Deletion of Asxl1 results in myelodysplasia and severe developmental defects in vivo - Wikidata - awgldk - TriplyDB

Deletion of Asxl1 results in myelodysplasia and severe developmental defects in vivo

Deletion of Asxl1 results in myelodysplasia and severe developmental defects in vivo

http://www.wikidata.org/entity/Q30413034

about

Functions of TET Proteins in Hematopoietic Transformation Molecular basis of cleft palates in mice Revisiting the case for genetically engineered mouse models in human myelodysplastic syndrome research Connections between TET proteins and aberrant DNA modification in cancer The TET2 interactors and their links to hematological malignancies Dose-dependent role of the cohesin complex in normal and malignant hematopoiesis.Next generation sequencing of acute myeloid leukemia: influencing prognosis.Next-generation sequencing of acute myeloid leukemia identifies the significance of TP53, U2AF1, ASXL1, and TET2 mutations Role of TET enzymes in DNA methylation, development, and cancer Age-related mutations associated with clonal hematopoietic expansion and malignancies Additional sex combs-like family genes are required for normal cardiovascular development Large-Scale Exome-wide Association Analysis Identifies Loci for White Blood Cell Traits and Pleiotropy with Immune-Mediated Diseases.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 The genomic landscape of core-binding factor acute myeloid leukemias Evaluation of allelic strength of human TET2 mutations and cooperation between Tet2 knockdown and oncogenic Nras mutation.ASXL genes and RUNX1: an intimate connection?Pathogenesis of myelodysplastic syndromes: an overview of molecular and non-molecular aspects of the disease.Myelodysplasia is in the niche: novel concepts and emerging therapies.The molecular basis of myeloid malignancies.Mutant U2AF1 Expression Alters Hematopoiesis and Pre-mRNA Splicing In Vivo.Role of ASXL1 and TP53 mutations in the molecular classification and prognosis of acute myeloid leukemias with myelodysplasia-related changes.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.TET proteins and 5-methylcytosine oxidation in hematological cancers 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.Assessment of the ExAC data set for the presence of individuals with pathogenic genotypes implicated in severe Mendelian pediatric disorders.DNA methylation and hydroxymethylation in hematologic differentiation and transformation.De novo dominant ASXL3 mutations alter H2A deubiquitination and transcription in Bainbridge-Ropers syndrome.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.Regulation of stem cell function by protein ubiquitylation Stem cell origin of myelodysplastic syndromes.

