A5005879024- CRISPR and Genetic Engineering
- RNA modifications and cancer
- CAR-T cell therapy research
- Cancer Cells and Metastasis
- Cancer Genomics and Diagnostics
- Single-cell and spatial transcriptomics
- Endoplasmic Reticulum Stress and Disease
- Innovative Microfluidic and Catalytic Techniques Innovation
- Virus-based gene therapy research
- Bioinformatics and Genomic Networks
- Cellular transport and secretion
- Epigenetics and DNA Methylation
- Lung Cancer Treatments and Mutations
- Phagocytosis and Immune Regulation
- Cancer Research and Treatments
- Glioma Diagnosis and Treatment
- Circular RNAs in diseases
- Mitochondrial Function and Pathology
- Tissue Engineering and Regenerative Medicine
- Cancer Immunotherapy and Biomarkers
The University of Texas Health Science Center at Houston
2021-2024
The University of Texas MD Anderson Cancer Center
2019-2024
Significance Exquisite lipid-binding specificity for phosphatidylserine (PtdSer) is hardwired into the structure of KRAS C-terminal plasma membrane (PM) anchor. This renders KRAS–PM localization and hence biological function potentially vulnerable to perturbations PM PtdSer content. Here, we show that all components recently described lipid transport machinery maintain content are indeed required support oncogenic function. In this context, demonstrate enzyme, PI4KIIIα, in particular has...
Conventional genetically engineered mouse models (GEMM) are time-consuming, laborious, and offer limited spatiotemporal control. Here, we describe the development of a streamlined platform for in vivo gene activation using CRISPR (CRISPRa) technology. Unlike conventional GEMMs, this model system allows flexible, sustained, timed one or more target genes single pooled lentiviral guides. Myc Yap1 were used as oncogenes to demonstrate primary pancreatic organoid cultures vitro enhanced...
Abstract Efforts to understand etiology of glioma led researchers investigate associated genetic factors. Genome Wide Association Studies (GWAS) conducted that end, uncovered an association various single nucleotide polymorphisms (SNP) among hallmark oncogenes and tumor suppressors as risk variants in incidence. Here, we perform vitro modeling four alleles/SNPs((rs723527 (EGFR), rs55705857 (MYC), rs7572263 (IDH1), rs78378222 (TP53)) mapped non-coding regulatory regions the genome, assess...
Abstract Deficiency of ATRX (Alpha Thalassemia/Mental Retardation Syndrome X-linked), a core member SWI/SNF family chromatin regulator is altered in diffuse gliomas and coexist with IDH1/2 mutations adults histone G34R/V alterations pediatric populations. Loss has been associated global accessibility epigenomics landscape, however, the detail mechanism behind oncogenic transformation remains elusive. Integrating transcriptomics in-depth positional epigenome analysis over repetitive DNA...
<div><p>Conventional genetically engineered mouse models (GEMM) are time-consuming, laborious, and offer limited spatiotemporal control. Here, we describe the development of a streamlined platform for <i>in vivo</i> gene activation using CRISPR (CRISPRa) technology. Unlike conventional GEMMs, this model system allows flexible, sustained, timed one or more target genes single pooled lentiviral guides. <i>Myc</i> <i>Yap1</i> were used as...
