Genomes and Genes
- Neurogenesis and cell cycle-reactivated neuronal death during pathogenic tau aggregationK Schindowski
INSERM, U837, Place de Verdun, Lille Cedex, France
Genes Brain Behav 7:92-100. 2008..Altogether, these data suggest that cell cycle events in THY-Tau22 are resulting from neurogenesis in young animals and cell death in older ones. It suggests that neuronal cell death in such models is much more complex than believed...
- Brain microvascular changes in Alzheimer's disease and other dementiasL Buee
INSERM U422, Lille, France
Ann N Y Acad Sci 826:7-24. 1997..This aspect of pathology is particularly interesting in view of its accessibility to therapeutic interventions...
- Comparative biochemistry of tau in progressive supranuclear palsy, corticobasal degeneration, FTDP-17 and Pick's diseaseL Buee
INSERM U422, F 59045 Lille, France
Brain Pathol 9:681-93. 1999..Thus, tau mutations and polymorphisms may also be instrumental in many neurodegenerative disorders...
- Tau exon 2 responsive elements deregulated in myotonic dystrophy type I are proximal to exon 2 and synergistically regulated by MBNL1 and MBNL2C Carpentier
Inserm UMR837 1 and Univ Lille Nord de France, Jean Pierre Aubert Research Center, Alzheimer and Tauopathies, F 59045 Lille, France Regional University Hospital of Lille, France
Biochim Biophys Acta 1842:654-64. 2014..In conclusion, both MBNL1 and MBNL2 are involved in the regulation of Tau exon 2 splicing and the mis-splicing of Tau in DM1 is due to the combined inactivation of both...
- Proteasome inhibition and Tau proteolysis: an unexpected regulationP Delobel
INSERM U422, Institut de Médecine Prédictive et Recherche Thérapeutique, Place de Verdun, 59045, Lille, France
FEBS Lett 579:1-5. 2005..Surprisingly, we showed that the inhibition of the proteasome led to a bidirectional degradation of Tau. Following this result, the cellular mechanisms that may degrade Tau were investigated...
- Overexpression of MBNL1 fetal isoforms and modified splicing of Tau in the DM1 brain: two individual consequences of CUG trinucleotide repeatsC M Dhaenens
INSERM, U837, Place de Verdun, 59045 Lille, France
Exp Neurol 210:467-78. 2008..The modified splicing of Tau thus results from a possibly CUG-mediated loss of function of MBNL1, but not from changes in the MBNL1 expression pattern...
- Alzheimer-specific epitope of AT100 in transfected cell lines with tau: toward an efficient cell model of tau abnormal phosphorylationC Mailliot
INSERM U422, Lille, France
Neurosci Lett 255:13-6. 1998..This represents a useful model to study abnormal tau phosphorylation in situ...
- Tau protein isoforms, phosphorylation and role in neurodegenerative disordersL Buee
INSERM U422, Place de Verdun, 59045 Cedex, Lille, France
Brain Res Brain Res Rev 33:95-130. 2000....
- Transcriptomic and genetic studies identify IL-33 as a candidate gene for Alzheimer's diseaseJ Chapuis
INSERM, U744, Universite de Lille 2, Institut Pasteur de Lille, BP 245, 1, rue du Professeur Calmette, Lille Cedex, France
Mol Psychiatry 14:1004-16. 2009..In conclusion, our data suggest that genetic variants in IL-33 gene may be associated with a decrease in AD risk potentially in modulating CAA formation...
- Increased expression of BIN1 mediates Alzheimer genetic risk by modulating tau pathologyJ Chapuis
1 INSERM U744, Universite Lille Nord de France, Institut Pasteur de Lille, Lille, France 2 Université Lille Nord de France, Institut Pasteur de Lille, Lille, France 3 Université Lille Nord de France, Institut Pasteur de Lille, Lille, France
Mol Psychiatry 18:1225-34. 2013..Finally, the 3 bp insertion was associated with Tau but not Amyloid loads in AD brains. We propose that BIN1 mediates AD risk by modulating Tau pathology. ..
- Neurotrophic factors in Alzheimer's disease: role of axonal transportK Schindowski
Institut National de la Santé et de la Research Médicale U837, Universite Lille 2, Lille Cedex, France
Genes Brain Behav 7:43-56. 2008....
- The peptidyl prolyl cis/trans isomerase Pin1 downregulates the Inhibitor of Apoptosis Protein SurvivinP Dourlen
INSERM, U837, Place de Verdun, 59045 Lille Cedex, France
Biochim Biophys Acta 1773:1428-37. 2007..The characterization of this functional relationship between Pin1 and Survivin might help to better understand mitosis control and cancer mechanisms...
- Loss of medial septum cholinergic neurons in THY-Tau22 mouse model: what links with tau pathology?K Belarbi
Universite Lille Nord de France, Lille, France
Curr Alzheimer Res 8:633-8. 2011..Finally, our data strongly support that tau pathology could be instrumental in the cholinergic neuronal loss observed in AD...
- Modelling Alzheimer-specific abnormal Tau phosphorylation independently of GSK3beta and PKA kinase activitiesP Delobel
INSERM U422, IMPRT, Institut de Médecine Prédictive et Recherche Thérapeutique, Place de Verdun, 59045, Lille, France
FEBS Lett 516:151-5. 2002..Our results demonstrate that a non-modified physiological process in a cell model can generate the most specific Alzheimer epitope of Tau pathology...
- Mis-splicing of Tau exon 10 in myotonic dystrophy type 1 is reproduced by overexpression of CELF2 but not by MBNL1 silencingC M Dhaenens
INSERM, U837 1, Alzheimer and Tauopathies, Place de Verdun, F 59045 Lille, France
Biochim Biophys Acta 1812:732-42. 2011....
- Sstr2A: a relevant target for the delivery of genes into human glioblastoma cells using fiber-modified adenoviral vectorsK Lécolle
INSERM, UMR837, rue Polonovski, Lille, France
Gene Ther 20:283-97. 2013..Adenoviral vectors targeting SRIF receptors might thus represent a promising therapeutic approach to brain tumors...
- Genome-wide haplotype association study identifies the FRMD4A gene as a risk locus for Alzheimer's diseaseJ C Lambert
INSERM, U744, Lille, France
Mol Psychiatry 18:461-70. 2013..4 × 10(-7)). In conclusion, combining both GWHA study and a conservative three-stage replication approach, we characterised FRMD4A as a new genetic risk factor of AD...