A5063179291- Cancer-related Molecular Pathways
- Pluripotent Stem Cells Research
- CRISPR and Genetic Engineering
- Cancer, Hypoxia, and Metabolism
- Epigenetics and DNA Methylation
- Genomics and Chromatin Dynamics
- RNA Research and Splicing
- RNA modifications and cancer
- Animal Genetics and Reproduction
- Reproductive System and Pregnancy
- Cancer-related gene regulation
- Renal and related cancers
- Bone health and treatments
- Genetic and Kidney Cyst Diseases
- Single-cell and spatial transcriptomics
- DNA Repair Mechanisms
- Computational Drug Discovery Methods
- Synthesis and Characterization of Heterocyclic Compounds
- Immune Cell Function and Interaction
- Parathyroid Disorders and Treatments
- 3D Printing in Biomedical Research
- Hedgehog Signaling Pathway Studies
- PARP inhibition in cancer therapy
- Genetics and Neurodevelopmental Disorders
- Bone Metabolism and Diseases
Weizmann Institute of Science
2010-2023
Hebrew University of Jerusalem
2010-2014
Tel Aviv University
2010
Johns Hopkins University
2010
Bar-Ilan University
2006
mRNA modification regulates pluripotency When stem cells progress from an embryonic pluripotent state toward a particular lineage, molecular switches dismantle the transcription factor network that keeps cell pluripotent. Geula et al. now show N6-methyladenosine (m6A), messenger RNA (mRNA) present on transcripts of factors, drives this transition. Methylation destabilized and limited their translation efficiency, which promoted timely decay naïve pluripotency. This m6A methylation was also...
Objective— Bone Gla Protein (BGP, osteocalcin) is commonly present in the calcified vasculature and was recently shown as energy metabolism-regulating hormone. This study investigates role of BGP cartilage mineralization. Methods Results— We established an vitro BGP-overexpression model chondrocytes (ATDC5) vascular smooth muscle cells (MOVAS). overexpression upregulated markers chondrogenic differentiation intensified staining for minerals. enhanced glucose uptake increased expression...
Mice deficient for all ten-eleven translocation (TET) genes exhibit early gastrulation lethality. However, separating cause and effect in such embryonic failure is challenging. To isolate cell-autonomous effects of TET loss, we used temporal single-cell atlases from embryos with partial or complete mutant contributions. Strikingly, when developing within a wild-type embryo, Tet-mutant cells retain near-complete differentiation potential, whereas solely comprising are defective epiblast to...
Abstract In this study, we focus on the analysis of a previously identified cancer-related gene signature (CGS) that underlies cross talk between p53 tumor suppressor and Ras oncogene. CGS consists large number known downstream target genes were synergistically upregulated by wild-type loss oncogenic H-RasG12V expression. Here show expression strongly correlates with malignancy. an attempt to elucidate molecular mechanisms underling cooperation H-RasG12V, distinguished pathways may account...
Compelling evidences have rendered the tumor microenvironment a crucial determinant in cancer outcome. Activating transcription factor 3 (ATF3), stress response factor, is known to dichotomous role cells, acting either as suppressor or an oncogene context-dependent manner. However, its expression and possible are hitherto unknown. Here we show that ATF3 upregulated stromal compartment of several types cancer. Accordingly, Cancer-associated fibroblasts (CAFs) ectopically expressing...
GNAO1-associated disorders are ultra-rare autosomal dominant conditions, which can manifest, depending on the exact pathogenic variant in GNAO1, as a spectrum of neurological phenotypes, including epileptic encephalopathy, developmental delay with movement disorders, or late-onset dystonia. There currently no effective treatments available, apart from symptomatic options. In this work, we suggest harnessing personalized RNA therapy to treat GNAO1 patients and focus specifically recurrent...
Abstract Mutations in p53 are ubiquitous human tumors. Some mutations not only result loss of wild-type (WT) activity but also grant additional functions, termed “gain function.” In this study, we explore how the status affects immediate response gene activating transcription factor 3 (ATF3) 12-O-tetradecanoylphorbol-13-acetate (TPA)-protein kinase C (PKC) pathway. We show that high doses TPA induce ATF3 a WT p53-independent manner correlating with PKCs depletion and cell death. cells...
Abstract Eviction of histones from nucleosomes and their exchange with newly synthesized or alternative variants is a central epigenetic determinant. Here, we define the genome-wide occupancy pattern canonical non-canonical histone in mouse embryonic stem cells by genetically encoded sensors. While all measured scales transcription, describe variant-specific associations transcription elongation Polycomb binding. We found considerable H3.1 H2B heterochromatin repeat elements, contrasting...
Measurement of Alkaline Phosphatase (ALP) level is a widely used procedure in clinical and basic research. We present simple inexpensive luminescence-based method that allows multiplexed measurement normalization intracellular ALP levels one sample well. The comprises two commercially available reagents enabling quantification cell number by sequential luminescence readouts. Using this we were able to detect analyze somatic reprogramming into pluripotent stem cells. highly applicable for...
The ability to reprogram somatic cells into induced pluripotent stem (iPSCs) with four transcription factors Oct4, Sox2, Klf4 and cMyc (abbreviated as OSKM) 1 has provoked interest define the molecular characteristics of this process 2-7 . Despite important progress, dynamics epigenetic reprogramming at high resolution in correctly reprogrammed iPSCs throughout entire remain largely undefined. This gap understanding results from inefficiency conventional methods coupled difficulty...