Lista de obras -

A rare motor neuron deleterious missense mutation in the DPYSL3 (CRMP4) gene is associated with ALS.

artículo científico publicado en 2013

APPepsilon, the epsilon-secretase-derived N-terminal product of the beta-amyloid precursor protein, behaves as a type I protein and undergoes alpha-, beta-, and gamma-secretase cleavages

artículo científico publicado en 2006

Assessment of a Screening Questionnaire to Identify Exposure to Lead in Pregnant Women

scientific article published on 10 December 2020

Calreticulin levels determine onset of early muscle denervation by fast motoneurons of ALS model mice.

artículo científico publicado en 2014

Caspase-3-derived C-terminal product of synphilin-1 displays antiapoptotic function via modulation of the p53-dependent cell death pathway.

artículo científico publicado en 2006

Combined pharmacological, mutational and cell biology approaches indicate that p53-dependent caspase 3 activation triggered by cellular prion is dependent on its endocytosis.

artículo científico publicado en 2005

Environmental Health in Perinatal and Early Childhood: Awareness, Representation, Knowledge and Practice of Southern France Perinatal Health Professionals

article

Knowledge and attitudes of midwives regarding reprotoxic agents during pregnancy: snapshot of the Marseille area, southern France

artículo científico publicado en 2018

LRP1 controls biosynthetic and endocytic trafficking of neuronal prion protein

artículo científico publicado en 2008

M1 and M3 muscarinic receptors control physiological processing of cellular prion by modulating ADAM17 phosphorylation and activity.

artículo científico publicado en 2007

Optimised and rapid pre-clinical screening in the SOD1(G93A) transgenic mouse model of amyotrophic lateral sclerosis (ALS).

artículo científico publicado en 2011

Presenilin-dependent gamma-secretase-mediated control of p53-associated cell death in Alzheimer's disease.

artículo científico publicado en 2006

Presenilin-dependent transcriptional control of the Abeta-degrading enzyme neprilysin by intracellular domains of betaAPP and APLP

scientific journal article

Primary cultured neurons devoid of cellular prion display lower responsiveness to staurosporine through the control of p53 at both transcriptional and post-transcriptional levels

artículo científico publicado en 2003

Reduced calreticulin levels link endoplasmic reticulum stress and Fas-triggered cell death in motoneurons vulnerable to ALS.

artículo científico publicado en 2012

Regulation of betaAPP and PrPc cleavage by alpha-secretase: mechanistic and therapeutic perspectives

scientific article published on April 2008

Response to Correspondence: Pardossi-Piquard et al., “Presenilin-Dependent Transcriptional Control of the Aβ-Degrading Enzyme Neprilysin by Intracellular Domains of βAPP and APLP.” Neuron 46, 541–554

article

Somatic and axonal LIGHT signaling elicit degenerative and regenerative responses in motoneurons, respectively

artículo científico publicado en 2014

The C-terminal products of cellular prion protein processing, C1 and C2, exert distinct influence on p53-dependent staurosporine-induced caspase-3 activation

artículo científico publicado en 2006

The alpha-secretase-derived N-terminal product of cellular prion, N1, displays neuroprotective function in vitro and in vivo

artículo científico publicado en 2009

The disintegrin ADAM9 indirectly contributes to the physiological processing of cellular prion by modulating ADAM10 activity

artículo científico publicado en 2005

The disintegrin ADAM9 indirectly contributes to the physiological processing of cellular prion by modulating ADAM10 activity.

artículo científico publicado en 2013

The gamma/epsilon-secretase-derived APP intracellular domain fragments regulate p53.

artículo científico publicado en 2007

The mechanism of internalization of glycosylphosphatidylinositol-anchored prion protein

artículo científico publicado en 2003

Transcriptional repression of p53 by parkin and impairment by mutations associated with autosomal recessive juvenile Parkinson's disease.

artículo científico publicado en 2009

p53-Dependent transcriptional control of cellular prion by presenilins. ⬇️

artículo científico publicado en 2009

α-Secretase-derived fragment of cellular prion, N1, protects against monomeric and oligomeric amyloid β (Aβ)-associated cell death

artículo científico publicado en 2011

α-Secretase-derived fragment of cellular prion, N1, protects against monomeric and oligomeric amyloid β (Aβ)-associated cell death

artículo científico publicado en 2013

Lista de obras de

A rare motor neuron deleterious missense mutation in the DPYSL3 (CRMP4) gene is associated with ALS.

