V
Vincent F. Vellucci
Researcher at Yale University
Publications - 14
Citations - 923
Vincent F. Vellucci is an academic researcher from Yale University. The author has contributed to research in topics: Transforming growth factor & Transforming growth factor beta. The author has an hindex of 14, co-authored 14 publications receiving 907 citations.
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Journal Article
Missense Mutations of the Transforming Growth Factor β Type II Receptor in Human Head and Neck Squamous Carcinoma Cells
Laure Garrigue-Antar,Teresita Muñoz-Antonia,Scott J. Antonia,Joan Gesmonde,Vincent F. Vellucci,Michael Reiss +5 more
TL;DR: These are the first reported naturally occurring nucleotide substitution mutations in the T beta R-11 gene in human head and neck cancer cells, which may explain their resistance to TGF beta 1-mediated cell cycle arrest.
Journal ArticleDOI
Smads 2 and 3 Are Differentially Activated by Transforming Growth Factor-β (TGF-β) in Quiescent and Activated Hepatic Stellate Cells CONSTITUTIVE NUCLEAR LOCALIZATION OF Smads IN ACTIVATED CELLS IS TGF-β-INDEPENDENT
Chenghai Liu,Marianna D. A. Gaça,E. Scott Swenson,Vincent F. Vellucci,Michael Reiss,Rebecca G. Wells +5 more
TL;DR: In this paper, the authors studied activation of the TGF-β downstream signaling molecules Smads 2, 3, and 4 in hepatic stellate cells (HSC) for 1, 4, and 7 days, with quiescent, intermediate, and fully transdifferentiated phenotypes, respectively.
Journal Article
Status of the p53 tumor suppressor gene in human squamous carcinoma cell lines.
Michael Reiss,Douglas E. Brash,Teresita Muñoz-Antonia,Jeffrey A. Simon,Annemarie Ziegler,Vincent F. Vellucci,Zhao ling Zhou +6 more
TL;DR: Three cell lines failed to express any p53 mRNA, and three of the lines expressed only mutant p53 protein resulting from missense mutations in codons 248 and 273, suggesting that the lack of transcription was the result of mutations in the regulatory region of the gene.
Journal Article
Activation of the Autocrine Transforming Growth Factor α Pathway in Human Squamous Carcinoma Cells
TL;DR: Human squamous carcinoma cell lines frequently exhibit a combination of the constitutive secretion of transforming growth factor alpha and the overexpression of epidermal growth factor receptors, suggesting that designing strategies to interrupt the transforming growth factors autocrine pathway might lead to new modalities to treat this class of malignant tumors.
Journal Article
Mutant p53 tumor suppressor gene causes resistance to transforming growth factor beta 1 in murine keratinocytes.
TL;DR: It is suggested that mutant forms of p53 inhibit the antiproliferative effect of TGF-beta 1 by interfering with its signaling pathway.