scispace - formally typeset
J

Jun-ichi Hanai

Researcher at Beth Israel Deaconess Medical Center

Publications -  56
Citations -  10141

Jun-ichi Hanai is an academic researcher from Beth Israel Deaconess Medical Center. The author has contributed to research in topics: SMAD & Transactivation. The author has an hindex of 35, co-authored 56 publications receiving 9429 citations. Previous affiliations of Jun-ichi Hanai include Harvard University & Japan Society for the Promotion of Science.

Papers
More filters
Journal ArticleDOI

Inhibition of lung cancer growth: ATP citrate lyase knockdown and statin treatment leads to dual blockade of mitogen-activated protein Kinase (MAPK) and Phosphatidylinositol-3-kinase (PI3K)/AKT pathways†

TL;DR: It is shown that ACL knockdown promotes apoptosis and differentiation, leading to the inhibition of tumor growth in vivo, and it is found that statins, inhibitors of 3‐hydroxy‐3‐methylglutaryl coenzyme A (HMG‐CoA) reductase, which act downstream of ACL in the cholesterol synthesis pathway, dramatically enhance the anti‐tumor effects of ACL inhibition, even regressing established tumors.
Journal ArticleDOI

Lipocalin 2 Diminishes Invasiveness and Metastasis of Ras-transformed Cells

TL;DR: Data characterize lipocalin 2 as an epithelial inducer in Ras malignancy and a suppressor of metastasis.
Journal ArticleDOI

Magic roundabout, a tumor endothelial marker: Expression and signaling

TL;DR: The tumor endothelial specific expression of a Robo family member, magic roundabout (MRB), functionally characterized its role in endothelial cell migration and defined a signaling pathway that might mediate this function.
Journal ArticleDOI

Statin-induced muscle damage and atrogin-1 induction is the result of a geranylgeranylation defect

TL;DR: It is reported here that lovastatin‐induced atrogin‐1 expression and muscle damage in cultured mouse myotubes and zebrafish can be prevented in the presence of geranylgeranol but not farnesol, and the concept that dysfunction of small GTP‐binding proteins lead to statin‐induced muscle damage is supported.
Journal ArticleDOI

E1A Inhibits Transforming Growth Factor-β Signaling through Binding to Smad Proteins

TL;DR: The Smad interaction domain (SID) in p300 is determined and it is found that two adjacent regions are required for the interaction, suggesting a novel mechanism whereby E1A antagonizes TGF-β signaling.