Martina Riva

ORCID: 0000-0001-9087-9685
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About
Contact & Profiles
Research Areas
  • Neuroscience and Neuropharmacology Research
  • Neurogenesis and neuroplasticity mechanisms
  • Neuroscience and Neural Engineering
  • Cardiac electrophysiology and arrhythmias
  • Genetics and Neurodevelopmental Disorders
  • Signaling Pathways in Disease
  • Wnt/β-catenin signaling in development and cancer
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Cell Adhesion Molecules Research
  • Glioma Diagnosis and Treatment
  • Photoreceptor and optogenetics research
  • RNA Research and Splicing
  • Genetic Syndromes and Imprinting

Université Paris Cité
2019-2024

Institut de Psychiatrie et Neurosciences de Paris
2019-2024

Institut des Maladies Génétiques Imagine
2019-2023

Inserm
1993-2021

Centre National de la Recherche Scientifique
2019

Institut Jacques Monod
2019

Abstract Cajal-Retzius cells (CRs) are transient neurons, disappearing almost completely in the postnatal neocortex by programmed cell death (PCD), with a percentage surviving up to adulthood hippocampus. Here, we evaluate CR’s role establishment of adult neuronal and cognitive function using mouse model preventing Bax-dependent PCD. CRs abnormal survival resulted impairment hippocampus-dependent memory, associated vivo attenuated theta oscillations enhanced gamma activity dorsal CA1. At...

10.1038/s41467-023-37249-7 article EN cc-by Nature Communications 2023-03-18

Programmed cell death and early activity contribute to the emergence of functional cortical circuits. While most neuronal populations are scaled-down by death, some subpopulations entirely eliminated, raising question importance such demise for wiring. Here, we addressed this issue focusing on Cajal-Retzius neurons (CRs), key players in development that eliminated postnatal mice part via Bax-dependent apoptosis. Using Bax-conditional mutants CR hyperpolarization, show survival electrically...

10.7554/elife.50503 article EN cc-by eLife 2019-12-31

Reelin (RELN) is a secreted glycoprotein essential for cerebral cortex development. In humans, recessive RELN variants cause cortical and cerebellar malformations, while heterozygous were associated to epilepsy, autism mild abnormalities. However, their functional effects remain unknown. We identified inherited de novo missense in patients with neuronal migration disorders (NMDs) as diverse pachygyria polymicrogyria. investigated culture the developing mouse how different impacted function....

10.1172/jci153097 article EN cc-by Journal of Clinical Investigation 2024-07-09

Human placenta contains, in addition to the ubiquitous p120-GTPase-activating protein (GAP), another isoform of 100 kDa, which is specific this organ. We have established a method for purifying placental p100-GAP near homogeneity. The purified allowed preparation polyclonal and monoclonal anti Ras-GAP antibodies. Two antibodies were selected two-site enzyme immunoassay. This simple accurate assay turn facilitated detection GAPs during purification. has activity identical catalytic properties...

10.1016/s0021-9258(17)46708-1 article EN cc-by Journal of Biological Chemistry 1993-09-01

ABSTRACT RELN is a large secreted glycoprotein that acts at multiple steps of cerebral cortex development, including neuronal migration. Only recessive mutations the Reelin gene ( ) have been associated with human cortical malformations and none has functionally characterized. We identified novel missense in both compound de novo heterozygous patients exhibiting an array migration disorders (NMDs) as diverse pachygyria, polymicrogyria heterotopia. Most caused defective secretion vitro and,...

10.1101/2021.05.25.445586 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2021-05-25
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