Ryoko Okamoto
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View article: Morphodynamics of human early brain organoid development
Morphodynamics of human early brain organoid development Open
Brain organoids enable the mechanistic study of human brain development and provide opportunities to explore self-organization in unconstrained developmental systems 1–3 . Here we establish long-term, live light-sheet microscopy on unguide…
View article: Fate and state transitions during human blood vessel organoid development
Fate and state transitions during human blood vessel organoid development Open
Human blood vessel organoids (hBVOs) have emerged as a system to model human vascular development and disease. Here, we use single-cell multi-omics together with genetic and signaling pathway perturbations to reconstruct hBVO development. …
View article: Multi-omic human neural organoid cell atlas of the posterior brain
Multi-omic human neural organoid cell atlas of the posterior brain Open
Patterning of the neural tube establishes midbrain and hindbrain structures that coordinate motor movement, process sensory input, and integrate cognitive functions. Cellular impairment within these structures underlie diverse neurological…
View article: Decoding morphogen patterning of human neural organoids with a multiplexed single-cell transcriptomic screen
Decoding morphogen patterning of human neural organoids with a multiplexed single-cell transcriptomic screen Open
Morphogens, secreted signalling molecules that direct cell fate and tissue development, are used to direct neuroepithelial progenitors towards discrete regional identities across the central nervous system. Neural tissues derived from plur…
View article: Human neuron subtype programming through combinatorial patterning with scRNA-seq readouts
Human neuron subtype programming through combinatorial patterning with scRNA-seq readouts Open
Human neurons programmed through transcription factor (TF) overexpression model neuronal differentiation and neurological diseases. However, programming specific neuron types remains challenging. Here, we modulate developmental signaling p…
View article: Morphodynamics of human early brain organoid development
Morphodynamics of human early brain organoid development Open
Brain organoids enable the mechanistic study of human brain development, and provide opportunities to explore self-organization in unconstrained developmental systems. Here, we establish long-term, live light sheet microscopy on unguided b…
View article: Morphodynamics of human early brain organoid development
Morphodynamics of human early brain organoid development Open
Brain organoids enable the mechanistic study of human brain development, and provide opportunities to explore self-organization in unconstrained developmental systems. Here, we establish long-term, live light sheet microscopy on unguided b…
View article: Supplementary Figure 2 from Off-Target Effects of c-MET Inhibitors on Thyroid Cancer Cells
Supplementary Figure 2 from Off-Target Effects of c-MET Inhibitors on Thyroid Cancer Cells Open
PDF - 3009KB, Effect of Tivantinib and Crizotinib on cell growth and c-MET phosphorylation of MDA-MB-231 and HT29 cells.
View article: Supplementary Figure 1 from Off-Target Effects of c-MET Inhibitors on Thyroid Cancer Cells
Supplementary Figure 1 from Off-Target Effects of c-MET Inhibitors on Thyroid Cancer Cells Open
PDF - 3892KB, Molecular structure of Cizotinib, Tivantinib, and SU11274.
View article: Data from Off-Target Effects of c-MET Inhibitors on Thyroid Cancer Cells
Data from Off-Target Effects of c-MET Inhibitors on Thyroid Cancer Cells Open
Aberrantly activated c-MET signaling occurs in several cancers, promoting the development of c-MET inhibitors. In this study, we found that eight of eight thyroid cancer cell lines (including six anaplastic thyroid cell lines) have promine…
View article: Supplementary Figure 2 from Off-Target Effects of c-MET Inhibitors on Thyroid Cancer Cells
Supplementary Figure 2 from Off-Target Effects of c-MET Inhibitors on Thyroid Cancer Cells Open
PDF - 3009KB, Effect of Tivantinib and Crizotinib on cell growth and c-MET phosphorylation of MDA-MB-231 and HT29 cells.
View article: Supplementary Table 1 from Off-Target Effects of c-MET Inhibitors on Thyroid Cancer Cells
Supplementary Table 1 from Off-Target Effects of c-MET Inhibitors on Thyroid Cancer Cells Open
PDF - 60KB, Antibodies for Western blotting.
View article: Supplementary Figure 1 from Off-Target Effects of c-MET Inhibitors on Thyroid Cancer Cells
Supplementary Figure 1 from Off-Target Effects of c-MET Inhibitors on Thyroid Cancer Cells Open
PDF - 3892KB, Molecular structure of Cizotinib, Tivantinib, and SU11274.
