UB Paderborn / Katalog / Suche / in CDI

Sortiert nach

Einfacher Volltextzugriff von (fast) überall

Installieren Sie die LibKey Nomad-Browsererweiterung und erhalten Sie von vielen Webseiten einfachen Zugriff auf lizenzierte Volltexte oder Open Access Publikationen. Mehr erfahren...

What's new in pontocerebellar hypoplasia? An update on genes and subtypes

Orphanet journal of rare diseases, 2018-06, Vol.13 (1), p.92-92, Article 92

2018

Volltextzugriff (PDF)

Classification, diagnosis and potential mechanisms in pontocerebellar hypoplasia

Orphanet journal of rare diseases, 2011-07, Vol.6 (1), p.50-50, Article 50

2011

Volltextzugriff (PDF)

Schwann cell autophagy, myelinophagy, initiates myelin clearance from injured nerves

The Journal of cell biology, 2015-07, Vol.210 (1), p.153-168

2015

Volltextzugriff (PDF)

Complement C1q-C3-associated synaptic changes in multiple sclerosis hippocampus

Annals of neurology, 2015-06, Vol.77 (6), p.1007-1026

2015

Volltextzugriff (PDF)

The Evolving Role of Next-Generation Sequencing in Screening and Diagnosis of Hemoglobinopathies

Frontiers in physiology, 2021-07, Vol.12, p.686689-686689

2021

Volltextzugriff (PDF)

Editorial: Complement in nervous system disease

Frontiers in cellular neuroscience, 2023-08, Vol.17, p.1268023-1268023

2023

Volltextzugriff (PDF)

Immunoglobulin G4+ clones identified by next-generation sequencing dominate the B cell receptor repertoire in immunoglobulin G4 associated cholangitis

Hepatology (Baltimore, Md.), 2013-06, Vol.57 (6), p.2390-2398

2013

Volltextzugriff (PDF)

A homozygous missense mutation in ERAL1, encoding a mitochondrial rRNA chaperone, causes Perrault syndrome

Human molecular genetics, 2017-07, Vol.26 (13), p.2541-2550

2017

Volltextzugriff (PDF)

Treatment with IFB-088 Improves Neuropathy in CMT1A and CMT1B Mice

Molecular neurobiology, 2022-07, Vol.59 (7), p.4159-4178

2022

Volltextzugriff (PDF)

C3-dependent mechanism of microglial priming relevant to multiple sclerosis

Proceedings of the National Academy of Sciences - PNAS, 2012-01, Vol.109 (3), p.965-970

2012

Volltextzugriff (PDF)

Complement activation at the motor end-plates in amyotrophic lateral sclerosis

Journal of neuroinflammation, 2016-04, Vol.13 (1), p.72-72, Article 72

2016

Volltextzugriff (PDF)

Recessive Mutations in the Putative Calcium-Activated Chloride Channel Anoctamin 5 Cause Proximal LGMD2L and Distal MMD3 Muscular Dystrophies

American journal of human genetics, 2010-02, Vol.86 (2), p.213-221

2010

Volltextzugriff (PDF)

Germline Mutation of INI1/SMARCB1 in Familial Schwannomatosis

American journal of human genetics, 2007-04, Vol.80 (4), p.805-810

2007

Volltextzugriff (PDF)

Molecular classification of amyotrophic lateral sclerosis by unsupervised clustering of gene expression in motor cortex

Neurobiology of disease, 2015-02, Vol.74, p.359-376

2015

Volltextzugriff (PDF)

Next-generation sequencing of microRNAs uncovers expression signatures in polarized macrophages

Physiological genomics, 2014-02, Vol.46 (3), p.91-103

2014

Volltextzugriff (PDF)

Loss-of-Function Variants in SUPT5H as Modifying Factors in Beta-Thalassemia

International journal of molecular sciences, 2024-08, Vol.25 (16), p.8928

2024

Volltextzugriff (PDF)

Therapeutic Intervention with Anti-Complement Component 5 Antibody Does Not Reduce NASH but Does Attenuate Atherosclerosis and MIF Concentrations in Ldlr-/-.Leiden Mice

International journal of molecular sciences, 2022-09, Vol.23 (18), p.10736

2022

Volltextzugriff (PDF)

Pontocerebellar hypoplasia due to bi-allelic variants in MINPP1

European journal of human genetics : EJHG, 2021-03, Vol.29 (3), p.411-421

2021

Volltextzugriff (PDF)

Clinical, neuroradiological and genetic findings in pontocerebellar hypoplasia

Brain (London, England : 1878), 2011-01, Vol.134 (Pt 1), p.143-156

2011

Volltextzugriff (PDF)

Ankle-Foot-Orthosis "Hermes" compensates pathological ankle stiffness of chronic stroke - A proof of concept

