Genomics of Pain - Resilience to Pain
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ABSTRACT:
PROVIDER: PRJNA498368 | ENA |
REPOSITORIES: ENA
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Project description:Genomics of Pain - Resilience to Pain
| PRJNA498369 | ENA
Project description:This clinical trial studies the effectiveness of a web-based cancer education tool called Helping Oncology Patients Explore Genomics (HOPE-Genomics) in improving patient knowledge of personal genomic testing results and cancer and genomics in general. HOPE-Genomics is a web-based education tool that teaches cancer/leukemia patients, and patients who may be at high-risk for developing cancer, about genomic testing and provide patients with information about their own genomic test results. The HOPE-Genomics tool may improve patient’s genomic knowledge and quality of patient-centered care. In addition, it may also improve education and care quality for future patients.
| 2378933 | ecrin-mdr-crc
Project description:OCT4, SOX2, and KLF4 (OSK) Yamanaka factors can reverse age-related epigenetic changes, yet alternate mechanisms by which they promote tissue resilience remain poorly understood. Oxidative stress contributes to retinal pigmented epithelium (RPE) degeneration in age-related macular degeneration. Here, we show that OSK expression in RPE promotes Tet2-independent oxidative resilience through acute, memory-free transcriptomic changes, and restores visual function in aged mice. Integrative functional genomics helped identify GSTA4, a detoxifying enzyme that clears the lipid peroxidation byproduct 4-HNE, as a key OSK downstream effector. OSK directly and dynamically activates GSTA4, recapitulating a stem cell-derived stress resilience program. GSTA4 overexpression alone enhances oxidative resilience, rejuvenates the aged RPE transcriptome, and reverses visual decline while avoiding OSK’s pleiotropic effects. GSTA4 is upregulated across diverse lifespan-extending interventions suggesting a broader pro-longevity role. These findings uncover a previously unrecognized protective axis directly regulated by OSK, that can be decoupled from reprogramming, providing a framework for developing more precise rejuvenation therapies.
2026-06-11 | GSE304037 | GEO
Project description:Chronic pain is a global public health problem, but the underlying molecular mechanisms are not fully understood. Here we examine genome-wide DNA methylation, first in 50 identical twins discordant for heat pain sensitivity and then in 50 further unrelated individuals. Whole blood DNA methylation was characterized at 5.2 million loci by MeDIP-sequencing and assessed longitudinally to identify differentially methylated regions associated with high or low pain-sensitivity (pain-DMRs). Nine meta-analysis pain-DMRs show robust evidence for association (false discovery rate 5%) with the strongest signal in the pain gene TRPA1 (P=1.2M-CM-^W10-13). Several pain-DMRs show longitudinal stability consistent with susceptibility effects, have similar methylation levels in brain, and altered expression in skin. Our approach identifies epigenetic changes in both novel and established candidate genes that provide molecular insights into pain and may generalize to other complex traits. MeDIP-sequencing in 100 individulas using a 2 stage design: paired-end MeDIP-seq in 50 monozygotic twins and single-end MeDIP-seq in 50 unrelated individuals.
2013-12-04 | E-GEOD-52965 | biostudies-arrayexpress
Project description:We used microarray-based expression genomics in 25 inbred mouse strains to identify dorsal root ganglion (DRG)-expressed genetic contributors to mechanical allodynia a prominent symptom of chronic pain. Expression genetics identifies a role for the Chrna6 (alpha 6-nicotinic receptor) gene in pain in mice and humans. Dorsal root ganglion tissue across multiple inbred mouse strains, both male and female
2015-02-18 | E-GEOD-65997 | biostudies-arrayexpress
Project description:OCT4, SOX2, and KLF4 (OSK) Yamanaka factors can reverse age-related epigenetic changes, yet alternate mechanisms by which they promote tissue resilience remain poorly understood. Oxidative stress contributes to retinal pigmented epithelium (RPE) degeneration in age-related macular degeneration. Here, we show that OSK expression in RPE promotes Tet2-independent oxidative resilience through acute, memory-free transcriptomic changes, and restores visual function in aged mice. Integrative functional genomics helped identify GSTA4, a detoxifying enzyme that clears the lipid peroxidation byproduct 4-HNE, as a key OSK downstream effector. OSK directly and dynamically activates GSTA4, recapitulating a stem cell-derived stress resilience program. GSTA4 overexpression alone enhances oxidative resilience, rejuvenates the aged RPE transcriptome, and reverses visual decline while avoiding OSK’s pleiotropic effects. GSTA4 is upregulated across diverse lifespan-extending interventions suggesting a broader pro-longevity role. These findings uncover a previously unrecognized protective axis directly regulated by OSK, that can be decoupled from reprogramming, providing a framework for developing more precise rejuvenation therapies.
