Pages that link to "Q38924048"
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The following pages link to Disease mutations in CMP-sialic acid transporter SLC35A1 result in abnormal α-dystroglycan O-mannosylation, independent from sialic acid. (Q38924048):
Displaying 13 items.
- The functional O-mannose glycan on α-dystroglycan contains a phospho-ribitol primed for matriglycan addition (Q32884479) (← links)
- Golgi post-translational modifications and associated diseases (Q34476104) (← links)
- ISPD produces CDP-ribitol used by FKTN and FKRP to transfer ribitol phosphate onto α-dystroglycan (Q36919737) (← links)
- A functional splice variant of the human Golgi CMP-sialic acid transporter. (Q38759339) (← links)
- Recent advancements in understanding mammalian O-mannosylation (Q40092479) (← links)
- O-mannosylation and N-glycosylation: two coordinated mechanisms regulating the tumour suppressor functions of E-cadherin in cancer. (Q42241744) (← links)
- NANS-mediated synthesis of sialic acid is required for brain and skeletal development (Q42696785) (← links)
- A New Mouse Model of Limb-Girdle Muscular Dystrophy Type 2I Homozygous for the Common L276I Mutation Mimicking the Mild Phenotype in Humans (Q50911860) (← links)
- Encephalopathy caused by novel mutations in the CMP-sialic acid transporter, SLC35A1 (Q57475865) (← links)
- Mammalian O-mannosyl glycans: Biochemistry and glycopathology (Q64233103) (← links)
- Disruption of sialic acid metabolism drives tumor growth by augmenting CD8 T cell apoptosis (Q64258056) (← links)
- Physical Principles of Membrane Shape Regulation by the Glycocalyx (Q91769178) (← links)
- Congenital Muscular Dystrophy due to Novel Compound Heterozygote Mutations in POMGNT1 Gene (Q92770935) (← links)