Differentiation defects in primary motoneurons from a SMARD1 mouse model that are insensitive to treatment with low dose PEGylated IGF1

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Differentiation defects in primary motoneurons from a SMARD1 mouse model that are insensitive to treatment with low dose PEGylated IGF1

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2014年の論文

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2014年論文

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Differentiation defects in pri ...... t with low dose PEGylated IGF1

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Differentiation defects in pri ...... t with low dose PEGylated IGF1

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Differentiation defects in pri ...... t with low dose PEGylated IGF1

@en

Differentiation defects in pri ...... t with low dose PEGylated IGF1

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Differentiation defects in pri ...... t with low dose PEGylated IGF1

@en

Differentiation defects in pri ...... t with low dose PEGylated IGF1

@nl

P1476

Differentiation defects in pri ...... t with low dose PEGylated IGF1

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P2093

Frank Krieger

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Friedrich Metzger

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Sibylle Jablonka

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P2860

Transmembrane receptor DCC associates with protein synthesis machinery and regulates translation

Biochemical and genetic evidence for a role of IGHMBP2 in the translational machinery

RNA helicases at work: binding and rearranging

Signalling pathways that mediate skeletal muscle hypertrophy and atrophy

Mutations in the gene encoding immunoglobulin mu-binding protein 2 cause spinal muscular atrophy with respiratory distress type 1

Characterization of Ighmbp2 in motor neurons and implications for the pathomechanism in a mouse model of human spinal muscular atrophy with respiratory distress type 1 (SMARD1)

Asymmetrical beta-actin mRNA translation in growth cones mediates attractive turning to netrin-1.

Role of Na(v)1.9 in activity-dependent axon growth in motoneurons.

Separation of fast from slow anabolism by site-specific PEGylation of insulin-like growth factor I (IGF-I).

Netrin-1-induced local β-actin synthesis and growth cone guidance requires zipcode binding protein 1

P304

e29415

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scholarly article

P356

10.4161/RDIS.29415

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P478

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P577

2014-06-10T00:00:00Z

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264429949

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P698

25083343

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P932

4116388

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