View article: Supplementary Table 1 from Off-Target Effects of c-MET Inhibitors on Thyroid Cancer Cells
Supplementary Table 1 from Off-Target Effects of c-MET Inhibitors on Thyroid Cancer Cells Open
PDF - 60KB, Antibodies for Western blotting.
View article: Data from Off-Target Effects of c-MET Inhibitors on Thyroid Cancer Cells
Data from Off-Target Effects of c-MET Inhibitors on Thyroid Cancer Cells Open
Aberrantly activated c-MET signaling occurs in several cancers, promoting the development of c-MET inhibitors. In this study, we found that eight of eight thyroid cancer cell lines (including six anaplastic thyroid cell lines) have promine…
View article: N-acetylcysteine overcomes NF1 loss-driven resistance to PI3Kα inhibition in breast cancer
N-acetylcysteine overcomes NF1 loss-driven resistance to PI3Kα inhibition in breast cancer Open
A genome-wide PiggyBac transposon-mediated screen and a resistance screen in a PIK3CAH1047R-mutated murine tumor model reveal NF1 loss in mammary tumors resistant to the phosphatidylinositol 3-kinase α (PI3Kα)-selective inhibitor alpelisib…
View article: Supplementary Table 1 from Cucurbitacin B Induces Apoptosis by Inhibition of the <i>JAK/STAT</i> Pathway and Potentiates Antiproliferative Effects of Gemcitabine on Pancreatic Cancer Cells
Supplementary Table 1 from Cucurbitacin B Induces Apoptosis by Inhibition of the <i>JAK/STAT</i> Pathway and Potentiates Antiproliferative Effects of Gemcitabine on Pancreatic Cancer Cells Open
Supplementary Table 1 from Cucurbitacin B Induces Apoptosis by Inhibition of the JAK/STAT Pathway and Potentiates Antiproliferative Effects of Gemcitabine on Pancreatic Cancer Cells
View article: Supplementary Table 1 from Cucurbitacin B Induces Apoptosis by Inhibition of the <i>JAK/STAT</i> Pathway and Potentiates Antiproliferative Effects of Gemcitabine on Pancreatic Cancer Cells
Supplementary Table 1 from Cucurbitacin B Induces Apoptosis by Inhibition of the <i>JAK/STAT</i> Pathway and Potentiates Antiproliferative Effects of Gemcitabine on Pancreatic Cancer Cells Open
Supplementary Table 1 from Cucurbitacin B Induces Apoptosis by Inhibition of the JAK/STAT Pathway and Potentiates Antiproliferative Effects of Gemcitabine on Pancreatic Cancer Cells
View article: Data from Cucurbitacin B Induces Apoptosis by Inhibition of the <i>JAK/STAT</i> Pathway and Potentiates Antiproliferative Effects of Gemcitabine on Pancreatic Cancer Cells
Data from Cucurbitacin B Induces Apoptosis by Inhibition of the <i>JAK/STAT</i> Pathway and Potentiates Antiproliferative Effects of Gemcitabine on Pancreatic Cancer Cells Open
Pancreatic cancer is an aggressive malignancy that is generally refractory to chemotherapy, thus posing experimental and clinical challenges. In this study, the antiproliferative effect of the triterpenoid compound cucurbitacin B was teste…
View article: Data from Cucurbitacin B Induces Apoptosis by Inhibition of the <i>JAK/STAT</i> Pathway and Potentiates Antiproliferative Effects of Gemcitabine on Pancreatic Cancer Cells
Data from Cucurbitacin B Induces Apoptosis by Inhibition of the <i>JAK/STAT</i> Pathway and Potentiates Antiproliferative Effects of Gemcitabine on Pancreatic Cancer Cells Open
Pancreatic cancer is an aggressive malignancy that is generally refractory to chemotherapy, thus posing experimental and clinical challenges. In this study, the antiproliferative effect of the triterpenoid compound cucurbitacin B was teste…
View article: Induction of PD-L1 by Nitric Oxide <i>via</i> JNK Activation in A172 Glioblastoma Cells
Induction of PD-L1 by Nitric Oxide <i>via</i> JNK Activation in A172 Glioblastoma Cells Open
Glioblastoma comprises 54% of all the gliomas derived from glial cells and are lethally malignant tumors of the central nervous system (CNS). Glioma cells disrupt the blood-brain barrier, leading to access of circulating immune cells to th…