P2860

Q26778323-7FE7D6A4-C2CF-48C6-AE52-424ECC3A705B Q26795762-6082F7E4-D0BD-4B8E-AF50-CCEEDA5B0ED9 Q26859843-68C33030-097D-4A1F-B149-A86480224743 Q26865671-2472CD91-580C-4BDB-AC0B-7BE157D930E3 Q27002485-C4232965-08A7-4D26-94A5-E291C31E8218 Q27308738-ED1795F4-74E7-476D-8CB4-D9ECEE4087B3 Q27690776-A1F6C997-EDF2-4857-8A21-A71FD800E9D8 Q27853094-7BAC1C85-D5E9-44B0-8949-C32012AD5347 Q28068541-B4887DA2-C717-4ED1-810C-0B9966819EDC Q28387160-F20B1C5D-1D79-4F34-9518-DDCF630AC019 Q28585968-1844C7CB-83FC-497B-B8F2-9DF39006AFB1 Q30276495-719A1689-2F86-4492-9D4D-4E7C5535AF6A Q33607609-8BCED9B3-8F11-44DE-9556-E531B908723B Q33753763-F81CC4B7-1ADA-4F81-8BAE-2927FF68CFB6 Q33802946-01665B2F-CA16-4277-A925-3062A1069351 Q33892323-7FD9918A-AAC1-4851-99C6-9504F2CF8F9B Q33901968-3AB32BC6-8FAF-45F4-BF01-C081280A5EC1 Q33934784-E033A6B6-F910-4F36-9D6D-1BCCD9DEEBE5 Q34106779-2E3CFE95-77CE-4E19-B9C1-6B07EFB3A72C Q34667249-49CF58D9-34A5-49C1-8A50-6208F09C26AA Q35059425-61E0D6F9-7AE6-4612-9D0B-E7E3C335A320 Q35103708-E48DF317-A0FE-4526-BBE6-A4D4C2807F74 Q35604082-6CB110FE-8F91-491E-847C-F920660E4B79 Q35781605-8C1F6DF8-298C-4F68-90B0-A9E042A992B9 Q35849733-9A3AA534-77C6-4E9E-8E45-5F2C8D4E3A45 Q36018603-B6FCED5B-55B8-4414-B328-4CE273A4E57C Q36197509-01992DF0-8FE5-4C56-B772-DE43D971D3D7 Q36292997-FA98D776-2D2E-4A2E-ACE1-C4CCE8DC5323 Q36360964-A414863B-AEA7-43C3-B4FB-85326018DE47 Q36362825-802EF725-7125-40F9-80A4-06D3262ADBBB Q36395976-5972E0CE-1D88-4CCE-A622-D558055369C2 Q36514637-C1036526-D78A-4D78-91DF-D6C5D7C93DA4 Q36523796-62F8567A-838B-4C73-8107-607594AB7EFA Q36608413-E631A4F3-144A-400E-BD4F-2B8683E8A681 Q36876853-E46E0E2D-66FE-4B9C-85B0-22838A8D9BE5 Q37014700-89E537C5-C9F6-416D-8800-03AA045C2EB7 Q37049843-3307FFFD-E43E-4BF2-B3BD-76E647A54099 Q37555315-338A0F5A-9D37-4F7F-9748-9714F03759B5 Q37707515-026CE8C1-2004-44B7-893B-8B0B7EAA140B Q38171230-6100EB97-8646-429A-9033-A031CD1D2EFD

P2860

Deletion of Asxl1 results in myelodysplasia and severe developmental defects in vivo

http://www.wikidata.org/entity/Q30413034

description

2013 nî lūn-bûn

@nan

2013 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած

@hyw

2013 թվականի նոյեմբերին հրատարակված գիտական հոդված

@hy

2013年の論文

@ja

2013年論文

@yue

2013年論文

@zh-hant

2013年論文

@zh-hk

2013年論文

@zh-mo

2013年論文

@zh-tw

2013年论文

@wuu

name

Deletion of Asxl1 results in myelodysplasia and severe developmental defects in vivo

@ast

Deletion of Asxl1 results in myelodysplasia and severe developmental defects in vivo

@en

type

label

Deletion of Asxl1 results in myelodysplasia and severe developmental defects in vivo

@ast

Deletion of Asxl1 results in myelodysplasia and severe developmental defects in vivo

@en

prefLabel

Deletion of Asxl1 results in myelodysplasia and severe developmental defects in vivo

@ast

Deletion of Asxl1 results in myelodysplasia and severe developmental defects in vivo

