Retention in the endoplasmic reticulum is the underlying mechanism of some hereditary haemorrhagic telangiectasia type 2 ALK1 missense mutations.
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Functional and splicing defect analysis of 23 ACVRL1 mutations in a cohort of patients affected by Hereditary Hemorrhagic TelangiectasiaInvestigation of endoglin wild-type and missense mutant protein heterodimerisation using fluorescence microscopy based IF, BiFC and FRET analyses.ALK5 and ALK1 play antagonistic roles in transforming growth factor β-induced podosome formation in aortic endothelial cells.Activin receptor-like kinase 1 as a target for anti-angiogenesis therapy.Differential molecular regulation of processing and membrane expression of Type-I BMP receptors: implications for signaling.Intracellular trafficking of transforming growth factor β receptors.
P2860
Retention in the endoplasmic reticulum is the underlying mechanism of some hereditary haemorrhagic telangiectasia type 2 ALK1 missense mutations.
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Retention in the endoplasmic r ...... ype 2 ALK1 missense mutations.
@en
Retention in the endoplasmic r ...... ype 2 ALK1 missense mutations.
@nl
type
label
Retention in the endoplasmic r ...... ype 2 ALK1 missense mutations.
@en
Retention in the endoplasmic r ...... ype 2 ALK1 missense mutations.
@nl
prefLabel
Retention in the endoplasmic r ...... ype 2 ALK1 missense mutations.
@en
Retention in the endoplasmic r ...... ype 2 ALK1 missense mutations.
@nl
P2093
P2860
P50
P1476
Retention in the endoplasmic r ...... ype 2 ALK1 missense mutations.
@en
P2093
Aydah M Al-Awadhi
Nadia A Akawi
Sarah S Al-Suwaidi
P2860
P2888
P304
P356
10.1007/S11010-012-1496-3
P577
2012-11-04T00:00:00Z