Kateri Moore

ORCID: 0000-0003-3049-5246
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About
Contact & Profiles
Research Areas
  • Hematopoietic Stem Cell Transplantation
  • Pluripotent Stem Cells Research
  • Epigenetics and DNA Methylation
  • Zebrafish Biomedical Research Applications
  • Immune Cell Function and Interaction
  • Virus-based gene therapy research
  • Mesenchymal stem cell research
  • T-cell and B-cell Immunology
  • CRISPR and Genetic Engineering
  • RNA Interference and Gene Delivery
  • Single-cell and spatial transcriptomics
  • Neonatal Respiratory Health Research
  • Cancer Cells and Metastasis
  • Cancer Genomics and Diagnostics
  • Acute Myeloid Leukemia Research
  • Cytomegalovirus and herpesvirus research
  • Pancreatic function and diabetes
  • Wnt/β-catenin signaling in development and cancer
  • Biomedical Ethics and Regulation
  • Acute Lymphoblastic Leukemia research
  • Liver physiology and pathology
  • CAR-T cell therapy research
  • Hematological disorders and diagnostics
  • Erythrocyte Function and Pathophysiology
  • Childhood Cancer Survivors' Quality of Life

Icahn School of Medicine at Mount Sinai
2012-2024

Stem Cell Institute
2013-2021

Tisch Cancer Institute
2021

Tisch Hospital
2021

Cancer Institute (WIA)
2021

The Graduate Center, CUNY
2017-2019

Graduate School USA
2018

New York Stem Cell Foundation
2015-2018

New York University
2016

Mount Sinai Hospital
2014-2015

Mechanisms regulating self-renewal and cell fate decisions in mammalian stem cells are poorly understood. We determined global gene expression profiles for mouse human hematopoietic other stages of the hierarchy. Murine share a number expressed products, which define key conserved regulatory pathways this developmental system. Moreover, mouse, portion genetic program is shared with embryonic neural cells. This overlapping set products represents molecular signature

10.1126/science.1073823 article EN Science 2002-10-17

Blood cell production originates from a rare population of multipotent, self-renewing stem cells. A genome-wide gene expression analysis was performed in order to define regulatory pathways cells as well their global genetic program. Subtracted complementary DNA libraries highly purified murine fetal liver were analyzed with bioinformatic and array hybridization strategies. large percentage the several thousand products that have been characterized correspond previously undescribed molecules...

10.1126/science.288.5471.1635 article EN Science 2000-06-02

The hematopoietic microenvironment provides a complex molecular milieu that regulates the self-renewal and differentiation activities of stem cells. We have characterized cell supportive stromal line, AFT024, was derived from murine fetal liver. Highly purified in vivo transplantable mouse cells are maintained AFT024 cultures at input levels, whereas other primitive progenitors expanded. In addition, human very effectively supported by AFT024. suggest line represents component an niche. To...

10.1073/pnas.192124499 article EN Proceedings of the National Academy of Sciences 2002-09-11

Primitive hematopoietic stem cells are closely associated with discrete in vivo microenvironments. These “niches” thought to provide the molecular signals that mediate cell differentiation and self-renewal. We have dissected fetal liver microenvironment into distinct cellular components by establishing an extensive panel of stromal lines. One particular line maintains repopulating for prolonged vitro culture periods. A subtraction cloning strategy has yielded a cDNA encodes surface...

10.1073/pnas.94.8.4011 article EN Proceedings of the National Academy of Sciences 1997-04-15

We investigated the homeostatic behavior of hematopoietic stem and progenitor cells (HSPCs) temporally defined according to their divisional histories using an HSPC-specific GFP label-retaining system. show that (HSCs) lose repopulating potential after limited cell divisions. Once HSCs exit dormancy accrue divisions, they also progressively ability return G0 functional activities associated with quiescent HSCs. In addition, dormant HSPCs phenotypically as multipotent display robust activity...

10.1016/j.stemcr.2014.01.016 article EN cc-by-nc-nd Stem Cell Reports 2014-03-22

Multiple replication-defective retrovirus vectors were tested for their ability to transfer and express human adenosine deaminase in vitro vivo a mouse bone marrow transplantation model. High-titer virus production was obtained from by using both long terminal repeat promoter internal transcriptional units with c-fos herpes thymidine kinase promoters. After infection of primary murine one these vectors, detected 60 85% spleen colony-forming the blood 14 syngeneic transplant recipients. This...

10.1128/mcb.8.12.5116 article EN Molecular and Cellular Biology 1988-12-01

The kinetics of label uptake and dilution in dividing stem cells, e.g., using Bromodeoxyuridine (BrdU) as a labeling substance, are common way to assess the cellular turnover all hematopoietic cells (HSCs) vivo. assumption that HSCs form homogeneous population which regularly undergo cell division has recently been challenged by new experimental results. For consistent functional explanation heterogeneity among HSCs, we propose concept flexibly reversibly adapt their cycling state according...

10.1371/journal.pcbi.1000447 article EN cc-by PLoS Computational Biology 2009-07-23

Somatic PTPN11 mutations cause juvenile myelomonocytic leukemia (JMML). Germline defects Noonan syndrome (NS), and specific inherited NS/JMML. Here, we report that hematopoietic cells differentiated from human induced pluripotent stem (hiPSCs) harboring NS/JMML-causing recapitulated JMML features. hiPSC-derived NS/JMML myeloid exhibited increased signaling through STAT5 upregulation of miR-223 miR-15a. Similarly, miR-15a were upregulated in 11/19 bone marrow mononuclear mutations, but not...

10.1016/j.celrep.2015.09.019 article EN cc-by Cell Reports 2015-10-01

Significance Li–Fraumeni syndrome is a rare disorder caused by germline TP53 mutations, predisposing patients to early-onset cancers, including osteosarcoma (OS). Here we demonstrate that strong expression of SFRP2, reported WNT antagonist, in OS patient samples correlates with poor survival and SFRP2 overexpression suppresses normal osteoblast differentiation, promotes features, facilitates angiogenesis via autocrine paracrine mechanisms an induced pluripotent stem cell disease model. We...

10.1073/pnas.1814044115 article EN Proceedings of the National Academy of Sciences 2018-11-01
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