about
ADAR1, inosine and the immune sensing system: distinguishing self from non-selfThe DNA helicase recql4 is required for normal osteoblast expansion and osteosarcoma formationRNA editing by ADAR1 prevents MDA5 sensing of endogenous dsRNA as nonselfSsb1 and Ssb2 cooperate to regulate mouse hematopoietic stem and progenitor cells by resolving replicative stress.The Rothmund-Thomson syndrome helicase RECQL4 is essential for hematopoiesis.Rb is dispensable for self-renewal and multilineage differentiation of adult hematopoietic stem cellsGeneration and analysis of Siah2 mutant mice.BET inhibitors induce apoptosis through a MYC independent mechanism and synergise with CDK inhibitors to kill osteosarcoma cellsHematopoietic AMPK β1 reduces mouse adipose tissue macrophage inflammation and insulin resistance in obesityHIF-1α is required for hematopoietic stem cell mobilization and 4-prolyl hydroxylase inhibitors enhance mobilization by stabilizing HIF-1α.Gene expression profiling to define the cell intrinsic role of the SKI proto-oncogene in hematopoiesis and myeloid neoplasmsA microenvironment-induced myeloproliferative syndrome caused by retinoic acid receptor gamma deficiency.Defining the Minimal Factors Required for Erythropoiesis through Direct Lineage ConversionCiliary neurotrophic factor has intrinsic and extrinsic roles in regulating B cell differentiation and bone structure.The Zinc-finger protein ASCIZ regulates B cell development via DYNLL1 and Bim.RARgamma is critical for maintaining a balance between hematopoietic stem cell self-renewal and differentiation.The Asymmetric Cell Division Regulators Par3, Scribble and Pins/Gpsm2 Are Not Essential for Erythroid Development or Enucleation.Terminal osteoblast differentiation, mediated by runx2 and p27KIP1, is disrupted in osteosarcomaRb intrinsically promotes erythropoiesis by coupling cell cycle exit with mitochondrial biogenesisGenetically engineered mouse models and human osteosarcoma.Darbepoietin-alfa has comparable erythropoietic stimulatory effects to recombinant erythropoietin whilst preserving the bone marrow microenvironmentPDGF-AB and 5-Azacytidine induce conversion of somatic cells into tissue-regenerative multipotent stem cells.Activation of PTHrP-cAMP-CREB1 signaling following p53 loss is essential for osteosarcoma initiation and maintenance.IAP antagonists sensitize murine osteosarcoma cells to killing by TNFαImmune response to RB1-regulated senescence limits radiation-induced osteosarcoma formation.Prostaglandin E2 regulates vertebrate haematopoietic stem cell homeostasis.MAD1 and c-MYC regulate UBF and rDNA transcription during granulocyte differentiationErythropoiesis, anemia and the bone marrow microenvironment.Defining the hematopoietic stem cell niche: the chicken and the egg conundrum.Deciphering hematopoietic stem cells in their niches: a critical appraisal of genetic models, lineage tracing, and imaging strategies.Cells of origin in osteosarcoma: mesenchymal stem cells or osteoblast committed cells?Src family kinases and their role in hematological malignancies.Brief report: the differential roles of mTORC1 and mTORC2 in mesenchymal stem cell differentiation.The SKI proto-oncogene enhances the in vivo repopulation of hematopoietic stem cells and causes myeloproliferative disease.Increased miR-155-5p and reduced miR-148a-3p contribute to the suppression of osteosarcoma cell death.The role of RNA editing by ADAR1 in prevention of innate immune sensing of self-RNA.Adenosine-to-inosine RNA editing by ADAR1 is essential for normal murine erythropoiesis.Retinoic acid receptor antagonism in vivo expands the numbers of precursor cells during granulopoiesis.The Transcription Factor ASCIZ and Its Target DYNLL1 Are Essential for the Development and Expansion of MYC-Driven B Cell Lymphoma.RARγ is a negative regulator of osteoclastogenesis.
