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1 MMTV Gag localizes to discrete cytoplasmic foci in mouse
2 MMTV isolated from infected mice lacking these LBPs cann
3 MMTV-bound bacterial lipopolysaccharide triggered Toll-l
4 MMTV-Cre- or adenoviral-Cre-mediated SmoM2 expression in
5 MMTV-Cre;NRP2(loxP/loxP) mice exhibited significant defe
6 MMTV-D stability could help direct activation-associated
7 MMTV-Espl1 mice in a C57BL/6 genetic background develop
8 MMTV-LTR promoter-driven HA-14-3-3zeta transgenic mice (
9 MMTV-neu transgenic mice developed anemia after tumor on
10 MMTV-neu;Nedd9(-/-) mammospheres had striking defects in
11 MMTV-SP uses endoplasmic reticulum-associated degradatio
12 ent ITAM-containing proteins, one encoding a MMTV provirus and the other a B cell receptor fusion pro
13 oteins from an immortalized cell line from a MMTV-neu mouse model and from MCF7 human breast cancers
16 MMTV Gag and YB-1 was RNA dependent, and an MMTV RNA reporter construct colocalized with Gag and YB-
17 Using both human breast tumor cells and an MMTV-Wnt mouse breast tumor model, we show that RKIP ind
18 of our MT prostate model with those from an MMTV-MT breast model (23) shows both tissue-specific and
21 to-mesenchymal transition and metastasis, an MMTV-PyMT transgenic mouse model of mammary tumour progr
26 creased apoptosis were seen in MMTV-HER2 and MMTV-Neu mammary glands lacking ErbB3, thus inhibiting p
30 ioned media (CM) obtained from MMTV-PyMT and MMTV-Her2/Neu tumor cells cultured in vitro were suffici
31 mouse mammary tumor virus (MMTV)- PyMT- and MMTV- Wnt1-driven mammary tumorigenesis and metastasis.
34 egulation of cap-independent translation and MMTV-induced tumorigenesis contrasts with the well estab
35 ogression of mammary tumors in MMTV-Wnt1 and MMTV-PyMT transgenic mice and by the tumor sphere cultur
36 /-) mice, arguing that mA3 is the major anti-MMTV restriction factor that is induced upon DC maturati
38 tumor virus-polyoma virus middle T antigen (MMTV-PyMT)-induced breast cancer to conduct such an eval
44 that mA3 expression in target cells blocked MMTV infection at a postentry step and acted together wi
45 To allow detection and localization of both MMTV-SP and the C-terminal cleavage product, we prepared
47 fap2c, in mouse mammary epithelium driven by MMTV-Cre promoted aberrant growth of the mammary tree le
48 t mechanistic breast cancer models driven by MMTV-Wnt1 and a human head and neck squamous cell carcin
49 trains for their abilities to be infected by MMTV and showed that susceptibility to infection correla
51 elopment in the mouse model of breast cancer MMTV-neu, a model characterized by amplification of the
52 induced mammary tumor formation in Chk1(+/-);MMTV-Cre animals with a median time to tumor latency of
55 nm) that partially activates an AR-dependent MMTV promoter (55% of maximal response) while antagonizi
56 on is diminished significantly in developing MMTV-Cre;NRP2(loxP/loxP) mammary glands compared with co
57 from Dmp1(+/+);MMTV-cyclin D1 and Dmp1(+/+);MMTV-D1T286A mice but significantly down-regulated in th
58 pre-malignant mammary glands from Dmp1(+/+);MMTV-cyclin D1 and Dmp1(+/+);MMTV-D1T286A mice but signi
