Loss of Asxl1 leads to myelodysplastic syndrome-like disease in mice - Wikidata - awgldk - TriplyDB

Loss of Asxl1 leads to myelodysplastic syndrome-like disease in mice

Loss of Asxl1 leads to myelodysplastic syndrome-like disease in mice

http://www.wikidata.org/entity/Q37512080

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The Hen or the Egg: Inflammatory Aspects of Murine MPN Models Additional sex combs-like family genes are required for normal cardiovascular development Epigenetics in normal and malignant hematopoiesis: An overview and update 2017.ASXL2 is essential for haematopoiesis and acts as a haploinsufficient tumour suppressor in leukemia.Loss of Asxl2 leads to myeloid malignancies in mice The distinct biological implications of Asxl1 mutation and its roles in leukemogenesis revealed by a knock-in mouse model Splicing factor 3b subunit 1 (Sf3b1) haploinsufficient mice display features of low risk Myelodysplastic syndromes with ring sideroblasts.The molecular basis of myeloid malignancies.ASXL1 mutations in younger adult patients with acute myeloid leukemia: a study by the German-Austrian Acute Myeloid Leukemia Study Group.Biology of BM failure syndromes: role of microenvironment and niches.Epigenetic Control of Stem Cell Potential during Homeostasis, Aging, and Disease SETBP1 mutations drive leukemic transformation in ASXL1-mutated MDS.Cancer-associated ASXL1 mutations may act as gain-of-function mutations of the ASXL1-BAP1 complex.Tumor suppressor ASXL1 is essential for the activation of INK4B expression in response to oncogene activity and anti-proliferative signals.Whole-exome and targeted sequencing identify ROBO1 and ROBO2 mutations as progression-related drivers in myelodysplastic syndromes.Digging deep into "dirty" drugs - modulation of the methylation machinery.Combined Loss of Tet1 and Tet2 Promotes B Cell, but Not Myeloid Malignancies, in Mice.Chronic myelomonocytic leukemia: Forefront of the field in 2015.Loss of Asxl1 Alters Self-Renewal and Cell Fate of Bone Marrow Stromal Cell, Leading to Bohring-Opitz-like Syndrome in Mice.ASXL1 plays an important role in erythropoiesis.Dynamics of ASXL1 mutation and other associated genetic alterations during disease progression in patients with primary myelodysplastic syndrome.Integrating genetics and epigenetics in myelodysplastic syndromes: advances in pathogenesis and disease evolution.Novel working hypothesis for pathogenesis of hematological malignancies: combination of mutations-induced cellular phenotypes determines the disease (cMIP-DD).Mutations in epigenetic modifiers in acute myeloid leukemia and their clinical utility.The Role of Additional Sex Combs-Like Proteins in Cancer.ASXL1 interacts with the cohesin complex to maintain chromatid separation and gene expression for normal hematopoiesis.Epigenetic dysregulation of hematopoietic stem cells and preleukemic state.Histone H2A Monoubiquitination in Neurodevelopmental Disorders.Surveillance Recommendations for Children with Overgrowth Syndromes and Predisposition to Wilms Tumors and Hepatoblastoma.Clonal hematopoiesis as determined by the HUMARA assay is a marker for acquired mutations in epigenetic regulators in older women.Gain-of-function of ASXL1 truncating protein in the pathogenesis of myeloid malignancies.Loss of ASXL1 in the bone marrow niche dysregulates hematopoietic stem and progenitor cell fates.Acute myeloid leukemia in a father and son with a germline mutation of ASXL1.Somatic Mutations and Clonal Hematopoiesis: Unexpected Potential New Drivers of Age-Related Cardiovascular Disease.The chromatin remodeling subunit Baf200 promotes normal hematopoiesis and inhibits leukemogenesis.CRISPR/Cas9-mediated ASXL1 mutations in U937 cells disrupt myeloid differentiation.Expression of mutant Asxl1 perturbs hematopoiesis and promotes susceptibility to leukemic transformation.Setd2 deficiency impairs hematopoietic stem cell self-renewal and causes malignant transformation.Clinical management of patients with ASXL1 mutations and Bohring-Opitz syndrome, emphasizing the need for Wilms tumor surveillance.Selective inhibition of BCL-2 is a promising target in patients with high-risk myelodysplastic syndromes and adverse mutational profile.

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Loss of Asxl1 leads to myelodysplastic syndrome-like disease in mice

http://www.wikidata.org/entity/Q37512080

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2013 nî lūn-bûn

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name

Loss of Asxl1 leads to myelodysplastic syndrome-like disease in mice

@en

Loss of Asxl1 leads to myelodysplastic syndrome-like disease in mice.

@nl

type

label

Loss of Asxl1 leads to myelodysplastic syndrome-like disease in mice

@en

Loss of Asxl1 leads to myelodysplastic syndrome-like disease in mice.

@nl

prefLabel

Loss of Asxl1 leads to myelodysplastic syndrome-like disease in mice

@en

Loss of Asxl1 leads to myelodysplastic syndrome-like disease in mice.

@nl

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Loss of Asxl1 leads to myelodysplastic syndrome-like disease in mice

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Chen-Leng Cai

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Feng Pan

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Feng-Chun Yang

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Hongyu Ni

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Jiapeng Wang

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Jiehao Zhou

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Jin Yuan

http://www.w3.org/2001/XMLSchema#string

Li Jiang

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Lihn Nguyen

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Mingjiang Xu

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ASXL1 mutations promote myeloid transformation through loss of PRC2-mediated gene repression

Histone H2A deubiquitinase activity of the Polycomb repressive complex PR-DUB

Additional sex comb-like 1 (ASXL1), in cooperation with SRC-1, acts as a ligand-dependent coactivator for retinoic acid receptor

The genetic basis of early T-cell precursor acute lymphoblastic leukaemia.

Genome-wide maps of chromatin state in pluripotent and lineage-committed cells

High-resolution profiling of histone methylations in the human genome

A bivalent chromatin structure marks key developmental genes in embryonic stem cells

ASXL1 represses retinoic acid receptor-mediated transcription through associating with HP1 and LSD1

A human homolog of Additional sex combs, ADDITIONAL SEX COMBS-LIKE 1, maps to chromosome 20q11

Exome sequencing identifies recurrent mutations of the splicing factor SF3B1 gene in chronic lymphocytic leukemia

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10.1182/BLOOD-2013-05-500272

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