V
Valentina M. Factor
Researcher at National Institutes of Health
Publications - 112
Citations - 11296
Valentina M. Factor is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Transforming growth factor & Genetically modified mouse. The author has an hindex of 56, co-authored 110 publications receiving 10450 citations. Previous affiliations of Valentina M. Factor include Russian Academy of Sciences.
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Journal ArticleDOI
Loss of miR-122 expression in liver cancer correlates with suppression of the hepatic phenotype and gain of metastatic properties.
Cédric Coulouarn,Valentina M. Factor,Jesper B. Andersen,Marian E. Durkin,Snorri S. Thorgeirsson +4 more
TL;DR: It is reported that miR-122 is specifically repressed in a subset of primary tumors that are characterized by poor prognosis, and it is shown that loss of microRNA-122 results in an increase of cell migration and invasion and that restoration of mi R-122 reverses this phenotype.
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Hepatocyte growth factor/c-met signaling pathway is required for efficient liver regeneration and repair
Chang-Goo Huh,Valentina M. Factor,Aránzazu Sánchez,Koichi Uchida,Elizabeth A. Conner,Snorri S. Thorgeirsson +5 more
TL;DR: Direct genetic evidence is provided in support of the critical role of c-met in efficient liver regeneration and disruption of c -met affects primarily hepatocyte survival and tissue remodeling and is suggested to affect primarily liver regeneration.
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Ubiquitous activation of Ras and Jak/Stat pathways in human HCC.
Diego F. Calvisi,Sara Ladu,Alexis Gorden,Miriam Farina,Elizabeth A. Conner,Ju Seog Lee,Valentina M. Factor,Snorri S. Thorgeirsson +7 more
TL;DR: Activation of Ras and Jak/Stat pathways was enhanced in all HCCs when compared with nonneoplastic surrounding and normal livers coincidently with the suppression of at least 1 Ras and Janus kinase (Jak)/signal transducer and activator of transcription (Stat) pathways.
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Hepatic expression of mature transforming growth factor beta 1 in transgenic mice results in multiple tissue lesions.
Nancy D. Sanderson,Valentina M. Factor,Peter Nagy,Jeffrey B. Kopp,Paturu Kondaiah,Lalage M. Wakefield,Anita B. Roberts,Michael B. Sporn,Snorri S. Thorgeirsson +8 more
TL;DR: The results from this transgenic model strongly support the proposed etiological role for TGF-beta 1 in a variety of fibrotic and inflammatory disorders and provide an appropriate paradigm for testing therapeutic interventions aimed at neutralizing the detrimental effects of this important cytokine.
Journal Article
Transgenic mice with increased plasma levels of TGF-beta 1 develop progressive renal disease.
Jeffrey B. Kopp,Valentina M. Factor,Miklos M. Mozes,Peter Nagy,Nancy D. Sanderson,Erwin P. Bottinger,Paul E. Klotman,Snorri S. Thorgeirsson +7 more
TL;DR: Increased levels of circulating TGF-beta 1 induced progressive renal disease that was characterized by mesangial expansion, accumulation of glomerular immune deposits and matrix proteins, and interstitial fibrosis in this transgenic mouse model, suggesting that chronically elevated circulating levels of TGF -beta 1 induce progressive glomerulosclerosis.