Alain Mauviel

ORCID: 0000-0002-0438-2793
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • TGF-β signaling in diseases
  • Cell Adhesion Molecules Research
  • Connective Tissue Growth Factor Research
  • Skin and Cellular Biology Research
  • Hedgehog Signaling Pathway Studies
  • NF-κB Signaling Pathways
  • Melanoma and MAPK Pathways
  • Cellular Mechanics and Interactions
  • Protease and Inhibitor Mechanisms
  • Kruppel-like factors research
  • Bone Metabolism and Diseases
  • Proteoglycans and glycosaminoglycans research
  • Inflammatory mediators and NSAID effects
  • Peptidase Inhibition and Analysis
  • Genetic factors in colorectal cancer
  • Osteoarthritis Treatment and Mechanisms
  • Wnt/β-catenin signaling in development and cancer
  • Hippo pathway signaling and YAP/TAZ
  • Wound Healing and Treatments
  • Skin Protection and Aging
  • Oral and Maxillofacial Pathology
  • Heterotopic Ossification and Related Conditions
  • Cancer-related gene regulation
  • melanin and skin pigmentation
  • Dermatology and Skin Diseases

Institut Curie
2012-2024

Centre National de la Recherche Scientifique
2010-2024

Inserm
2011-2024

Université Paris Sciences et Lettres
2010-2024

Université Paris-Sud
2018-2024

Université Paris-Saclay
2010-2017

Université Paris Cité
2002-2015

La Ligue Contre le Cancer
2013

University of Virginia
2010-2012

National Cancer Institute
1994-2012

Despite major advances in the understanding of intimate mechanisms transforming growth factor-β (TGF-β) signaling through Smad pathway, little progress has been made identification direct target genes. In this report, using cDNA microarrays, we have focussed our attention on characterization extracellular matrix-related genes rapidly induced by TGF-β human dermal fibroblasts and attempted to identify ones whose up-regulation is Smad-mediated. For a gene qualify as target, postulated that it...

10.1074/jbc.m100754200 article EN cc-by Journal of Biological Chemistry 2001-05-01

Abstract Hedgehog (Hh) and transforming growth factor-β (TGF-β) family members are involved in numerous overlapping processes during embryonic development, hair cycle, cancer. Herein, we show that TGF-β induces the expression of Hh signaling molecules Gli1 Gli2 various human cell types, including normal fibroblasts keratinocytes, as well cancer lines. induction by is rapid, independent from receptor signaling, requires a functional Smad pathway. subsequently activated Gli2-dependent manner....

10.1158/0008-5472.can-07-0491 article EN Cancer Research 2007-07-15

Previous studies have shown that transforming growth factor-β (TGF-β) and tumor necrosis factor-α (TNF-α) modulate type I collagen gene expression in fibroblasts. To fine-map the corresponding response elements human α2(I) (COL1A2) promoter, we generated a series of 5′ deletion promoter/chloramphenicol acetyltransferase (CAT) reporter constructs. Transient cell transfection assays using dermal fibroblasts stable experiments NIH 3T3 identified region located between residues −265 −241, as...

10.1074/jbc.271.6.3272 article EN cc-by Journal of Biological Chemistry 1996-02-01

Melanoma often metastasizes to bone where it is exposed high concentrations of TGF-β. Constitutive Smad signaling occurs in human melanoma. Because TGF-β promotes metastases by several types solid tumors including breast cancer, we hypothesized that pharmacologic blockade the pathway may interfere with capacity melanoma cells metastasize bone. In this study, tested effect a small molecule inhibitor receptor I kinase (TβRI), SD-208, on various parameters affecting development and progression...

10.1158/0008-5472.can-10-2651 article EN Cancer Research 2010-11-18

The effect of transforming growth factor β (TGF‐β) on the production matrix macromolecules was studied in cultures rabbit articular chondrocytes. A 24 h exposure to TGF‐β at concentrations 0.1, 1 and 10 ng/ml markedly stimulated synthesis collagen non‐collagen protein. Similar increases glycosaminoglycan observed same experimental conditions. distribution these newly synthesized between cell layer medium not altered by treatment with TGF‐β. slightly enhanced proliferation chondrocytes...

10.1016/0014-5793(88)81327-9 article EN FEBS Letters 1988-07-04

Melanoma has a propensity to metastasize bone, where it is exposed high concentrations of transforming growth factor-beta (TGF-beta). Because TGF-beta promotes bone metastases from other solid tumors, such as breast cancer, we tested the role in melanoma bone. 1205Lu cells, stably transfected overexpress natural TGF-beta/Smad signaling inhibitor Smad7, were studied an experimental model metastasis whereby tumor cells are inoculated into left cardiac ventricle nude mice. All mice bearing...

10.1158/0008-5472.can-06-3950 article EN Cancer Research 2007-03-01

Radiation-induced fibrosis is an untoward effect of high dose therapeutic and inadvertent exposure to ionizing radiation. Transforming growth factor-β (TGF-β) has been proposed be critical in tissue repair mechanisms resulting from radiation injury. Previously, we showed that interruption TGF-β signaling by deletion Smad3 results resistance radiation-induced In the current study, a small molecular weight molecule, halofuginone (100 nm), demonstrated reporter assays inhibit pathway, Northern...

10.1074/jbc.m309798200 article EN cc-by Journal of Biological Chemistry 2004-04-01

Summary There is growing evidence that the metastatic spread of melanoma driven not by a linear increase in tumorigenic aggressiveness, but rather switching back and forth between two different phenotypes potential. In vitro these are respectively defined characteristics strong proliferation/weak invasiveness weak proliferation/strong invasiveness. Melanoma cell phenotype tightly linked to gene expression. Taking advantage this, we have developed expression–based tool for predicting called...

10.1111/j.1755-148x.2012.00986.x article EN Pigment Cell & Melanoma Research 2012-02-15

GLI2 (GLI-Kruppel family member 2), a zinc finger transcription factor that mediates Hedgehog signaling, is implicated in the progression of an ever-growing number human malignancies, including prostate and pancreatic cancer, as well basal cell carcinoma skin. Its expression up-regulated by transforming growth factor-beta (TGF-beta) variety types, both normal transformed. We report herein TGF-beta-driven transcriptional does not result from stabilization transcripts. describe...

10.1074/jbc.m109.059964 article EN cc-by Journal of Biological Chemistry 2009-09-22

YAP and its paralog protein TAZ are downstream effectors of the Hippo pathway. Both amplified in many human cancers promote cell proliferation epithelial-mesenchymal transition. Little is known about status pathway cutaneous melanoma. We profiled component expression a panel melanoma lines melanocytic lesions, characterized capacity to control behavior. immuno-staining samples revealed mixed cytoplasmic nuclear staining for both proteins benign nevi superficial spreading was expressed at...

10.1038/jid.2013.319 article EN cc-by-nc-nd Journal of Investigative Dermatology 2013-07-29

TGF-β signaling is involved in pancreatic ductal adenocarcinoma (PDAC) tumorigenesis, representing one of the four major pathways genetically altered 100% PDAC cases. exerts complex and pleiotropic effects cancers, notably via activation SMAD pathways, predominantly SMAD2/3/4. Though SMAD2 3 are rarely mutated SMAD4 lost about 50% PDAC, role SMAD2/3 a SMAD4-null context remains understudied. We herein provide evidence oncogenic effect response to TGF-β1 human cancer cells. report that...

10.1038/s42003-022-03994-6 article EN cc-by Communications Biology 2022-10-07
Coming Soon ...