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Person

René Feichtinger (1946-)

Biologe

Name	René Feichtinger
Time	1946- (Date of birth and death)
Place	Salzburg (Geburtsort) Österreich
Academic degree	Dr.
Profession	Biologe (characteristic profession)
Variant	René Günther Feichtinger René G. Feichtinger R. G. Feichtinger
Related	Landesklinik für Kinder- und Jugendheilkunde (Salzburg) Genetik (Thema) Cytologie (Thema)
Record type	Person
GND-Identifier	1242637486
Record ID	1242637486
Involved in show all Anaplerotic Therapy Using Triheptanoin in Two Brothers Suffering from Aconitase 2 Deficiency Characterising a homozygous two‐exon deletion in UQCRH : comparing human and mouse phenotypes A spoonful of L‐fucose—an efficient therapy for GFUS‐CDG, a new glycosylation disorder Characterising a homozygous two‐exon deletion in UQCRH: comparing human and mouse phenotypes PRUNE1 Deficiency: Expanding the Clinical and Genetic Spectrum Bi-allelic mutations in NDUFA6 establish its role in early-onset isolated mitochondrial complex I deficiency Biallelic mutations in TMEM126B cause severe complex i deficiency with a variable clinical phenotype Mutations in TTC19: expanding the molecular, clinical and biochemical phenotype Sengers syndrome: six novel AGK mutations in seven new families and review of the phenotypic and mutational spectrum of 29 patients

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Katalog der Deutschen Nationalbibliothek

René Feichtinger (1946-)

Anaplerotic Therapy Using Triheptanoin in Two Brothers Suffering from Aconitase 2 Deficiency

Characterising a homozygous two‐exon deletion in UQCRH : comparing human and mouse phenotypes

A spoonful of L‐fucose—an efficient therapy for GFUS‐CDG, a new glycosylation disorder

Characterising a homozygous two‐exon deletion in UQCRH: comparing human and mouse phenotypes

PRUNE1 Deficiency: Expanding the Clinical and Genetic Spectrum

Bi-allelic mutations in NDUFA6 establish its role in early-onset isolated mitochondrial complex I deficiency

Biallelic mutations in TMEM126B cause severe complex i deficiency with a variable clinical phenotype

Mutations in TTC19: expanding the molecular, clinical and biochemical phenotype

Sengers syndrome: six novel AGK mutations in seven new families and review of the phenotypic and mutational spectrum of 29 patients