A5033939534- Cancer Mechanisms and Therapy
- CRISPR and Genetic Engineering
- Chromatin Remodeling and Cancer
- Protein Degradation and Inhibitors
- Genomics and Chromatin Dynamics
- interferon and immune responses
- Hair Growth and Disorders
- Melanoma and MAPK Pathways
- Advanced biosensing and bioanalysis techniques
- Machine Learning in Bioinformatics
- Mechanisms of cancer metastasis
- Ubiquitin and proteasome pathways
- Ovarian cancer diagnosis and treatment
- Glutathione Transferases and Polymorphisms
- Neuroinflammation and Neurodegeneration Mechanisms
- Cancer and Skin Lesions
- Genomics and Rare Diseases
- RNA regulation and disease
- Thyroid Disorders and Treatments
- melanin and skin pigmentation
- Urological Disorders and Treatments
- Cellular transport and secretion
- Histone Deacetylase Inhibitors Research
- Immune Response and Inflammation
- Autophagy in Disease and Therapy
Stanford University
2017-2023
Howard Hughes Medical Institute
2013-2021
Stratford University
2021
Stanford Medicine
2021
Institute of Molecular Biology, Academia Sinica
2011
National Defense Medical Center
2011
Institute of Zoology
2006
Abstract Mutations in ARID1A rank among the most common molecular aberrations human cancer. However, oncogenic consequences of mutation cells remain poorly defined due to lack forward genetic models. Here, CRISPR/Cas9-mediated knockout (KO) primary TP53−/− gastric organoids induced morphologic dysplasia, tumorigenicity, and mucinous differentiation. Genetic WNT/β-catenin activation rescued differentiation, but not hyperproliferation, suggesting alternative pathways KO-mediated...
Dendritic arborization is a critical neuronal differentiation process. Here, we demonstrate that syndecan-2 (Sdc2), synaptic heparan sulfate proteoglycan triggers dendritic filopodia and spine formation, regulates in cultured hippocampal neurons. This process controlled by sterile α TIR motif–containing 1 protein (Sarm1), negative regulator of Toll-like receptor 3 (TLR3) innate immunity signaling. We show Sarm1 interacts with receives signal from Sdc2 controls through the MKK4–JNK pathway....
Autophagy is a catabolic membrane-trafficking mechanism conserved in all eukaryotic cells. In addition to the nonselective transport of bulk cytosol, autophagy responsible for efficient delivery vacuolar enzyme Ape1 precursor (prApe1) budding yeast Saccharomyces cerevisiae, suggesting presence prApe1 sorting machinery. Sequential interactions between Atg19-Atg11 and Atg19-Atg8 pairs are thought targeting vesicle formation site, preautophagosomal structure (PAS), loading it into vesicles,...
SWI/SNF (BAF) complexes are a diverse family of ATP-dependent chromatin remodelers produced by combinatorial assembly that mutated in and thought to contribute 20% human cancers large number neurologic diseases. The gene-activating functions BAF essential for viability many cell types, limiting the development small molecule inhibitors. To circumvent potential toxicity inhibition, we identified molecules inhibit specific repressive function these but relatively nontoxic importantly synergize...
SWI/SNF (BAF) complexes are a diverse family of ATP-dependent chromatin remodelers produced by combinatorial assembly that mutated in and thought to contribute 20% human cancers large number neurologic diseases. The gene-activating functions BAF essential for viability many cell types, limiting the development small molecule inhibitors. To circumvent potential toxicity inhibition, we identified molecules inhibit specific repressive function these but relatively non-toxic importantly...
ABSTRACT Genes that drive the proliferation, survival, invasion and metastasis of malignant cells have been identified for many human cancers 1–6 . Independent studies cell death pathways eliminate good organism 7–10 The coexistence with driver mutations suggest cancer could be rewired to activate death. We invented a new class molecules: TCIPs (Transcriptional/Epigenetic Chemical Inducers Proximity) recruit endogenous driver, or downstream transcription factor, promoters genes thereby...
Abstract Recent unbiased exome and whole-genome sequencing studies have identified ARID1B (originally BAF250b) as the most frequently mutated gene in human de novo neurodevelopmental disorders a high confidence autism gene. is subunit of multimeric SWI/SNF or Brg/Brahma-Associated Factor (BAF) ATP-dependent chromatin remodeling complex. Studies Arid1b+/- mice well other BAF mutants found defects neural progenitor proliferation activity-dependent neuronal dendritogenesis; however, to date,...
Abstract Mutations in ARID1A, encoding a subunit of the BAF chromatin remodeling complex, rank amongst most common molecular aberrations human cancer. However, oncogenic consequences ARID1A mutation cells remain poorly defined due to lack forward genetic model systems. Here, CRISPR/Cas9 knockout primary TP53-/- gastric organoids induced morphologic dysplasia, tumorigenicity and mucinous differentiation but impaired Wnt/β-catenin signaling. Genetic Wnt pathway activation rescued...
<div>Abstract<p>Mutations in <i>ARID1A</i> rank among the most common molecular aberrations human cancer. However, oncogenic consequences of mutation cells remain poorly defined due to lack forward genetic models. Here, CRISPR/Cas9-mediated knockout (KO) primary <i>TP53<sup>−/−</sup></i> gastric organoids induced morphologic dysplasia, tumorigenicity, and mucinous differentiation. Genetic WNT/β-catenin activation rescued differentiation, but...
<p>Key Resources Tables</p>
<p>Key Resources Tables</p>
<p>Supplementary Figure 1</p>
<p>Supplementary Figure 1</p>
<div>Abstract<p>Mutations in <i>ARID1A</i> rank among the most common molecular aberrations human cancer. However, oncogenic consequences of mutation cells remain poorly defined due to lack forward genetic models. Here, CRISPR/Cas9-mediated knockout (KO) primary <i>TP53<sup>−/−</sup></i> gastric organoids induced morphologic dysplasia, tumorigenicity, and mucinous differentiation. Genetic WNT/β-catenin activation rescued differentiation, but...
<p>Supplementary Figure 7</p>