IEEE transactions on neural systems and rehabilitation engineering, 2023-01, Vol.31, p.1-1

2023

Volltextzugriff (PDF)

Corrigendum: Ldlr-/-.Leiden mice develop neurodegeneration, age-dependent astrogliosis and obesity-induced changes in microglia immunophenotype which are partly reversed by complement component 5 neutralizing antibody

Frontiers in cellular neuroscience, 2023-08, Vol.17, p.1267913-1267913

2023

Volltextzugriff (PDF)

Evaluation of locked nucleic acid–modified small interfering RNA in vitro and in vivo

Molecular cancer therapeutics, 2007-03, Vol.6 (3), p.833-843

2007

Volltextzugriff (PDF)

Ldlr-/-.Leiden mice develop neurodegeneration, age-dependent astrogliosis and obesity-induced changes in microglia immunophenotype which are partly reversed by complement component 5 neutralizing antibody

Frontiers in cellular neuroscience, 2023-06, Vol.17, p.1205261-1205261

2023

Volltextzugriff (PDF)

Focal chromosomal copy number aberrations identify CMTM8 and GPR177 as new candidate driver genes in osteosarcoma

PloS one, 2014-12, Vol.9 (12), p.e115835

2014

Volltextzugriff (PDF)

LAD-1/variant syndrome is caused by mutations in FERMT3

Blood, 2009-05, Vol.113 (19), p.4740-4746

2009

Volltextzugriff (PDF)

1 – 25 von 457

Suche als RSS-Feed

Suchergebnisse filtern

Filter anzeigen

Nur zeigen

Geprüft (Peer-Review)
(433)
Mit Volltextzugriff
(404)

Publikationsform

1 weiteren anzeigen...

Weniger anzeigen...

Sprache

Erscheinungsjahr

n.n

Thema

15 weitere anzeigen...

Weniger anzeigen...

Zeitschrift / Serie

5 weitere anzeigen...

Weniger anzeigen...

Neu hinzugefügt

... seit 30 Tagen
(2)
... seit 90 Tagen
(3)

Menü

Weitere Dienste

Einstellungen

What's new in pontocerebellar hypoplasia? An update on genes and subtypes

Classification, diagnosis and potential mechanisms in pontocerebellar hypoplasia

Schwann cell autophagy, myelinophagy, initiates myelin clearance from injured nerves

Complement C1q-C3-associated synaptic changes in multiple sclerosis hippocampus

The Evolving Role of Next-Generation Sequencing in Screening and Diagnosis of Hemoglobinopathies

Editorial: Complement in nervous system disease

Immunoglobulin G4+ clones identified by next-generation sequencing dominate the B cell receptor repertoire in immunoglobulin G4 associated cholangitis

A homozygous missense mutation in ERAL1, encoding a mitochondrial rRNA chaperone, causes Perrault syndrome

Treatment with IFB-088 Improves Neuropathy in CMT1A and CMT1B Mice

C3-dependent mechanism of microglial priming relevant to multiple sclerosis

Complement activation at the motor end-plates in amyotrophic lateral sclerosis

Recessive Mutations in the Putative Calcium-Activated Chloride Channel Anoctamin 5 Cause Proximal LGMD2L and Distal MMD3 Muscular Dystrophies

Germline Mutation of INI1/SMARCB1 in Familial Schwannomatosis

Molecular classification of amyotrophic lateral sclerosis by unsupervised clustering of gene expression in motor cortex

Next-generation sequencing of microRNAs uncovers expression signatures in polarized macrophages

Loss-of-Function Variants in SUPT5H as Modifying Factors in Beta-Thalassemia

Therapeutic Intervention with Anti-Complement Component 5 Antibody Does Not Reduce NASH but Does Attenuate Atherosclerosis and MIF Concentrations in Ldlr-/-.Leiden Mice

Pontocerebellar hypoplasia due to bi-allelic variants in MINPP1

Clinical, neuroradiological and genetic findings in pontocerebellar hypoplasia

Ankle-Foot-Orthosis "Hermes" compensates pathological ankle stiffness of chronic stroke - A proof of concept

Corrigendum: Ldlr-/-.Leiden mice develop neurodegeneration, age-dependent astrogliosis and obesity-induced changes in microglia immunophenotype which are partly reversed by complement component 5 neutralizing antibody

Evaluation of locked nucleic acid–modified small interfering RNA in vitro and in vivo

Ldlr-/-.Leiden mice develop neurodegeneration, age-dependent astrogliosis and obesity-induced changes in microglia immunophenotype which are partly reversed by complement component 5 neutralizing antibody

Focal chromosomal copy number aberrations identify CMTM8 and GPR177 as new candidate driver genes in osteosarcoma

LAD-1/variant syndrome is caused by mutations in FERMT3

Suchergebnisse filtern