P
Phyllus Mong
Researcher at Icahn School of Medicine at Mount Sinai
Publications - 4
Citations - 525
Phyllus Mong is an academic researcher from Icahn School of Medicine at Mount Sinai. The author has contributed to research in topics: Wnt signaling pathway & Enhancer. The author has an hindex of 3, co-authored 4 publications receiving 454 citations.
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Journal ArticleDOI
Canonical and noncanonical Wnts use a common mechanism to activate completely unrelated coreceptors
Luca Grumolato,Guizhong Liu,Phyllus Mong,Raksha Mudbhary,Romi Biswas,Randy Arroyave,Sapna Vijayakumar,Aris N. Economides,Stuart A. Aaronson +8 more
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.
Journal ArticleDOI
β-Catenin-independent activation of TCF1/LEF1 in human hematopoietic tumor cells through interaction with ATF2 transcription factors.
Luca Grumolato,Guizhong Liu,Tomomi Haremaki,Sathish Kumar Mungamuri,Phyllus Mong,Gal Akiri,Pablo Lopez-Bergami,Adriana Arita,Youssef Anouar,Marek Mlodzik,Ze'ev Ronai,Joshua Brody,Daniel C. Weinstein,Stuart A. Aaronson +13 more
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.
Proceedings ArticleDOI
Abstract A02: Beta-catenin-independent activation of TCF1/LEF1 in human hematopoietic tumor cells through interaction with ATF2 transcription factors
Luca Grumolato,Guizhong Liu,Tomomi Haremaki,Sathish Kumar Mungamuri,Phyllus Mong,Gal Akiri,Pablo Lopez-Bergami,Adriana Arita,Anouar Youssef,Marek Mlodzik,Ze'ev Ronai,Joshua Brody,Daniel C. Weinstein,Stuart A. Aaronson +13 more
TL;DR: Together, these findings indicate that, through interaction with ATF2 factors, TCF1/LEF1 promote the growth of hematopoietic malignancies in the absence of beta-catenin stabilization, thus establishing a new mechanism for TCF/ LEF1 transcriptional activity distinct from that associated with canonical Wnt signaling.