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Luca Grumolato

Researcher at French Institute of Health and Medical Research

Publications -  53
Citations -  1893

Luca Grumolato is an academic researcher from French Institute of Health and Medical Research. The author has contributed to research in topics: Wnt signaling pathway & Cancer. The author has an hindex of 22, co-authored 50 publications receiving 1661 citations. Previous affiliations of Luca Grumolato include University of Rouen & Icahn School of Medicine at Mount Sinai.

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Canonical and noncanonical Wnts use a common mechanism to activate completely unrelated coreceptors

TL;DR: It is demonstrated here that prototype canonical Wnt3a and noncanonical Wnt5a ligands specifically trigger completely unrelated endogenous coreceptors-LRP5/6 and Ror1/2, respectively-through a common mechanism that involves their Wnt-dependent coupling to the Frizzled (Fzd) coreceptor and recruitment of shared components.
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Canonical Wnts function as potent regulators of osteogenesis by human mesenchymal stem cells.

TL;DR: This study investigates the functions of canonical Wnts on differentiation of adult multipotent human mesenchymal stem cells (hMSCs) in vitro and in vivo, arguing for an important role of a canonical WNT gradient in hMSC osteogenesis in vivo.
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Selenoprotein T is a PACAP-regulated gene involved in intracellular Ca2+ mobilization and neuroendocrine secretion

TL;DR: Results suggested a possible role of SelT in PACAP signaling during PC12 cell differentiation and demonstrated the implication of a selenoprotein in the regulation of Ca2+ homeostasis and neuroendocrine secretion in response to a cAMP‐stimulating trophic factor.
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High-Frequency Canonical Wnt Activation in Multiple Sarcoma Subtypes Drives Proliferation through a TCF/β-Catenin Target Gene, CDC25A

TL;DR: In Wnt autocrine cell lines, alterations including overexpression or gene amplification of Wnt ligands and/or LRP5/6 coreceptors and epigenetic silencing of different cell surface Wnt antagonists are identified and inhibited sarcoma cell proliferation both in vitro and in vivo.
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β-Catenin-independent activation of TCF1/LEF1 in human hematopoietic tumor cells through interaction with ATF2 transcription factors.

TL;DR: Together, these findings indicate that, through interaction with ATF2 factors, TCF1/LEF1 promote the growth of hematopoietic malignancies in the absence of β-catenin stabilization, thus establishing a new mechanism for TCF/ LEF1 transcriptional activity distinct from that associated with canonical Wnt signaling.