60 r data support the hypothesis that efficient MMTV particle assembly is dependent upon the interaction
63 mammary hyperplasia and carcinoma in female MMTV-neu mice without causing weight loss or affecting n
66 signal peptidase in the ER is necessary for MMTV-SP function in a reporter assay, but many requireme
68 F-1alpha levels and tumor cells created from MMTV-Neu mice harboring deletion of Hif1alpha alleles re
71 s established from tumor tissue derived from MMTV-Neu/Tcfap2c(L/L) control animals and parallel cell
72 atic Mvt-1 mammary cancer cells derived from MMTV-PyVmT/FVB-N transgenic mice and c-Myc/vegf tumor ex
73 al delay in tumor growth, cells derived from MMTV-PyVT;Nedd9(-/-) tumors are characteristically hyper
78 h high levels of MELK in mammary tumors from MMTV-Wnt1/MELK-GFP bitransgenic mice resulted in a signi
80 tritransgenic mice (TetO-MYC;TetO-Kras(G12D);MMTV-rtTA) in which MYC and mutant Kras can be regulated
84 alysis of the Akt2/miR-21 pathway in hypoxic MMTV-PyMT-induced mouse mammary adenocarcinomas and huma
86 ngle-cell transplantation assays to identify MMTV-Her2/Neu mouse mammary TICs as CD24(+):JAG1(-) at a
89 reast cancer, and constitutive activation in MMTV-SmoM2 transgenic mice caused alterations in mammary
93 n vivo analysis, indicated tumors arising in MMTV-neu;Nedd9(-/-) mice had undergone mutational select
95 the casr gene in mammary epithelial cells in MMTV-PymT mice reduced tumor PTHrP expression and inhibi
97 f YB-1 resulted in a significant decrease in MMTV particle production, indicating that YB-1 plays a r
100 blation impeded mammary tumor development in MMTV-Wnt1 mice, further underscoring a requirement of TG
101 22 promotes aggressive metastatic disease in MMTV-miR-22 TG mice, as well as compound MMTV-neu or -Py
103 this difference is replicated faithfully in MMTV-PyMT and MMTV-Her2 transgenic mouse models of breas
106 that only a limited effect on metastasis in MMTV-neu;Nedd9(-/-) mice compared with MMTV-neu;Nedd9(+/
107 in a reduction of branching morphogenesis in MMTV-PyMT- and Her2/neu-amplified tumor organoids, incre
109 ed mammary tumour formation were observed in MMTV-RANK transgenic mice after multiparity or treatment
111 significantly delays mammary tumor onset in MMTV-Wnt1 females, whereas acute deletion of Pygo2 in MM
114 that epithelia-specific ablation of Pygo2 in MMTV-Wnt1 transgenic mice results in delayed mammary duc
115 females, whereas acute deletion of Pygo2 in MMTV-Wnt1 tumor cells leads to a significant decrease in
117 eration and increased apoptosis were seen in MMTV-HER2 and MMTV-Neu mammary glands lacking ErbB3, thu
118 TFAP2C, we examined mammary tumorigenesis in MMTV-Neu transgenic female mice with or without conditio
119 ased during progression of mammary tumors in MMTV-Wnt1 and MMTV-PyMT transgenic mice and by the tumor
120 C59 blocked progression of mammary tumors in MMTV-WNT1 transgenic mice while downregulating Wnt/beta-
121 matrix metalloproteinases are upregulated in MMTV-LRP6 mice that could contribute to the hyperplasia
122 nts indicated that overexpression of Zpo2 in MMTV-PyMT mammary tumor cell lines enhances lung metasta
127 mor development and metastasis, we interbred MMTV-PyMT mice with E2F1, E2F2, or E2F3 knockout mice.
