Caspase-8: a key role in the pathogenesis of diabetic embryopathy. - Wikidata - awgldk - TriplyDB

Caspase-8: a key role in the pathogenesis of diabetic embryopathy.

Caspase-8: a key role in the pathogenesis of diabetic embryopathy.

http://www.wikidata.org/entity/Q33726220

about

Genetic, epigenetic, and environmental contributions to neural tube closure Oxidative stress, unfolded protein response, and apoptosis in developmental toxicity Reduction in embryonic malformations and alleviation of endoplasmic reticulum stress by nitric oxide synthase inhibition in diabetic embryopathy.Epigallocatechin-3-gallate ameliorates hyperglycemia-induced embryonic vasculopathy and malformation by inhibition of Foxo3a activation.Dynamic glucoregulation and mammalian-like responses to metabolic and developmental disruption in zebrafish.Protein kinase Cβ2 inhibition reduces hyperglycemia-induced neural tube defects through suppression of a caspase 8-triggered apoptotic pathway.Resveratrol prevents embryonic oxidative stress and apoptosis associated with diabetic embryopathy and improves glucose and lipid profile of diabetic dam.The essential role of protein kinase Cδ in diabetes-induced neural tube defects What neonatal complications should the pediatrician be aware of in case of maternal gestational diabetes?SOD1 suppresses maternal hyperglycemia-increased iNOS expression and consequent nitrosative stress in diabetic embryopathy Immunohistochemical study of NF-κB p65, c-IAP2 and caspase-3 expression in cervical cancer.Oxidative stress-induced JNK1/2 activation triggers proapoptotic signaling and apoptosis that leads to diabetic embryopathy.Dominant negative FADD dissipates the proapoptotic signalosome of the unfolded protein response in diabetic embryopathy.Amelioration of intracellular stress and reduction of neural tube defects in embryos of diabetic mice by phytochemical quercetin.Maternal hyperglycemia activates an ASK1-FoxO3a-caspase 8 pathway that leads to embryonic neural tube defects New concepts in diabetic embryopathy The status of diabetic embryopathy.Diabetes-induced birth defects: what do we know? What can we do?Effect of maternal diabetes on the embryo, fetus, and children: congenital anomalies, genetic and epigenetic changes and developmental outcomes.Formation of neurodegenerative aggresome and death-inducing signaling complex in maternal diabetes-induced neural tube defects.Down regulation of the proliferation and apoptotic pathways in the embryonic brain of diabetic rats.

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P2860

Caspase-8: a key role in the pathogenesis of diabetic embryopathy.

http://www.wikidata.org/entity/Q33726220

description

2009 nî lūn-bûn

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2009 թուականի Փետրուարին հրատարակուած գիտական յօդուած

@hyw

2009 թվականի փետրվարին հրատարակված գիտական հոդված

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2009年の論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年論文

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2009年论文

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name

Caspase-8: a key role in the pathogenesis of diabetic embryopathy.

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Caspase-8: a key role in the pathogenesis of diabetic embryopathy.

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Caspase-8: a key role in the pathogenesis of diabetic embryopathy.

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Caspase-8: a key role in the pathogenesis of diabetic embryopathy.

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Caspase-8: a key role in the pathogenesis of diabetic embryopathy.

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Caspase-8: a key role in the pathogenesis of diabetic embryopathy.

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Birth Defects Research Part B: Developmental and Reproductive Toxicology

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Caspase-8: a key role in the pathogenesis of diabetic embryopathy

@en

P2093

E Albert Reece

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Peixin Yang

http://www.w3.org/2001/XMLSchema#string

Richard L Eckert

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P2860

Mechanisms of caspase activation

Folic acid supplementation affects ROS scavenging enzymes, enhances Vegf-A, and diminishes apoptotic state in yolk sacs of embryos of diabetic rats

The roles of Bid

Apoptosis: controlled demolition at the cellular level

Pathogenesis of diabetes-induced congenital malformations.

Redox stress and the contributions of BH3-only proteins to infarction.

The role of pro- and anti-apoptotic molecular interactions in embryonic maldevelopment.

Control of mitochondrial permeability by Bcl-2 family members.

Current perspectives on the causes of neural tube defects resulting from diabetic pregnancy.

Apoptotic signaling pathways: caspases and stress-activated protein kinases.

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72-77

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scholarly article

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10.1002/BDRB.20185

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1

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86

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2009-02-01T00:00:00Z

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23981386

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19194987

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2838243

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