Additional sex comb-like 1 (ASXL1), in cooperation with SRC-1, acts as a ligand-dependent coactivator for retinoic acid receptor
about
ASXL1 mutations promote myeloid transformation through loss of PRC2-mediated gene repressionNegative regulation of ERα by a novel protein CAC1 through association with histone demethylase LSD1Additional sex comb-like (ASXL) proteins 1 and 2 play opposite roles in adipogenesis via reciprocal regulation of peroxisome proliferator-activated receptor {gamma}MED25 is distinct from TRAP220/MED1 in cooperating with CBP for retinoid receptor activationThe ubiquitin carboxyl hydrolase BAP1 forms a ternary complex with YY1 and HCF-1 and is a critical regulator of gene expressionASXL1 mutations identify a high-risk subgroup of older patients with primary cytogenetically normal AML within the ELN Favorable genetic category.ASXL1 exon 12 mutations are frequent in AML with intermediate risk karyotype and are independently associated with an adverse outcome.ASXL1 represses retinoic acid receptor-mediated transcription through associating with HP1 and LSD1Loss-of-function Additional sex combs like 1 mutations disrupt hematopoiesis but do not cause severe myelodysplasia or leukemiaMyelodysplastic syndromes are induced by histone methylation–altering ASXL1 mutationsAdditional sex combs-like 1 belongs to the enhancer of trithorax and polycomb group and genetically interacts with Cbx2 in miceThe HARE-HTH and associated domains: novel modules in the coordination of epigenetic DNA and protein modificationsCurrent outlook on molecular pathogenesis and treatment of myeloproliferative neoplasms.Functional proteomics of the epigenetic regulators ASXL1, ASXL2 and ASXL3: a convergence of proteomics and epigenetics for translational medicine.The BAP1/ASXL2 Histone H2A Deubiquitinase Complex Regulates Cell Proliferation and Is Disrupted in Cancer.Mutations in epigenetic modifiers in the pathogenesis and therapy of acute myeloid leukemia.Additional sex combs-like 2 is required for polycomb repressive complex 2 binding at select targetsThe molecular basis of myeloid malignancies.De novo dominant ASXL3 mutations alter H2A deubiquitination and transcription in Bainbridge-Ropers syndrome.Isolation and characterization of a novel H1.2 complex that acts as a repressor of p53-mediated transcription.Loss of Asxl1 Alters Self-Renewal and Cell Fate of Bone Marrow Stromal Cell, Leading to Bohring-Opitz-like Syndrome in Mice.Functional and cancer genomics of ASXL family membersASXL1 plays an important role in erythropoiesis.Heterogeneous breakpoints in patients with acute lymphoblastic leukemia and the dic(9;20)(p11-13;q11) show recurrent involvement of genes at 20q11.21.Loss of Asxl1 leads to myelodysplastic syndrome-like disease in miceUnraveling the molecular pathophysiology of myelodysplastic syndromes.Update on cytogenetic and molecular changes in myelodysplastic syndromes.Molecular biology of myelodysplastic syndromes.Mutations in epigenetic regulators in myelodysplastic syndromes.Mutations in ASXL1 are associated with poor prognosis across the spectrum of malignant myeloid diseases.Role of TET2 and ASXL1 mutations in the pathogenesis of myeloproliferative neoplasms.The ASXL-BAP1 axis: new factors in myelopoiesis, cancer and epigenetics.The genetic basis of phenotypic heterogeneity in myelodysplastic syndromes.Genetic and epigenetic alterations of myeloproliferative disorders.Genetic basis of MPN: Beyond JAK2-V617F.Asxl1 deficiency in embryonic fibroblasts leads to cellular senescence via impairment of the AKT-E2F pathway and Ezh2 inactivation.ASXL1 interacts with the cohesin complex to maintain chromatid separation and gene expression for normal hematopoiesis.Molecular Mutations and Their Cooccurrences in Cytogenetically Normal Acute Myeloid Leukemia.A novel cytoplasmic adaptor for retinoic acid receptor (RAR) and thyroid receptor functions as a Derepressor of RAR in the absence of retinoic acidMutations with epigenetic effects in myeloproliferative neoplasms and recent progress in treatment: Proceedings from the 5th International Post-ASH Symposium.
