نتایج جستجو برای: merzbacher

تعداد نتایج: 317  

2013
Stefano Regis Fabio Corsolini Serena Grossi Barbara Tappino David N. Cooper Mirella Filocamo

An exonic missense mutation, c.436C>G, in the PLP1 gene of a patient affected by the hypomyelinating leukodystrophy, Pelizaeus-Merzbacher disease, has previously been found to be responsible for the alteration of the canonical alternative splicing profile of the PLP1 gene leading to the loss of the longer PLP isoform. Here we show that the presence of the c.436C>G mutation served to introduce r...

2016
Moones Heidari Sam H. Gerami Brianna Bassett Ross M. Graham Anita C.G. Chua Ritambhara Aryal Michael J. House Joanna F. Collingwood Conceição Bettencourt Henry Houlden Mina Ryten John K. Olynyk Debbie Trinder Daniel M. Johnstone Elizabeth A. Milward

We previously demonstrated elevated brain iron levels in myelinated structures and associated cells in a hemochromatosis Hfe (-/-) xTfr2 (mut) mouse model. This was accompanied by altered expression of a group of myelin-related genes, including a suite of genes causatively linked to the rare disease family 'neurodegeneration with brain iron accumulation' (NBIA). Expanded data mining and ontolog...

2010
Julia M Edgar Mailis C McCulloch Paul Montague Angus M Brown Sebastian Thilemann Laura Pratola Fredrik I Gruenenfelder Ian R Griffiths Klaus-Armin Nave

It is widely thought that demyelination contributes to the degeneration of axons and, in combination with acute inflammatory injury, is responsible for progressive axonal loss and persistent clinical disability in inflammatory demyelinating disease. In this study we sought to characterize the relationship between demyelination, inflammation and axonal transport changes using a Plp1-transgenic m...

Journal: :American journal of medical genetics 1995
V M Pratt S Boyadjiev K Green M E Hodes S R Dlouhy

Pelizaeus-Merzbacher disease (PMD) is an X-linked dysmyelinating disorder of the central nervous system. Many cases of PMD can be attributed to defects in the proteolipid protein gene (PLP). To date, with one exception, each family has had either no or a unique mutation in one of the seven exons of PLP. We describe a new missense mutation in exon 2 of the PLP gene of an affected individual. Thi...

Journal: :Cell 2007
Jennifer A. Lee Claudia M.B. Carvalho James R. Lupski

The prevailing mechanism for recurrent and some nonrecurrent rearrangements causing genomic disorders is nonallelic homologous recombination (NAHR) between region-specific low-copy repeats (LCRs). For other nonrecurrent rearrangements, nonhomologous end joining (NHEJ) is implicated. Pelizaeus-Merzbacher disease (PMD) is an X-linked dysmyelinating disorder caused most frequently (60%-70%) by non...

Journal: :Clinical genetics 2013
P Martínez-Montero M Muñoz-Calero E Vallespín J Campistol L Martorell M J Ruiz-Falcó A Santana R Pons A Dinopoulos C Sierra J Nevado J Molano

Pelizaeus-Merzbacher disease (PMD) is caused in most cases by either duplications or point mutations in the PLP1 gene. This disease, a dysmyelinating disorder affecting mainly the central nervous system, has a wide clinical spectrum and its causing mutations act through different molecular mechanisms. Eighty-eight male patients with leukodystrophy were studied. PLP1 gene analysis was performed ...

2015
Christine R. Beck Claudia M. B. Carvalho Linda Banser Tomasz Gambin Danielle Stubbolo Bo Yuan Karen Sperle Suzanne M. McCahan Marco Henneke Pavel Seeman James Y. Garbern Grace M. Hobson James R. Lupski

Inverted repeats (IRs) can facilitate structural variation as crucibles of genomic rearrangement. Complex duplication-inverted triplication-duplication (DUP-TRP/INV-DUP) rearrangements that contain breakpoint junctions within IRs have been recently associated with both MECP2 duplication syndrome (MIM#300260) and Pelizaeus-Merzbacher disease (PMD, MIM#312080). We investigated 17 unrelated PMD su...

Journal: :Proceedings of the National Academy of Sciences of the United States of America 2007
Ajit-Singh Dhaunchak Klaus-Armin Nave

A large number of mutations in the human PLP1 gene lead to abnormal myelination and oligodendrocyte death in Pelizaeus-Merzbacher disease (PMD). Here we show that a major subgroup of PMD mutations that map into the extracellular loop region of PLP/DM20 leads to the failure of oligodendrocytes to form the correct intramolecular disulfide bridges. This leads to abnormal protein cross-links and en...

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