C. Alexander

发表

OPA1 mutations in patients with autosomal dominant optic atrophy and evidence for semi-dominant inheritance.

E. Zrenner, B. Jurklies, B. Wissinger, 2001, Human molecular genetics.

A comprehensive survey of mutations in the OPA1 gene in patients with autosomal dominant optic atrophy.

T. Rosenberg, S. Bhattacharya, H. Eiberg, 2002, Investigative ophthalmology & visual science.

Characterization of OPA1 isoforms isolated from mouse tissues

E. Müller, A. Otto, H. Strauss, 2008, Journal of neurochemistry.

Proteomics Out of the Archive: Two-dimensional Electrophoresis and Mass Spectrometry Using HOPE-fixed, Paraffin-embedded Tissues

T. Goldmann, E. Vollmer, H. Schultz, 2010, The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society.

Solving a 50 year mystery of a missing OPA1 mutation: more insights from the first family diagnosed with autosomal dominant optic atrophy

E. Zrenner, B. Wissinger, G. Auburger, 2010, Molecular Neurodegeneration.

OPA1 processing controls mitochondrial fusion and is regulated by mRNA splicing, membrane potential, and Yme1L

D. Chan, C. Alexander, Zhiyin Song, 2007, The Journal of cell biology.

OPA1, the disease gene for autosomal dominant optic atrophy, is specifically expressed in ganglion cells and intrinsic neurons of the retina.

H. Kalbacher, S. Bette, K. Kohler, 2004, Investigative ophthalmology & visual science.

OPA1, encoding a dynamin-related GTPase, is mutated in autosomal dominant optic atrophy linked to chromosome 3q28

S. Bhattacharya, M. Votruba, A. Moore, 2000, Nature Genetics.

OPA1 processing controls mitochondrial fusion and is regulated by mRNA splicing, membrane potential, and Yme1L

D. Chan, C. Alexander, Zhiyin Song, 2007, The Journal of cell biology.

SLP‐2 is required for stress‐induced mitochondrial hyperfusion

Jean-Claude Martinou, Christiane Alexander, Alexis A. Jourdain, 2009, The EMBO journal.

A frameshift mutation in exon 28 of the OPA1 gene explains the high prevalence of dominant optic atrophy in the Danish population: evidence for a founder effect

T. Rosenberg, S. Bhattacharya, H. Eiberg, 2001, Human Genetics.

A major marker for normal tension glaucoma: association with polymorphisms in the OPA1 gene

M. Krawczak, S. Bhattacharya, T. Aung, 2001, Human Genetics.

Identification of the physiological promoter for spinocerebellar ataxia 2 gene reveals a CpG island for promoter activity situated into the exon 1 of this gene and provides data about the origin of the nonmethylated state of these types of islands.

W. Schulz, G. Auburger, C. Alexander, 1999, Biochemical and biophysical research communications.

Saturating density of STSs (1/6 kb) in a 1.1 Mb region on 3q28-q29: a valuable resource for cloning of disease genes

M. Rocchi, S. Bernstein, G. Auburger, 2001, European Journal of Human Genetics.

Fine scale mapping places DLG1, the gene encoding hDlg, telomeric to the OPA1 candidate region

P. Bryant, A. Chishti, G. Auburger, 1997, Mammalian Genome.

Expression and regulation of phospholipase D in the human keratinocyte cell line HaCaT

T. Wieder, A. Höer, C. Alexander, 1998, FEBS letters.

OPA 1 processing controls mitochondrial fusion and is regulated by mRNA splicing , membrane potential , and Yme 1 L

D. Chan, C. Alexander, Zhiyin Song, 2007 .