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Inflammatory Stress on Autophagy in Peripheral Blood Mononuclear Cells from Patients with Alzheimer's Disease during 24 Months of Follow-UpLongitudinal follow-up of autophagy and inflammation in brain of APPswePS1dE9 transgenic miceImpairment of autophagy in the central nervous system during lipopolysaccharide-induced inflammatory stress in miceInvolvement of interleukin-1β in the autophagic process of microglia: relevance to Alzheimer's diseasePost-translational modifications of tau protein: implications for Alzheimer's disease.Tau protein kinases: involvement in Alzheimer's disease.Tau protein phosphatases in Alzheimer's disease: the leading role of PP2A.Autophagy dysfunction and its link to Alzheimer's disease and type II diabetes mellitus.GSM-900MHz at low dose temperature-dependently downregulates α-synuclein in cultured cerebral cells independently of chaperone-mediated-autophagy.Induction of antiproliferative effect by diosgenin through activation of p53, release of apoptosis-inducing factor (AIF) and modulation of caspase-3 activity in different human cancer cells.PP2A blockade inhibits autophagy and causes intraneuronal accumulation of ubiquitinated proteins.Maladaptative Autophagy Impairs Adipose Function in Congenital Generalized Lipodystrophy due to Cavin-1 Deficiency.Correction: Inflammatory Stress on Autophagy in Peripheral Blood Mononuclear Cells from Patients with Alzheimer's Disease during 24 Months of Follow-Up.In vivo activation and nuclear translocation of phosphorylated glycogen synthase kinase-3beta in neuronal apoptosis: links to tau phosphorylation.Neurons overexpressing mutant presenilin-1 are more sensitive to apoptosis induced by endoplasmic reticulum-Golgi stress.BAD and Bcl-2 regulation are early events linking neuronal endoplasmic reticulum stress to mitochondria-mediated apoptosis.Linking alterations in tau phosphorylation and cleavage during neuronal apoptosis.Study of p53 expression and post-transcriptional modifications after GSM-900 radiofrequency exposure of human amniotic cells.Brefeldin A-induced apoptosis is expressed in rat neurons with dephosphorylated tau protein.Should the chromosome region 15q11q13 be tested systematically by FISH in the case of an autistic-like syndrome?Lithium down-regulates tau in cultured cortical neurons: a possible mechanism of neuroprotection.Brefeldin A induces apoptosis and cell cycle blockade in glioblastoma cell lines.First prenatally diagnosed case of 16p11.2p12.1 duplicationCytogenetic Studies in Human Cells ExposedIn Vitroto GSM-900 MHz Radiofrequency Radiation Using R-Banded KaryotypingPhosphorylated neurofilament expression and resistance to kainate toxicityN-methyl-D-aspartate receptor blockade enhances neuronal apoptosis induced by serum deprivationNeuronal APP accumulates in toxic membrane blebbingsRevaluation twenty-three years later of a supernumerary derivative chromosome 9First familial case of ring chromosome 18 and monosomy 18 mosaicismTwo unusual chromosome aberrations ascertained by sonographic anomaliesAneuploidy studies in human cells exposed in vitro to GSM-900 MHz radiofrequency radiation using FISHFamilial 18 centromere variant resulting in difficulties in interpreting prenatal interphase FISHTau phosphorylation and neuronal apoptosis induced by the blockade of PP2A preferentially involve GSK3β
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P50
description
researcher ORCID ID = 0000-0002-3655-3964
@en
wetenschapper
@nl
name
Faraj Terro
@ast
Faraj Terro
@en
Faraj Terro
@es
Faraj Terro
@nl
type
label
Faraj Terro
@ast
Faraj Terro
@en
Faraj Terro
@es
Faraj Terro
@nl
prefLabel
Faraj Terro
@ast
Faraj Terro
@en
Faraj Terro
@es
Faraj Terro
@nl
P106
P1153
6602670596
P31
P496
0000-0002-3655-3964