129 d-type bone marrow, into lethally irradiated MMTV-PyVmT mice (a model of metastatic breast cancer) de
131 lore this possibility, the highly metastatic MMTV-PyMT mice were crossed with 25 AKXD (AKR/J x DBA/2J
132 omoter-driven HA-14-3-3zeta transgenic mice (MMTV-HA-14-3-3zeta) developed mammary tumors, whereas co
135 ed dynamics compared to a nearby nucleosome (MMTV-B) that is the initial target of transcription acti
136 mary Tumor Virus promoter-region nucleosome (MMTV-D) has greater inherent stability than and reduced
137 ary tumor virus (MMTV)-neu and 50 nuliparous MMTV-wnt1 transgenic mice were treated with RARalpha ago
139 ne deamination by virion-packaged APOBEC3 of MMTV early reverse transcription DNA occurred only at lo
143 n (KD) miR-155 in the myeloid compartment of MMTV-PyMT mice, a mouse model of spontaneous breast carc
144 ile APOBEC3-mediated cytidine deamination of MMTV may occur, it is not the major means by which APOBE
147 agonist, Mesd, markedly suppressed growth of MMTV-Wnt1 tumors without causing undesirable side effect
150 is essential for the efficient production of MMTV particles, a process directed by the viral Gag prot
151 reversal suggests the specific selection of MMTV-PyVT;Nedd9(-/-) cells for growth in an in vivo micr
155 , we used virions from the mammary tissue of MMTV-infected inbred wild-type mice with different allel
156 rity of the late-appearing mammary tumors of MMTV-polyoma virus middle T;Nedd9(-/-) mice are characte
162 gly, in spite of their aggressive phenotype, MMTV-PyVT;Nedd9(-/-) cells persistently have low levels
163 Deletion of the Bcl3 gene in ErbB2-positive (MMTV-Neu) mice resulted in a 75% reduction in metastatic
164 ase-mediated collagen crosslinking prevented MMTV-Neu-induced fibrosis, decreased focal adhesions and
167 Here, the normal microenvironment redirects MMTV-neu-transformed tumorigenic cells to participate in
168 that the timed secretion of Wingless-related MMTV (mouse mammary tumor virus) integration site 3 (WNT
169 which secrete the morphogen Wingless-related MMTV (mouse mammary tumor virus) integration site 3 (WNT
172 secreted modulator of WNT (Wingless-related MMTV integration site)/beta-catenin signaling, is both n
173 ammary epithelium of our previously reported MMTV-tva transgenic mice, we detected high-grade, poorly
175 (MEC) populations, and oncogenic signaling, MMTV-ErbB2 transgenic mice were administered AZD4547 (2-
176 mouse mammary tumor virus-Polyoma Middle T (MMTV-PyMT) model of luminal breast cancer, induction of
177 mouse mammary tumor virus-Polyoma Middle T (MMTV-PyMT), which mimics RANK and RANKL expression patte
180 ivated in the MMTV-expressing cells and that MMTV-induced apoptosis resistance was completely restore
184 awn from the free energy profiles, show that MMTV folds by a hierarchical mechanism with parallel pat
189 this LPS to stimulate TLR4, suggesting that MMTV intensifies these immunostimulatory properties.
191 Overexpression of L9 in cells expressing the MMTV(C3H) provirus resulted in specific, robust accumula
192 model of mammary tumorigenesis harboring the MMTV-HER2 oncogene and mutation of MED1 to evaluate its
193 ing antisense oligonucleotides (ASOs) in the MMTV (mouse mammary tumor virus)-PyMT mouse mammary carc
194 xycycline-induced expression of FIP1C in the MMTV-ErbB2 mouse model resulted in delayed mammary tumor
195 o found that Src kinase was activated in the MMTV-expressing cells and that MMTV-induced apoptosis re
198 eless, our analysis of tumors arising in the MMTV-Myc model of mammary carcinogenesis reveals substan
209 gh studies of CaSR-PTHrP interactions in the MMTV-PymT transgenic mouse model of breast cancer and in
210 n Src inhibitor, SKI-606 (bosutinib), in the MMTV-PyVmT transgenic mouse model of breast cancer.
