDGFA, PDGFB, and TGFB1) and increased expression of tumor supp
47 arkers near PDGFalpha (PDGFA) and PDGFbeta, (PDGFB) also failed to maintain significance after correc
48                       Transplantation of PGK-PDGFB-transduced Sca1(+) cells increased MSC proliferati
49 elet-derived growth factor beta polypeptide [PDGFB], vascular endothelial growth factor [VEGF], vascu
50                            Platelets produce PDGFB to activate HSC and promote fibrosis in MDR2-null
51  involving 9p23-p22.3 (NFIB) and 22q12-qter (PDGFB) may be of importance for disease progression in a
52 d has thus far been associated with SLC20A2, PDGFB or PDGFRB mutations.
53                                    Adult SPC-PDGFB transgenic mice exhibited lung pathology character
54 ly among individual mice within the same SPC-PDGFB transgenic lineage.
55 moving inhibitory regulatory elements in the PDGFB mRNA, we are able to substantially elevate its exp
56                                Levels of the PDGFB were increased in serum samples from patients with
57                                        Thus, PDGFB and IL18R1 represent plausible candidates for stud
58       Here we switch the therapeutic gene to PDGFB, another potent mitogen for mesenchymal stem cells
59 iability of cells coexpressing IGFBP2 versus PDGFB expression alone.
60 ic beta-catenin, which was not observed with PDGFB, ras or erbB2 transfectants.

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