APPepsilon, the epsilon-secretase-derived N-terminal product of the beta-amyloid precursor protein, behaves as a type I protein and undergoes alpha-, beta-, and gamma-secretase cleavages

Assessment of a Screening Questionnaire to Identify Exposure to Lead in Pregnant Women

Calreticulin levels determine onset of early muscle denervation by fast motoneurons of ALS model mice.

Caspase-3-derived C-terminal product of synphilin-1 displays antiapoptotic function via modulation of the p53-dependent cell death pathway.

Combined pharmacological, mutational and cell biology approaches indicate that p53-dependent caspase 3 activation triggered by cellular prion is dependent on its endocytosis.

Environmental Health in Perinatal and Early Childhood: Awareness, Representation, Knowledge and Practice of Southern France Perinatal Health Professionals

Knowledge and attitudes of midwives regarding reprotoxic agents during pregnancy: snapshot of the Marseille area, southern France

LRP1 controls biosynthetic and endocytic trafficking of neuronal prion protein

M1 and M3 muscarinic receptors control physiological processing of cellular prion by modulating ADAM17 phosphorylation and activity.

Optimised and rapid pre-clinical screening in the SOD1(G93A) transgenic mouse model of amyotrophic lateral sclerosis (ALS).

Presenilin-dependent gamma-secretase-mediated control of p53-associated cell death in Alzheimer's disease.

Presenilin-dependent transcriptional control of the Abeta-degrading enzyme neprilysin by intracellular domains of betaAPP and APLP

Primary cultured neurons devoid of cellular prion display lower responsiveness to staurosporine through the control of p53 at both transcriptional and post-transcriptional levels

Reduced calreticulin levels link endoplasmic reticulum stress and Fas-triggered cell death in motoneurons vulnerable to ALS.

Regulation of betaAPP and PrPc cleavage by alpha-secretase: mechanistic and therapeutic perspectives

Response to Correspondence: Pardossi-Piquard et al., “Presenilin-Dependent Transcriptional Control of the Aβ-Degrading Enzyme Neprilysin by Intracellular Domains of βAPP and APLP.” Neuron 46, 541–554

Somatic and axonal LIGHT signaling elicit degenerative and regenerative responses in motoneurons, respectively

The C-terminal products of cellular prion protein processing, C1 and C2, exert distinct influence on p53-dependent staurosporine-induced caspase-3 activation

The alpha-secretase-derived N-terminal product of cellular prion, N1, displays neuroprotective function in vitro and in vivo

The disintegrin ADAM9 indirectly contributes to the physiological processing of cellular prion by modulating ADAM10 activity

The disintegrin ADAM9 indirectly contributes to the physiological processing of cellular prion by modulating ADAM10 activity.

The gamma/epsilon-secretase-derived APP intracellular domain fragments regulate p53.

The mechanism of internalization of glycosylphosphatidylinositol-anchored prion protein

Transcriptional repression of p53 by parkin and impairment by mutations associated with autosomal recessive juvenile Parkinson's disease.

p53-Dependent transcriptional control of cellular prion by presenilins. ⬇️

α-Secretase-derived fragment of cellular prion, N1, protects against monomeric and oligomeric amyloid β (Aβ)-associated cell death

α-Secretase-derived fragment of cellular prion, N1, protects against monomeric and oligomeric amyloid β (Aβ)-associated cell death