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Genetic architecture of 11 major psychiatric disorders at biobehavioral, functional genomic and molecular genetic levels of analysis

Joint analysis of 11 major psychiatric disorders identifies four broad factor underlying genetic correlations among the disorders. Association analyses detect 152 loci acting on these factors and identify 9 loci that act heterogeneously across disorders.

Andrew D. Grotzinger
Travis T. Mallard
Michel G. Nivard
Research05 May 2022
Nature Genetics

Volume: 54, P: 548-559
Bone marrow–derived stem cells initiate pancreatic regeneration

David Hess
Li Li
Mickie Bhatia
Research22 Jun 2003
Nature Biotechnology

Volume: 21, P: 763-770
PADI4 acts as a coactivator of Tal1 by counteracting repressive histone arginine methylation

Peptidylarginine deiminase 4 (PADI4) is a transcriptional co-regulator that converts arginine residues at histone tails to citrulline. The authors show that PADI4 interacts with the central haematopoietic transcription factor TAL1 to regulate gene expression in an erythroleukemia cell line.

Stephan Kolodziej
Olga N. Kuvardina
Jörn Lausen
ResearchOpen Access29 May 2014
Nature Communications

Volume: 5, P: 1-12
α-synuclein interacts with PrP^C to induce cognitive impairment through mGluR5 and NMDAR2B

The precise underpinnings of Parkinson's disease and other disorders associated with the accumulation of α-synuclein are unclear. This study shows that PrP^C mediates α-synuclein-associated synaptic dysfunction and memory deficits. Blocking specific events in receptor biology rescued cognitive deficits in mice, suggesting new possibilities for intervention in synucleinopathies.

Diana G Ferreira
Mariana Temido-Ferreira
Tiago F Outeiro
Research25 Sept 2017
Nature Neuroscience

Volume: 20, P: 1569-1579
Sip1 regulates sequential fate decisions by feedback signaling from postmitotic neurons to progenitors

Smad-interacting protein 1 (Sip1) is a transcriptional repressor that acts in the TGF-β signaling pathway. This study finds that Sip1 is involved in a feedback signaling mechanism in which newly generated postmitotic cells in neocortical layers instruct progenitor cells for proper cell-fate switch and proliferation.

Eve Seuntjens
Anjana Nityanandam
Victor Tarabykin
Research18 Oct 2009
Nature Neuroscience

Volume: 12, P: 1373-1380
Observation of the rare B_s⁰ →µ⁺µ⁻ decay from the combined analysis of CMS and LHCb data

Combined analysis of proton-proton collision data from the Large Hadron Collider at CERN by the CMS and LHCb collaborations leads to the observation of the extremely rare decay of the strange B meson into muons; the result is compatible with the standard model of particle physics, and does not show any signs of new physics, such as supersymmetry.

V. Khachatryan
A.M. Sirunyan
E. Pesen
ResearchOpen Access13 May 2015
Nature

Volume: 522, P: 68-72
Disruption of NEUROD2 causes a neurodevelopmental syndrome with autistic features via cell-autonomous defects in forebrain glutamatergic neurons

Karen Runge
Rémi Mathieu
Antoine de Chevigny
ResearchOpen Access29 Jun 2021
Molecular Psychiatry

Volume: 26, P: 6125-6148

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Genetic architecture of 11 major psychiatric disorders at biobehavioral, functional genomic and molecular genetic levels of analysis

Bone marrow–derived stem cells initiate pancreatic regeneration

PADI4 acts as a coactivator of Tal1 by counteracting repressive histone arginine methylation

α-synuclein interacts with PrP^C to induce cognitive impairment through mGluR5 and NMDAR2B

Sip1 regulates sequential fate decisions by feedback signaling from postmitotic neurons to progenitors

Observation of the rare B_s⁰ →µ⁺µ⁻ decay from the combined analysis of CMS and LHCb data

Disruption of NEUROD2 causes a neurodevelopmental syndrome with autistic features via cell-autonomous defects in forebrain glutamatergic neurons

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Genetic architecture of 11 major psychiatric disorders at biobehavioral, functional genomic and molecular genetic levels of analysis

Bone marrow–derived stem cells initiate pancreatic regeneration

PADI4 acts as a coactivator of Tal1 by counteracting repressive histone arginine methylation

α-synuclein interacts with PrPC to induce cognitive impairment through mGluR5 and NMDAR2B

Sip1 regulates sequential fate decisions by feedback signaling from postmitotic neurons to progenitors

Observation of the rare Bs0 →µ+µ− decay from the combined analysis of CMS and LHCb data

Disruption of NEUROD2 causes a neurodevelopmental syndrome with autistic features via cell-autonomous defects in forebrain glutamatergic neurons

Search

Quick links

α-synuclein interacts with PrP^C to induce cognitive impairment through mGluR5 and NMDAR2B

Observation of the rare B_s⁰ →µ⁺µ⁻ decay from the combined analysis of CMS and LHCb data