Supplementary Figure from A Programmable <i>In Vivo</i> CRISPR Activation Model Elucidates the Oncogenic and Immunosuppressive Functions of MYC in Lung Adenocarcinoma
Supplementary Figure from A Programmable <i>In Vivo</i> CRISPR Activation Model Elucidates the Oncogenic and Immunosuppressive Functions of MYC in Lung Adenocarcinoma
Supplementary Figure from A Programmable <i>In Vivo</i> CRISPR Activation Model Elucidates the Oncogenic and Immunosuppressive Functions of MYC in Lung Adenocarcinoma
Supplementary Figure from A Programmable <i>In Vivo</i> CRISPR Activation Model Elucidates the Oncogenic and Immunosuppressive Functions of MYC in Lung Adenocarcinoma
Supplementary Data from A Programmable <i>In Vivo</i> CRISPR Activation Model Elucidates the Oncogenic and Immunosuppressive Functions of MYC in Lung Adenocarcinoma
Supplementary Figure from A Programmable <i>In Vivo</i> CRISPR Activation Model Elucidates the Oncogenic and Immunosuppressive Functions of MYC in Lung Adenocarcinoma
Supplementary Figure from A Programmable <i>In Vivo</i> CRISPR Activation Model Elucidates the Oncogenic and Immunosuppressive Functions of MYC in Lung Adenocarcinoma
Supplementary Data from A Programmable <i>In Vivo</i> CRISPR Activation Model Elucidates the Oncogenic and Immunosuppressive Functions of MYC in Lung Adenocarcinoma
Supplementary Figure from A Programmable <i>In Vivo</i> CRISPR Activation Model Elucidates the Oncogenic and Immunosuppressive Functions of MYC in Lung Adenocarcinoma
Supplementary Figure from A Programmable <i>In Vivo</i> CRISPR Activation Model Elucidates the Oncogenic and Immunosuppressive Functions of MYC in Lung Adenocarcinoma
Supplementary Figure from A Programmable <i>In Vivo</i> CRISPR Activation Model Elucidates the Oncogenic and Immunosuppressive Functions of MYC in Lung Adenocarcinoma
Supplementary Figure from A Programmable <i>In Vivo</i> CRISPR Activation Model Elucidates the Oncogenic and Immunosuppressive Functions of MYC in Lung Adenocarcinoma
Supplementary Figure from A Programmable <i>In Vivo</i> CRISPR Activation Model Elucidates the Oncogenic and Immunosuppressive Functions of MYC in Lung Adenocarcinoma
Supplementary Figure from A Programmable <i>In Vivo</i> CRISPR Activation Model Elucidates the Oncogenic and Immunosuppressive Functions of MYC in Lung Adenocarcinoma
<div><p>Conventional genetically engineered mouse models (GEMM) are time-consuming, laborious, and offer limited spatiotemporal control. Here, we describe the development of a streamlined platform for <i>in vivo</i> gene activation using CRISPR (CRISPRa) technology. Unlike conventional GEMMs, this model system allows flexible, sustained, timed one or more target genes single pooled lentiviral guides. <i>Myc</i> <i>Yap1</i> were used as...
Abstract Introduction: Pancreatic cancer is characterized by early metastasis and resistance to chemotherapy. To elucidate the transcriptional reprogramming drug that emerges during metastatic cascade, we set out characterize transcriptomic profiles response of matched sets cell organoids derived from multiple sites (primary tumor, lesion, circulating tumor cells) in tumor-bearing PKCY (p53L/wt, KrasLSL-G12D/wt, ptf1acre/wt, Rosa26LSL-YFP/LSL-YFP) mice. Methods: establish primary organoids,...
Abstract Conventional genetically engineered mouse models (GEMMs) are time consuming, laborious and offer limited spatio-temporal control. We have developed a streamlined platform for in vivo gene activation using CRISPR (CRISPRa) technology. Our model system allows flexible, sustained timed of one or more target genes, vitro vivo, single pooled lentiviral guides. Using Myc Yap1 as oncogenes, we implemented this to study the effect oncogene on tumorigenic potential primary pancreatic...
Abstract Conventional genetically engineered mouse models (GEMMs) are time consuming, laborious and offer limited spatio-temporal control. Here, we describe the development of a streamlined platform for in vivo gene activation using CRISPR (CRISPRa) technology. Unlike conventional GEMMs, our model system allows flexible, sustained timed one or more target genes single pooled lentiviral guides. Using Myc Yap1 as oncogenes, demonstrate primary pancreatic organoid cultures vitro enhanced...