P50
Q26773989-0085CACC-A352-4EA2-88C7-CCFE5610796DQ27311269-E3BADFE3-0653-4B34-BCB9-729D69D20CCCQ28266296-57C953EA-E573-481F-96C4-D57D5214E6D3Q33640202-3B2E57D3-169D-4907-8B0F-27E76BBB84C3Q33944167-0B7A7D2E-62AC-463C-9B3E-43326D690B05Q34657898-3DFB68E3-F448-48C9-B1FD-60BD0A1BA24EQ34986884-82DA8E34-EF01-4647-8CCF-4B33FA0197C7Q35574955-8125AB7D-392F-4BC3-84BD-365766C5F452Q35578618-3B67AE4F-BE6C-4284-BBE9-91E725A7C97BQ35838285-F9FF9A08-C21F-4108-93ED-DC0B6E6E47A1Q35951466-59C0D705-2903-4C44-B700-B0048D9F992EQ35987653-0B1BC7CC-D513-4CE6-89D5-875446F194A1Q36041465-B448AEF6-0FAA-42E5-BBCA-C980176F6D30Q36187605-7C5F341A-889C-43DC-B65E-20CD4CB2C4C4Q36193554-0C625F55-AD20-4C16-AD8F-033076E27CBCQ36238093-D6E81558-4903-406B-92D3-596CE33A298FQ36251360-77E07E19-20DE-4CDB-A55E-31C088A73CEAQ36322562-3518E223-F0C7-4C2A-A72C-97B1F2A5AF5CQ36453536-22119E4C-F75D-4924-A34F-414E26F3B65BQ36468644-5C2A6550-E405-41A0-8693-E333F5E14F66Q36805820-78D7ABF5-AA0D-4176-8DA4-BCA31016448FQ36831498-8CF92F01-A22F-4718-A556-0D2B29E2FC2DQ36862527-CBE2E82B-4B8B-46D7-A3EC-87085611AF25Q37376164-33BA7950-3C42-4E24-A7FB-A713567C037AQ37383985-A9EA8078-A1D4-4237-BAE5-669434A72C8CQ37416219-96046F37-2BD0-4AB5-8DF2-2CE6EB61806FQ37485846-FC6622CA-2EB0-406C-B911-477E8909F73EQ37827440-BB2E3DEA-86B9-4B1A-9B79-D6F8BBDC013BQ37866721-0748DDE9-CCCD-427A-8403-D8775A18BB8DQ38161064-DEAA3BBB-DED6-4BDB-98B5-6C49583AC3A7Q38188304-B1776272-8656-459A-873F-9A0C08D03C87Q38217719-4ED75D68-D8AE-41EB-B6B4-040E6E3FFCA7Q38302018-33E9B3E7-0D3C-4E0B-B56A-F0E02CE63511Q38572519-F1EB9E3D-E87A-4764-8388-462E5DD78EBFQ38780991-1C1890C1-A0BB-4E3A-A0EC-5F38C6298435Q38797973-06F6A929-3C69-4563-A149-2FA5DACF0D28Q39635966-1FE0AC7D-1138-4ADE-B76A-1119928DDB88Q40708012-5EC350F2-E185-4FC1-9E2F-CFEA4A75DCBEQ40937420-C29CEECC-95E1-45E3-81FA-F20357FFEB0AQ41175656-FD9085B4-2620-4B30-82D5-3860D99ADBE8
P50
description
hulumtues
@sq
researcher
@en
wetenschapper
@nl
հետազոտող
@hy
name
Carl R Walkley
@ast
Carl R Walkley
@en
Carl R Walkley
@es
Carl R Walkley
@nl
Carl R Walkley
@sl
type
label
Carl R Walkley
@ast
Carl R Walkley
@en
Carl R Walkley
@es
Carl R Walkley
@nl
Carl R Walkley
@sl
prefLabel
Carl R Walkley
@ast
Carl R Walkley
@en
Carl R Walkley
@es
Carl R Walkley
@nl
Carl R Walkley
@sl
P106
P21
P31
P4012
P496
0000-0002-4784-9031