@en

P1433

Q30413034-A024C071-AA43-40D8-B8A2-C71A6F356A06

P1476

Q30413034-35CE4E75-0F9A-40EA-A511-E9AF59955367

P2093

Q30413034-1A5C247E-BF95-49C4-8A6A-CE2C582429F4

Q30413034-1F5F8316-7AE3-46EC-B988-574F033A114C

Q30413034-232FD229-C0ED-4F96-BB56-B71920B56F2C

Q30413034-2B2EC9E1-ACFA-4885-90CC-A424FE569834

Q30413034-2C55E7BE-DDE5-4835-8CA9-860BF063442F

Q30413034-2F9F0BA0-6C0E-4DD5-AF3A-4E6668361E04

Q30413034-33C8A3B3-3776-4E50-A03C-31585A3B5D2D

Q30413034-3BB79C29-9329-403D-AB72-09363F660348

Q30413034-57F8834D-CD3D-4A5D-860E-DAD052F94B9F

Q30413034-5C4F6CC8-5448-4067-A8D4-F4F2F3B78F9B

P2860

Q30413034-05C07BD0-5B83-4C05-9A73-153A074E0B5B

Q30413034-09576916-3318-479F-B733-87FC3E4CCECA

Q30413034-1BFB1C68-6F0B-4C5A-8553-CCA2E071D79D

Q30413034-1DEC5BCA-EB95-4491-911D-7D0295FC647D

Q30413034-2249FA93-F1C0-4339-B26B-63BEF0509FEF

Q30413034-260D90F1-A35A-49A0-9A5B-3D0EC8D22E67

Q30413034-336C7C39-DA00-4E3F-B0C3-8A1167E9EFC0

Q30413034-390B8791-9A36-4655-92A9-E5E79909D1BB

Q30413034-3AEA8054-A1EE-4F19-80B8-D2D6F90E8A3D

Q30413034-413269B8-EEAD-4821-BE97-DFD8DEB9A107

P304

Q30413034-F0CADCE2-3DC9-49EF-AFA9-6F8BA9227226

P31

Q30413034-1F9F0B9D-D04F-4082-BC44-FB3C0269238D

P356

Q30413034-BF94D4C2-E39F-4EB4-847D-DC639C1A24DD

P407

Q30413034-39D4AB7F-9021-470E-90EC-7A1CD2923F4F

P433

Q30413034-EAE38928-8839-424D-8FE0-1EBC07DBF90E

P478

Q30413034-97BB68CB-8060-4761-860A-E4ADF8AA7DDA

P50

Q30413034-2D523986-9D65-4DEB-AA5A-55E538F60DF9

Q30413034-3C854762-B5FB-49B6-AA00-A65378DF3327

Q30413034-5735665C-C935-4D30-8A2A-CC7E6116259D

Q30413034-D90CD371-8FE9-4399-97B8-A7E7B0C8DD3E

Q30413034-E6D7CA62-A6E8-4886-B26E-B207451B2723

P577

Q30413034-0F05184C-6220-4F0A-A4C8-B190BF509615

P5875

Q30413034-7D2E4537-C3BC-4750-B466-8389313A219C

P698

Q30413034-8A310BEB-E9E5-40E8-A532-D1618B037FCD

P921

Q30413034-D104C93D-74A4-490E-83AC-AD8D3DC6298F

P932

Q30413034-3B338548-6983-4E22-9855-005BFB9CD4C0

P356

P1433

Journal of Experimental Medicine

P1476

Deletion of Asxl1 results in myelodysplasia and severe developmental defects in vivo

@en

P2093

Alan H Shih

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

Anwesha Dey

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

Bradley E Bernstein

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

Christopher E Mason

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

Christopher Y Park

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

Delphine Ndiaye-Lobry

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

Iannis Aifantis

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

Jie Gao

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

Joseph Y Shin

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

Leon Telis

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

P2860

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

Gene set enrichment analysis: a knowledge-based approach for interpreting genome-wide expression profiles.

Germline deletion of the miR-17∼92 cluster causes skeletal and growth defects in humans

The Polycomb group proteins bind throughout the INK4A-ARF locus and are disassociated in senescent cells

ASXL1 mutations identify a high-risk subgroup of older patients with primary cytogenetically normal AML within the ELN Favorable genetic category.

Prognostic relevance of integrated genetic profiling in acute myeloid leukemia.

TET2 inactivation results in pleiotropic hematopoietic abnormalities in mouse and is a recurrent event during human lymphomagenesis

Tet2 loss leads to increased hematopoietic stem cell self-renewal and myeloid transformation

Ten-Eleven-Translocation 2 (TET2) negatively regulates homeostasis and differentiation of hematopoietic stem cells in mice

Loss-of-function Additional sex combs like 1 mutations disrupt hematopoiesis but do not cause severe myelodysplasia or leukemia

P304

2641-2659

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

P31

scholarly article

P356

10.1084/JEM.20131141

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

P407

P433

12

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

P478

210

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

P50

Omar Abdel-Wahab

P577

2013-11-11T00:00:00Z

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

P5875

258445598

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

P698

24218140

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

P921

P932

3832937

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