Repression of the Heat Shock Response Is a Programmed Event at the Onset of Reproduction.
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Developmental Drift and the Role of Wnt Signaling in AgingEngineering and Evolution of Molecular Chaperones and Protein Disaggregases with Enhanced ActivityA network approach to discerning the identities of C. elegans in a free moving population.Uncoupling the Trade-Off between Somatic Proteostasis and Reproduction in Caenorhabditis elegans Models of Polyglutamine Diseases.The genome-wide role of HSF-1 in the regulation of gene expression in Caenorhabditis elegansVitellogenin-RNAi and ovariectomy each increase lifespan, increase protein storage, and decrease feeding, but are not additive in grasshoppers.Innate immunity mediated longevity and longevity induced by germ cell removal converge on the C-type lectin domain protein IRG-7.Caenorhabditis elegans glp-4 Encodes a Valyl Aminoacyl tRNA SynthetaseHSF-1 activates the ubiquitin proteasome system to promote non-apoptotic developmental cell death in C. elegans.A transcriptional signature of Alzheimer's disease is associated with a metastable subproteome at risk for aggregationTwo Conserved Histone Demethylases Regulate Mitochondrial Stress-Induced Longevity.The Aging EpigenomeUBQLN2 Mediates Autophagy-Independent Protein Aggregate Clearance by the Proteasome.Identification of SET Domain-Containing Proteins in Gossypium raimondii and Their Response to High Temperature Stress.Small heat shock proteins mediate cell-autonomous and -nonautonomous protection in a Drosophila model for environmental-stress-induced degeneration.E2F coregulates an essential HSF developmental program that is distinct from the heat-shock response.Reducing translation through eIF4G/IFG-1 improves survival under ER stress that depends on heat shock factor HSF-1 in Caenorhabditis elegans.Hormetic heat stress and HSF-1 induce autophagy to improve survival and proteostasis in C. elegans.Heat Shock Proteins and Maternal Contribution to Oogenesis and Early Embryogenesis.Interaction between epigenetic and metabolism in aging stem cells.Shaping proteostasis at the cellular, tissue, and organismal level.The Intersection Of Aging Biology and The Pathobiology of Lung Diseases: A Joint NHLBI/NIA Workshop.Assessing Health Span in Caenorhabditis elegans: Lessons From Short-Lived Mutants.Life-extending Dietary Restriction Reduces Oxidative Damage of Proteins in Grasshoppers but Does Not Alter Allocation of Ingested Nitrogen to Somatic Tissues.Suppression of transcriptional drift extends C. elegans lifespan by postponing the onset of mortality.Dietary-Induced Signals That Activate the Gonadal Longevity Pathway during Development Regulate a Proteostasis Switch in Caenorhabditis elegans AdulthoodCaenorhabditis elegans ATPase inhibitor factor 1 (IF1) MAI-2 preserves the mitochondrial membrane potential (Δψm) and is important to induce germ cell apoptosis.Chaperone co-inducer BGP-15 inhibits histone deacetylases and enhances the heat shock response through increased chromatin accessibility.C. elegans neurons jettison protein aggregates and mitochondria under neurotoxic stressHSF1-dependent and -independent regulation of the mammalian in vivo heat shock response and its impairment in Huntington's disease mouse models.The homeodomain-interacting protein kinase HPK-1 preserves protein homeostasis and longevity through master regulatory control of the HSF-1 chaperone network and TORC1-restricted autophagy in Caenorhabditis elegans.In vivo properties of the disaggregase function of J-proteins and Hsc70 in Caenorhabditis elegans stress and aging.The mitochondrial UPR: mechanisms, physiological functions and implications in ageing.Temporal dynamics of gene expression in heat-stressed Caenorhabditis elegans.Proteome Stability as a Key Factor of Genome Integrity.Transcriptional control of non-apoptotic developmental cell death in C. elegans.Mitochondrial Stress Restores the Heat Shock Response and Prevents Proteostasis Collapse during Aging.The chromatin remodeling factor ISW-1 integrates organismal responses against nuclear and mitochondrial stress.Pathways of cellular proteostasis in aging and disease.Rethinking HSF1 in Stress, Development, and Organismal Health.
P2860
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P2860
Repression of the Heat Shock Response Is a Programmed Event at the Onset of Reproduction.
description
2015 nî lūn-bûn
@nan
2015年の論文
@ja
2015年論文
@yue
2015年論文
@zh-hant
2015年論文
@zh-hk
2015年論文
@zh-mo
2015年論文
@zh-tw
2015年论文
@wuu
2015年论文
@zh
2015年论文
@zh-cn
name
Repression of the Heat Shock Response Is a Programmed Event at the Onset of Reproduction.
@ast
Repression of the Heat Shock Response Is a Programmed Event at the Onset of Reproduction.
@en
type
label
Repression of the Heat Shock Response Is a Programmed Event at the Onset of Reproduction.
@ast
Repression of the Heat Shock Response Is a Programmed Event at the Onset of Reproduction.
@en
prefLabel
Repression of the Heat Shock Response Is a Programmed Event at the Onset of Reproduction.
@ast
Repression of the Heat Shock Response Is a Programmed Event at the Onset of Reproduction.
@en
P2860
P1433
P1476
Repression of the Heat Shock Response Is a Programmed Event at the Onset of Reproduction.
@en
P2093
Johnathan Labbadia
Richard I Morimoto
P2860
P304
P356
10.1016/J.MOLCEL.2015.06.027
P577
2015-07-22T00:00:00Z