about
Phenotypic diversity of breast cancer-related mutations in metalloproteinase-disintegrin ADAM12Control of muscle formation by the fusogenic micropeptide myomixer.CRISPR-Cpf1 correction of muscular dystrophy mutations in human cardiomyocytes and mice.Altered ion transport by thyroid epithelia from CFTR(-/-) pigs suggests mechanisms for hypothyroidism in cystic fibrosis.Alternative mRNA splicing generates two distinct ADAM12 prodomain variants.Intracellular complexes of the early-onset torsion dystonia-associated AAA+ ATPase TorsinA.An essential role of metalloprotease-disintegrin ADAM12 in triple-negative breast cancerAnalysis of nitrite and nitrate in biological samples using high-performance liquid chromatography.Postnatal genome editing partially restores dystrophin expression in a mouse model of muscular dystrophy.Severe muscle wasting and denervation in mice lacking the RNA-binding protein ZFP106.Metalloproteinase-disintegrin ADAM12 is associated with a breast tumor-initiating cell phenotype.Metalloprotease-disintegrin ADAM12 actively promotes the stem cell-like phenotype in claudin-low breast cancerThe role of Delta-like 1 shedding in muscle cell self-renewal and differentiation.Requirement of the fusogenic micropeptide myomixer for muscle formation in zebrafish.Single-cut genome editing restores dystrophin expression in a new mouse model of muscular dystrophy.Correction of diverse muscular dystrophy mutations in human engineered heart muscle by single-site genome editing.Gene editing restores dystrophin expression in a canine model of Duchenne muscular dystrophyProteomic Characterization of the Heart and Skeletal Muscle Reveals Widespread Arginine ADP-Ribosylation by the ARTC1 EctoenzymeIntracellular sources of ornithine for polyamine synthesis in endothelial cellsCRISPR-Cas9 corrects Duchenne muscular dystrophy exon 44 deletion mutations in mice and human cellsEnhanced CRISPR-Cas9 correction of Duchenne muscular dystrophy in mice by a self-complementary AAV delivery systemIn vivo non-invasive monitoring of dystrophin correction in a new Duchenne muscular dystrophy reporter mouse
P50
Q30360467-BCFA225C-5E56-4C59-8469-AEAE9945260FQ33112265-2C146196-7585-430A-B69D-2C76B30EF873Q33558467-5D1E889F-60E4-41E1-835B-8CDC023798EDQ34348064-D83C8075-1E6C-4BD2-8060-1E71DB4513E0Q35014541-D00FB2E0-2A3D-46CE-A9F9-85838FCBDD47Q35059239-2BAF4DF3-C081-4508-B713-70AFB35FD807Q36315707-C0E590A4-E6CF-4E66-A837-7572B82D4D52Q36564264-766AB030-71DA-4F0D-8556-6B5037CB942EQ36598414-E8819B3C-480F-4DA9-A748-5FE53B4645FBQ37161716-E110467D-80BF-4CCD-A3F3-74063016D234Q37352137-9580BBFF-6ACE-4A41-A60E-8B5C380F9643Q37620891-93CC7806-B0E3-4A71-8F89-28F888C1CC11Q39924099-A922E9F5-3FD6-4D28-8709-5339E99A45DFQ46273123-608E7B42-06FB-465E-93DF-D3DEF463DB50Q47153293-63E65AB4-AFEA-4341-98EB-198F0DA383FFQ48041681-D9AF101D-D144-4127-A4C4-536FF37FC5AEQ56986031-C8C461F8-5259-465C-A311-7C3294AC36C9Q57583016-E779DB5A-31C4-449E-A473-C8E27EFD1CF0Q61411930-EC1669FE-CE25-4F9F-BE58-74D639C7B824Q64059247-146CB9ED-0B23-44DB-8250-E56C70124CD0Q90017264-D24D4E10-667B-4E43-8C4B-FC5970A8D906Q90496381-45E681E1-A3B2-4FE1-A15E-4E061A03C40B
P50
description
researcher (ORCID 0000-0002-4114-8349)
@en
name
Hui Li
@en
Hui Li
@nl
type
label
Hui Li
@en
Hui Li
@nl
prefLabel
Hui Li
@en
Hui Li
@nl
P31
P496
0000-0002-4114-8349