2026-06-11 | GSE304043 | GEO
Project description:OCT4, SOX2, and KLF4 (OSK) Yamanaka factors can reverse age-related epigenetic changes, yet alternate mechanisms by which they promote tissue resilience remain poorly understood. Oxidative stress contributes to retinal pigmented epithelium (RPE) degeneration in age-related macular degeneration. Here, we show that OSK expression in RPE promotes Tet2-independent oxidative resilience through acute, memory-free transcriptomic changes, and restores visual function in aged mice. Integrative functional genomics helped identify GSTA4, a detoxifying enzyme that clears the lipid peroxidation byproduct 4-HNE, as a key OSK downstream effector. OSK directly and dynamically activates GSTA4, recapitulating a stem cell-derived stress resilience program. GSTA4 overexpression alone enhances oxidative resilience, rejuvenates the aged RPE transcriptome, and reverses visual decline while avoiding OSK’s pleiotropic effects. GSTA4 is upregulated across diverse lifespan-extending interventions suggesting a broader pro-longevity role. These findings uncover a previously unrecognized protective axis directly regulated by OSK, that can be decoupled from reprogramming, providing a framework for developing more precise rejuvenation therapies.
2026-06-11 | GSE304040 | GEO
Project description:OCT4, SOX2, and KLF4 (OSK) Yamanaka factors can reverse age-related epigenetic changes, yet alternate mechanisms by which they promote tissue resilience remain poorly understood. Oxidative stress contributes to retinal pigmented epithelium (RPE) degeneration in age-related macular degeneration. Here, we show that OSK expression in RPE promotes Tet2-independent oxidative resilience through acute, memory-free transcriptomic changes, and restores visual function in aged mice. Integrative functional genomics helped identify GSTA4, a detoxifying enzyme that clears the lipid peroxidation byproduct 4-HNE, as a key OSK downstream effector. OSK directly and dynamically activates GSTA4, recapitulating a stem cell-derived stress resilience program. GSTA4 overexpression alone enhances oxidative resilience, rejuvenates the aged RPE transcriptome, and reverses visual decline while avoiding OSK’s pleiotropic effects. GSTA4 is upregulated across diverse lifespan-extending interventions suggesting a broader pro-longevity role. These findings uncover a previously unrecognized protective axis directly regulated by OSK, that can be decoupled from reprogramming, providing a framework for developing more precise rejuvenation therapies.
2026-06-11 | GSE304042 | GEO
Project description:OCT4, SOX2, and KLF4 (OSK) Yamanaka factors can reverse age-related epigenetic changes, yet alternate mechanisms by which they promote tissue resilience remain poorly understood. Oxidative stress contributes to retinal pigmented epithelium (RPE) degeneration in age-related macular degeneration. Here, we show that OSK expression in RPE promotes Tet2-independent oxidative resilience through acute, memory-free transcriptomic changes, and restores visual function in aged mice. Integrative functional genomics helped identify GSTA4, a detoxifying enzyme that clears the lipid peroxidation byproduct 4-HNE, as a key OSK downstream effector. OSK directly and dynamically activates GSTA4, recapitulating a stem cell-derived stress resilience program. GSTA4 overexpression alone enhances oxidative resilience, rejuvenates the aged RPE transcriptome, and reverses visual decline while avoiding OSK’s pleiotropic effects. GSTA4 is upregulated across diverse lifespan-extending interventions suggesting a broader pro-longevity role. These findings uncover a previously unrecognized protective axis directly regulated by OSK, that can be decoupled from reprogramming, providing a framework for developing more precise rejuvenation therapies.
2026-06-11 | GSE304039 | GEO
Project description:OCT4, SOX2, and KLF4 (OSK) Yamanaka factors can reverse age-related epigenetic changes, yet alternate mechanisms by which they promote tissue resilience remain poorly understood. Oxidative stress contributes to retinal pigmented epithelium (RPE) degeneration in age-related macular degeneration. Here, we show that OSK expression in RPE promotes Tet2-independent oxidative resilience through acute, memory-free transcriptomic changes, and restores visual function in aged mice. Integrative functional genomics helped identify GSTA4, a detoxifying enzyme that clears the lipid peroxidation byproduct 4-HNE, as a key OSK downstream effector. OSK directly and dynamically activates GSTA4, recapitulating a stem cell-derived stress resilience program. GSTA4 overexpression alone enhances oxidative resilience, rejuvenates the aged RPE transcriptome, and reverses visual decline while avoiding OSK’s pleiotropic effects. GSTA4 is upregulated across diverse lifespan-extending interventions suggesting a broader pro-longevity role. These findings uncover a previously unrecognized protective axis directly regulated by OSK, that can be decoupled from reprogramming, providing a framework for developing more precise rejuvenation therapies.
2026-06-11 | GSE304038 | GEO