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1 lular carcinoma (HCC) progression in X/c-myc bitransgenics.
2 loidy was frequently observed in tumors from bitransgenic and p53172R-H mice, but not from mice expre
10 Both biological and foster pups nursed by bitransgenic dams exhibited a dramatic decrease in survi
13 sults were found in mammary tumors from mice bitransgenic for the neu and transforming growth factor-
17 similar in WT, hemizygous SP-C-hCFTR+/-, and bitransgenic gut-corrected FABP-hCFTR+/+-mCFTR-/-, the l
19 of several reporter genes in the corneas of bitransgenic Krt12cre/+/ROSA(EGFP), Krt12Cre/+/ZEG, and
21 ferative and preneoplastic stages in X/c-myc bitransgenic livers, whereas BAMBI and PLK1 were overexp
24 Significantly, liver tumors from HBx/c-myc bitransgenic mice and chronically HBV-infected patients
25 nd Suz12/Znf198 in liver tumors from X/c-myc bitransgenic mice and woodchuck hepatitis virus (WHV)-in
27 latency, however, was reduced by 8 months in bitransgenic mice as compared to mice of the other three
29 e expression of the LacZ gene was induced in bitransgenic mice by administration of doxycycline in th
32 ant p53 in mammary tumorigenesis by creating bitransgenic mice carrying MMTV-neu and 172Arg-to-His p5
33 the lung tumors were lung adenocarcinomas in bitransgenic mice compared to only 3% in wild-type mice.
34 and cerebrovascular Abeta deposition in the bitransgenic mice compared with their singly transgenic
36 ell lines derived from MMTV-c-Rel x CK2alpha bitransgenic mice displayed a highly invasive phenotype.
41 gillus species extract-challenged CC10-IL-15 bitransgenic mice exhibited significantly reduced levels
42 mous epithelia, the resulting Bi-L E7/K5-tTA bitransgenic mice expressed E7 and luciferase in the ski
43 tently expressed in NPC and can cooperate in bitransgenic mice expressed from the keratin-14 promoter
44 rmed RIDNs on amyloid deposition, we crossed bitransgenic mice expressing APP and presenilin 1 (PS1)
47 epatocellular carcinomas (HCCs) derived from bitransgenic mice harboring TGF-alpha and c-myc transgen
48 lial cells in CCSP-rtTA/(tetO)(7)-CMV-Stat3C bitransgenic mice induces chronic inflammation and lung
49 transforming growth factor (TGF)-alpha/c-myc bitransgenic mice leads to inhibition of NF-kappaB and p
50 ithelial cells of CCSP-rtTA/(tetO)(7)-Stat3C bitransgenic mice leads to severe pulmonary inflammation
55 LK in mammary tumors from MMTV-Wnt1/MELK-GFP bitransgenic mice resulted in a significant enrichment o
56 -1(+) cells from lung of doxycycline-treated bitransgenic mice strongly inhibited proliferation and f
57 This synchrony of tumor development in the bitransgenic mice suggests that trophic maintenance of t
61 actosidase enzyme activity by doxycycline in bitransgenic mice took place in 24 hours and reached a p
66 endocrine or neural features, and Atp4b-Cre bitransgenic mice with a Cre reporter confirmed that the
67 ofiles of Kras(G12D)-induced lung cancers in bitransgenic mice with and without Sp1 inhibition, 542 g
68 t5B were significantly suppressed in MECs of bitransgenic mice with constitutive miR-150 expression a
69 ranial self-stimulation (ICSS) and inducible bitransgenic mice with enriched expression of mCREB in f
70 chanism of Rb effects on the somatic growth, bitransgenic mice with tetracycline-regulated Rb express
71 , and cingulate cortex in different lines of bitransgenic mice, and CREB expression was blocked by ad
72 sed in lung and blood of doxycycline-treated bitransgenic mice, but CD4(+) and CD8(+) T cells were de
73 vage fluid and plasma of doxycycline-treated bitransgenic mice, concentrations of MDSC-stimulating cy
74 was elevated in tumors from WAP-DES, but not bitransgenic mice, indicating an alteration in the p53/I
76 n of deltaFosB in NAc and dorsal striatum of bitransgenic mice, or specifically in the NAc core of ra
106 ieved overexpression of DeltaFosB by using a bitransgenic mouse line that inducibly expresses the pro
107 tion between Myc and E2Fs in vivo, we used a bitransgenic mouse model of Myc-induced T cell lymphomag
109 eloid-specific c-fms-rtTA/(TetO)(7)-CMV-Api6 bitransgenic mouse model under the control of the c-fms
115 cre expression, tumors develop by design in bitransgenic mouse progeny derived by crossing Cre-produ
117 tors PKI 166 and erlotinib and a conditional bitransgenic mouse that expressed a constitutively activ
119 ew, we address two distinct c-myc-containing bitransgenic murine mammary tumor models and discuss the
120 ively repressed in primary thyrocytes from a bitransgenic murine model (Bi-Tg) of thyroid-specific PB
123 xpressed in primary and secondary lesions of bitransgenic offspring and its expression is particularl
124 rom a bicistronic message is accomplished in bitransgenic progeny by Cre-mediated excision of a segme
127 R2 receptor activation in vivo by generating bitransgenic reporter mice in which the chemokine recept
128 e and male reproductive tract, we employed a bitransgenic system to target FGF-3 to these organs.
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