about
Wnt-14 plays a pivotal role in inducing synovial joint formation in the developing appendicular skeletonCanonical Wnt/beta-catenin signaling prevents osteoblasts from differentiating into chondrocytesWnt9a signaling is required for joint integrity and regulation of Ihh during chondrogenesisCbfa1-independent decrease in osteoblast proliferation, osteopenia, and persistent embryonic eye vascularization in mice deficient in Lrp5, a Wnt coreceptorWnt/β-catenin signaling in the dental mesenchyme regulates incisor development by regulating Bmp4The calmodulin pathway and evolution of elongated beak morphology in Darwin's finches.Role of canonical Wnt-signalling in joint formation.Autophagy facilitates secretion and protects against degeneration of the Harderian gland.Dual pathways to endochondral osteoblasts: a novel chondrocyte-derived osteoprogenitor cell identified in hypertrophic cartilageThe Drosophila fork head domain protein crocodile is required for the establishment of head structures.β-catenin activity in late hypertrophic chondrocytes locally orchestrates osteoblastogenesis and osteoclastogenesis.Transcriptional networks controlling skeletal development.WNTing embryonic stem cells.Differential requirement for the dual functions of β-catenin in embryonic stem cell self-renewal and germ layer formation.Non-steroidal anti-inflammatory drug indometacin enhances endogenous remyelination.Role of Wnt5a-Ror2 signaling in morphogenesis of the metanephric mesenchyme during ureteric buddingDeletion of beta catenin in hypertrophic growth plate chondrocytes impairs trabecular bone formation.Increased survival and cell cycle progression pathways are required for EWS/FLI1-induced malignant transformation.Krüppel target gene knockout participates in the proper innervation of a specific set of Drosophila larval muscles.Tissue specific regulation of VEGF expression during bone development requires Cbfa1/Runx2.Mice lacking the orphan receptor ror1 have distinct skeletal abnormalities and are growth retarded.Wnt9a deficiency discloses a repressive role of Tcf7l2 on endocrine differentiation in the embryonic pancreas.Cloning and expression of a novel cysteine-rich secreted protein family member expressed in thyroid and pancreatic mesoderm within the chicken embryo.Dual roles of Wnt signaling during chondrogenesis in the chicken limb.Arthritis induces lymphocytic bone marrow inflammation and endosteal bone formation.Putative Krüppel target gene of novel sequence expressed in Drosophila VO5 muscle precursors.Genetic and molecular insights into genotype-phenotype relationships in osteopathia striata with cranial sclerosis (OSCS) through the analysis of novel mouse Wtx mutant alleles.Wif-1 is expressed at cartilage-mesenchyme interfaces and impedes Wnt3a-mediated inhibition of chondrogenesis.Spatiotemporal relationships between a novel Drosophila stripe expressing gene and known segmentation genes by simultaneous visualization of transcript patterns.Ectodysplasin and Wnt pathways are required for salivary gland branching morphogenesis.Wnt-signaling and skeletogenesis.Specific muscle identities are regulated by Krüppel during Drosophila embryogenesis.A two-step mode of stripe formation in the Drosophila blastoderm requires interactions among primary pair rule genes.Ca2+/Calmodulin-dependent kinase II signaling causes skeletal overgrowth and premature chondrocyte maturation.Sclerostin inhibition promotes TNF-dependent inflammatory joint destruction.Wnt Signaling in Cartilage DevelopmentAbstract 61: A mouse model for small round cell tumors induced by the Ewing sarcoma oncogene EWS/FLI1Skeletal development--Wnts are in controlMultiple roles of mesenchymal -catenin during murine limb patterningWnt signalling regulates myogenic differentiation in the developing avian wing
P50
Q28203665-3369D1C8-6DA2-4D21-AB88-1DEED416C416Q28505614-8701C997-4FAF-4BE7-B246-5C57D9861AA9Q28508484-6BFC6890-7ED3-42F4-A76E-CE9231734B2AQ28590950-256EFF39-FA9C-4579-A75B-74928EE075E3Q34382103-3E01EF0D-01E6-4225-8481-AD9D32E7B4B5Q34553831-E98E7945-0715-4BE8-A168-1B6EEC90FCADQ34582978-2B1C779F-B043-4786-82F7-4445BFA774E5Q35498851-1E08965A-82AD-4508-B968-97B116227016Q35616579-56F2C102-F3A9-4990-859D-2A55775FFD11Q36671327-B741710F-791B-4EBA-BC21-87F925F21E80Q37381251-0D31B0D0-C7CE-431A-B516-52AE2C75B953Q37616352-238A51D5-C5E7-4695-9E7A-6EF984825E0CQ37971088-4FB9C0F6-63DD-4D62-80DA-36D34A72CBEDQ38473082-93F5201E-8DDA-46F0-88E4-3E06E8640C1CQ38878763-4D49EF38-9046-47C3-AB91-68300193FA8BQ38988843-A2F40DB6-CD9A-4D28-90FA-A6CC607FCADEQ39169428-0FEE7EB0-1F78-443A-A1F9-CACC732B39FEQ42126638-9BA72837-60CE-40FE-9E3F-E636C8A86600Q42628586-A0700288-2F2F-418E-8F9B-74EB6543A517Q42826927-052C3443-4587-400A-8729-F4DB8CE1CF8FQ42996554-43BA11A7-B1B7-4C6C-81C5-75D7A642EA00Q43069532-7EB1DA8D-568D-407D-BD76-A9A37F5096DAQ43565084-0F0F2841-B883-4A56-9F35-3F0EBFE08C10Q44509921-C8718865-06A0-4BA2-BC2B-FF384F975611Q47654090-67B9DF88-C5A3-4F09-B4CC-36E87858ADBDQ47681918-6655EF0C-6946-4D1A-ADD8-D11D722F6E18Q50062521-B5DF34EB-EEA0-4760-88F9-60DD66908047Q50336920-BFE4A337-889E-4707-8C36-B33E6A18E520Q50756806-83E413B0-DD99-48F3-8944-D43256383557Q51864812-E1C6D6CF-D831-4936-BCCF-DCFC6B5E1BCFQ52055483-0267B3C0-FB79-4B45-BA7F-B2AC29DD9031Q52192642-D61AD978-B4E0-441D-9B0A-7C4BD8192198Q52543572-C8D3D32E-F50C-4CB6-B648-8083D7DC483AQ53491968-47A610C2-20E4-4C1E-8A06-1210BD3AF4F3Q55025334-BEB7D9C6-635F-42D0-BCE1-5E9B41839D6FQ60178649-DD650601-D4CA-499C-8BEE-64D31C2840B3Q60178651-43656812-0F55-476C-B5ED-446B4F71E3B0Q60178655-CAD26773-3DA5-457D-94BD-4B84A08CDB40Q60178657-44251635-3A18-4667-812A-EF157798B876Q60178658-C057C442-81F0-4233-9603-B8162B67D246
P50
description
hulumtuese
@sq
onderzoeker
@nl
researcher
@en
հետազոտող
@hy
name
Christine Hartmann
@ast
Christine Hartmann
@en
Christine Hartmann
@es
Christine Hartmann
@nl
Christine Hartmann
@sl
type
label
Christine Hartmann
@ast
Christine Hartmann
@en
Christine Hartmann
@es
Christine Hartmann
@nl
Christine Hartmann
@sl
prefLabel
Christine Hartmann
@ast
Christine Hartmann
@en
Christine Hartmann
@es
Christine Hartmann
@nl
Christine Hartmann
@sl
P106
P21
P31
P496
0000-0002-6854-8633