212 The treatment was more effective in the MMTV-wnt1 model in which Am580 also induced differentiat
216 ective Dmp1 deletion was found in 21% of the MMTV-D1 and D1T286A mammary carcinomas, and the Dmp1 het
217 expressing human FLAG-PAD2 downstream of the MMTV-LTR promoter develop spontaneous neoplastic skin le
224 in (GFP) from the NS promoter and bred it to MMTV-Wnt1 mice, so that NS-expressing cells can be prosp
226 n in animals, we have generated a transgenic MMTV-Espl1 mouse model that overexpresses Separase prote
227 mammary tumor tissues from double-transgenic MMTV-Hoxb7/Her2 mice than tumors from single-transgenic
230 ide additional evidence in triple transgenic MMTV/QR/Arom mice, wherein the QR expression is induced
232 not only in hormone- and carcinogen-treated MMTV-RANK and wild-type mice, but also in the MMTV-neu t
233 nduced lung fibrosis model we used wild-type MMTV mice and a triple transgenic mouse SPC-rtTA(+/-)Tet
234 Fibroblast growth factor (Fgf)-Wingless type MMTV integration site family (Wnt) genetic module in the
235 the sonic hedgehog pathway and Wingless type MMTV integration site family were validated by immunohis
236 eas the roles of the canonical wingless-type MMTV (mouse mammary tumor virus) integration site family
237 d 3 main clusters of HCCs: the wingless-type MMTV integration site (32 of 89; 36%), interferon-relate
238 cued by local treatment with a Wingless-type MMTV integration site (Wnt) antagonist, Dickkopf-1 (Dkk1
240 converging to dysregulate the Wingless-type MMTV integration site (Wnt)/beta-catenin signaling, a ke
241 errant activation of canonical Wingless-type MMTV integration site family (Wnt) signaling is pathogno
245 bone morphogenetic protein and wingless-type MMTV integration site family member (Wnt) superfamilies,
246 s in SP7 transcription factor, wingless-type MMTV integration site family member 1 (WNT1), trimeric i
248 ted protein, which retains the Wingless-type MMTV integration site family member-ligand-binding domai
253 re characteristically hyperaggressive versus MMTV-PyVT;Nedd9(+/+) cells in anchorage-independent grow
255 betaretroviruses, mouse mammary tumor virus (MMTV) and human endogenous retrovirus type K, encode ana
256 icts infection by mouse mammary tumor virus (MMTV) and murine leukemia virus (MLV) and that there are
257 ol infection with mouse mammary tumor virus (MMTV) and murine leukemia virus (MuLV) via an adaptive i
258 Integration of mouse mammary tumor virus (MMTV) at the common integration site Int6 occurs in the
265 m2s driven by the mouse mammary tumor virus (MMTV) long terminal repeat (LTR) promoter were morpholog
268 murine retrovirus mouse mammary tumor virus (MMTV) orchestrates the assembly of immature virus partic
271 mitted retrovirus mouse mammary tumor virus (MMTV) requires the intestinal microbiota for persistence
272 e first time that mouse mammary tumor virus (MMTV), a mammalian retrovirus that assembles intracytopl
273 iruses, including mouse mammary tumor virus (MMTV), are transmitted most efficiently through mucosal
275 eletion inhibited mouse mammary tumor virus (MMTV)- PyMT- and MMTV- Wnt1-driven mammary tumorigenesis
277 in breast cancer, mouse mammary tumor virus (MMTV)-Her2/neu transgenic mice that develop mammary tumo
279 l of 50 uniparous mouse mammary tumor virus (MMTV)-neu and 50 nuliparous MMTV-wnt1 transgenic mice we
281 in xenograft and mouse mammary tumor virus (MMTV)-neu mouse models in a manner associated with activ
284 ary tumors in the mouse mammary tumor virus (MMTV)-polyoma virus middle T (PyVT) genetic model is del
285 crossed with the mouse mammary tumor virus (MMTV)-Polyoma virus middle T antigen (PyMT) or MMTV-c-Ne
286 on factors in the mouse mammary tumor virus (MMTV)-polyomavirus middle T oncoprotein (PyMT) mouse mod
287 (R175H) mice and mouse mammary tumor virus (MMTV)-Wnt-1 transgenic (mWnt-1) mice to specifically add
288 mammary tumors of mouse mammary tumor virus (MMTV)-Wnt1-transgenic mice and in aggressive basal subty
290 ain-of-function (mouse mammary tumour virus (MMTV)-RANK transgenic mice) and loss-of function (pharma
293 ing factors, prompting us to examine whether MMTV utilizes a similar set of host proteins to facilita
295 ) have increased tumor latency compared with MMTV-ErbB2 wild-type (deltaWT) mice, and the tumors show
297 is in MMTV-neu;Nedd9(-/-) mice compared with MMTV-neu;Nedd9(+/+) mice, but instead a dramatic reducti
298 umber of CD39(+)CD73(+) TDMMCs compared with MMTV-PyMT/TGFbetaRII(WT) control tumors with intact TGF-
300 or growth, we interbred FABP5-null mice with MMTV-ErbB2/HER2 oncomice, which spontaneously develop ma
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