P2860
0d28ecdcf0fa052979a02360f9af56e41312abbf197309a90ca2f835853843f929d3b3c82cee75193ce881414aee742961eeb6eaafccaf41e42c5d8d44b660b7b0af73035d3d734d4e5c674183f9bb6779fc179f3ea0b3e975104755bd5f31faa3a6c84682853225ec6b52ec5ca25b42a8aeb5e69aa61e2fb18642af2a11130f483bf1be3206a39b5439f971bca6ce2e63ac17a4cf6be78a842b6be5abdf046dc9db969c408ccc7221b5743305658ab3b0b610ede84667df82c210eaa4647d4565f69048d60956fc
P248
Q24296658-50DCCD72-DC70-4F4C-8CE7-455757E0710BQ24304751-D56F1DCB-ED83-4E2E-837E-9A51E6A32526Q24305362-F2670B0C-BDA4-4ABA-9A75-6D9227FA2F77Q24321381-761B3E05-9674-4356-AE2D-2D1098A3DD9CQ24633127-45058E5C-020D-494A-932D-46824E041C1DQ27851679-C6B3F45F-FB1D-40A4-8B5C-77EC86507E50Q27851909-EA9BD1C4-A6CE-4460-A44D-3E6E7D5DFB8CQ28115338-1D01A567-21BC-4DAF-8D5C-9C750D62FD3FQ28585869-2D1DBA20-667D-42F1-B1D8-CB8E0F680FA9Q28590040-77786CDF-056D-4266-A2ED-379CA0A62446Q33595603-04800465-8692-4ACA-B19C-3BE4D53DF405Q34107107-C10CD0B7-2043-4340-8893-546B074879BCQ34302770-A572DDC5-DC4A-42E6-8767-E0A973C4854FQ34469971-F94E8070-DC24-45E7-B957-CB6CB867128DQ34496129-8688ADB9-928A-46D8-BA2D-9CE885F9D16FQ34651312-8CFB1554-597B-403C-AB0B-F0617228C6F7Q34989584-E8F17CF5-B35E-4771-9F2B-E691EE51B490Q35103708-684F0A3A-F807-4F01-A839-682E570A0B55Q36514637-A344247D-FF4B-4896-8A07-C57CF9AF2250Q36727277-CAFAADE8-6F62-449F-BB1A-65749814E3BBQ37014700-048AA38C-7B25-481F-AEA0-A4B662A3BABFQ37040682-5AA35C35-3A7B-4D60-91B2-D9E3842D971CQ37049843-4EE4D4A6-206A-40C6-975F-0C307D597E32Q37284420-63F12A68-D422-4932-8012-D6A108E2EF86Q37512080-3079A4B8-0CA6-4220-B276-5B6F042C97CFQ37671806-77482C47-F7A1-4A75-85F5-C27FD9250B56Q37923939-2366B5AC-5C66-4250-92B8-380DC71F2395Q37937809-CC8EA110-5B13-46D5-B361-66E17BCF1DACQ37974844-178D02A5-2F8B-49E6-9F2B-CF985BD27D85Q37995804-C7F515E1-4291-4A59-BC0E-43B80AC54465Q38046319-56ADB798-3ED8-43D2-A153-7D206B340793Q38059391-77B06BC1-E064-4DFC-8C7A-19E35835AAB5Q38061848-43911EC5-61F2-41BF-B75C-16894D0F1DE2Q38066786-03BB6146-0A44-4E60-8076-39A3E7623AA1Q38159973-27D1C5D3-27B6-4702-AB92-70DB4772E8A3Q38401146-8E9F3B88-9244-42FD-ACB8-11F8721ADB18Q39003064-6C9C4E5D-20A4-484C-BBE7-7933ED6E9AE3Q39135620-20E5EB3E-7064-47EC-A2BB-6BE55B56BC11Q39663814-7D8CA3CC-2FA8-426F-BAF9-05E7FF3E2D47Q40298579-B1226D0A-B4DD-44C4-8761-037C4EC61621
P2860
Additional sex comb-like 1 (ASXL1), in cooperation with SRC-1, acts as a ligand-dependent coactivator for retinoic acid receptor
description
2006 nî lūn-bûn
@nan
2006 թուականի Յունիսին հրատարակուած գիտական յօդուած
@hyw
2006 թվականի հունիսին հրատարակված գիտական հոդված
@hy
2006年の論文
@ja
2006年学术文章
@wuu
2006年学术文章
@zh-cn
2006年学术文章
@zh-hans
2006年学术文章
@zh-my
2006年学术文章
@zh-sg
2006年學術文章
@yue
name
Additional sex comb-like 1 (AS ...... tor for retinoic acid receptor
@ast
Additional sex comb-like 1 (AS ...... tor for retinoic acid receptor
@en
Additional sex comb-like 1 (AS ...... tor for retinoic acid receptor
@en-gb
Additional sex comb-like 1 (AS ...... tor for retinoic acid receptor
@nl
type
label
Additional sex comb-like 1 (AS ...... tor for retinoic acid receptor
@ast
Additional sex comb-like 1 (AS ...... tor for retinoic acid receptor
@en
Additional sex comb-like 1 (AS ...... tor for retinoic acid receptor
@en-gb
Additional sex comb-like 1 (AS ...... tor for retinoic acid receptor
@nl
prefLabel
Additional sex comb-like 1 (AS ...... tor for retinoic acid receptor
@ast
Additional sex comb-like 1 (AS ...... tor for retinoic acid receptor
@en
Additional sex comb-like 1 (AS ...... tor for retinoic acid receptor
@en-gb
Additional sex comb-like 1 (AS ...... tor for retinoic acid receptor
@nl
P2093
P2860
P3181
P356
P1476
Additional sex comb-like 1 (AS ...... tor for retinoic acid receptor
@en
P2093
Eun-Joo Kim
Hong-Sig Sin
Soo-Jong Um
Ui-Hyun Park
Yang-Sook Cho
P2860
P304
P3181
P356
10.1074/JBC.M512616200
P407
P577
2006-06-30T00:00:00Z