Rhizomelic chondrodysplasia punctata is caused by deficiency of human PEX7, a homologue of the yeast PTS2 receptor (Q24311572)

ether lipid biosynthetic process

GOA release 2020-03-11

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rhizomelic chondrodysplasia punctata

GOA release 2020-03-11

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3

M Skoneczny

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author name string

P E Purdue

series ordinal

1

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J W Zhang

series ordinal

2

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P B Lazarow

series ordinal

4

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language of work or name

English

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publication date

April 1997

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published in

Nature Genetics

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volume

15

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issue

4

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page(s)

381-4

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cites work

PEB1 (PAS7) in Saccharomyces cerevisiae encodes a hydrophilic, intra-peroxisomal protein that is a member of the WD repeat family and is essential for the import of thiolase into peroxisomes

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Targeting of human catalase to peroxisomes is dependent upon a novel COOH-terminal peroxisomal targeting sequence

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PAS7 encodes a novel yeast member of the WD-40 protein family essential for import of 3-oxoacyl-CoA thiolase, a PTS2-containing protein, into peroxisomes

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The import receptor for the peroxisomal targeting signal 2 (PTS2) in Saccharomyces cerevisiae is encoded by the PAS7 gene.

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Amino-terminal presequence of the precursor of peroxisomal 3-ketoacyl-CoA thiolase is a cleavable signal peptide for peroxisomal targeting.

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Rhizomelic chondrodysplasia punctata: Biochemical studies of peroxisomes isolated from cultured skin fibroblasts

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Aberrant subcellular localization of peroxisomal 3-ketoacyl-CoA thiolase in the Zellweger syndrome and rhizomelic chondrodysplasia punctata.

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Molecular evolution of alanine/glyoxylate aminotransferase 1 intracellular targeting. Analysis of the marmoset and rabbit genes

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Deficiency of acyl-CoA: dihydroxyacetone phosphate acyltransferase in patients with Zellweger (cerebro-hepato-renal) syndrome

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