LIVIVO - Search results -

Search results

Result 1 - 10 of total 64

Search options

Article: "Holy cow, where do I sign up?" Attitudes of Military Veterans toward Epigenomic Biomarker Toxic Exposure Testing.

Pereira, Stacey / Apodaca, Calvin / Slominski, Kyle / Lipsky, Rachele K / Coarfa, Cristian / Walker, Cheryl L / McGuire, Amy L / Steele, Lea / Helmer, Drew A

medRxiv : the preprint server for health sciences

2024

Abstract: Background: With the signing of the PACT Act in 2022, there is great interest and investment in studying toxic exposures encountered during military service. One way to address this is through the identification of epigenomic biomarkers associated with ... ...

Abstract	Background: With the signing of the PACT Act in 2022, there is great interest and investment in studying toxic exposures encountered during military service. One way to address this is through the identification of epigenomic biomarkers associated with exposures. There is increasing evidence suggesting that exposure to toxic substances may result in alterations to DNA methylation and resultant gene expression. These epigenomic changes may lead to adverse health effects for exposed individuals and their offspring. While the development of epigenomic biomarkers for exposures could facilitate understanding of these exposure-related health effects, such testing could also provide unwanted information. Objectives: Explore Veterans' attitudes toward epigenomic biomarker research and the potential to test for past exposures that could pose intergenerational risk. Methods: Semi-structured interviews with Veterans (n=22) who experienced potentially harmful exposures during their military service. Results: Twenty Veterans said they would hypothetically want to receive epigenomic information related to their toxic exposures and potential health impacts as part of a research study. Veterans identified nine potential benefits of this research, including promoting insights concerning intergenerational health, identification of early health interventions to mitigate the impact of exposures, and additional knowledge or explanation for their experiences. At the same time, 16 participants noted potential risks, including psychological distress in response to results, concerns about receiving non-actionable, uncertain, or inaccurate results, and issues related to privacy and discrimination. Ten participants also identified at least one condition in their children that they thought could be related to their exposure and most said they would be interested in receiving research results related to their children's and grandchildren's risk of developing a health condition associated with their exposure. Discussion: Results suggest that Veterans might welcome benefits of epigenomic research related to military exposures yet have some concerns about potential negative impacts.
Language	English
Publishing date	2024-04-18
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.04.09.24305554
Database	MEDical Literature Analysis and Retrieval System OnLINE

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Details ▾

Article: Lysine Demethylase 4A is a Centrosome Associated Protein Required for Centrosome Integrity and Genomic Stability.

Chowdhury, Pratim / Wang, Xiaoli / Love, Julia F / Vargas-Hernandez, Sofia / Nakatani, Yuya / Grimm, Sandra L / Mezquita, Dereck / Mason, Frank M / Martinez, Elisabeth D / Coarfa, Cristian / Walker, Cheryl L / Gustavsson, Anna-Karin / Dere, Ruhee

bioRxiv : the preprint server for biology

2024

Abstract: Centrosomes play a fundamental role in nucleating and organizing microtubules in the cell and are vital for faithful chromosome segregation and maintenance of genomic stability. Loss of structural or functional integrity of centrosomes causes genomic ... ...

Abstract	Centrosomes play a fundamental role in nucleating and organizing microtubules in the cell and are vital for faithful chromosome segregation and maintenance of genomic stability. Loss of structural or functional integrity of centrosomes causes genomic instability and is a driver of oncogenesis. The lysine demethylase 4A (KDM4A) is an epigenetic 'eraser' of chromatin methyl marks, which we show also localizes to the centrosome with single molecule resolution. We additionally discovered KDM4A demethylase enzymatic activity is required to maintain centrosome homeostasis, and is required for centrosome integrity, a new functionality unlinked to altered expression of genes regulating centrosome number. We find rather, that KDM4A interacts with both mother and daughter centriolar proteins to localize to the centrosome in all stages of mitosis. Loss of
Language	English
Publishing date	2024-02-21
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.02.20.581246
Database	MEDical Literature Analysis and Retrieval System OnLINE

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Details ▾

Article ; Online: The Maternal and Infant Environmental Health Riskscape study of perinatal disparities in greater Houston: rationale, study design and participant profiles.

Symanski, Elaine / Whitworth, Kristina W / Mendez-Figueroa, Hector / Aagaard, Kjersti M / Moussa, Iman / Alvarez, Juan / Chardon Fabian, Adrien / Kannan, Kurunthachalam / Walker, Cheryl L / Coarfa, Cristian / Suter, Melissa A / Salihu, Hamisu M

Frontiers in reproductive health

2024 Volume 6, Page(s) 1304717

Abstract: Introduction: The Maternal and Infant Environmental Health Riskscape (MIEHR) Center was established to address the interplay among chemical and non-chemical stressors in the biological, physical, social, and built environments that disproportionately ... ...

Abstract	Introduction: The Maternal and Infant Environmental Health Riskscape (MIEHR) Center was established to address the interplay among chemical and non-chemical stressors in the biological, physical, social, and built environments that disproportionately impact perinatal health among Black pregnant people in a large and diverse urban area with documented disparities in the U.S. Methods: The MIEHR cohort is recruiting non-Hispanic Black and non-Hispanic white pregnant people who deliver their infants at major obstetric hospitals in Houston, Texas. At enrollment, all participants are asked to provide urine samples for chemical [metals, cotinine, and polycyclic aromatic hydrocarbons (PAHs)] analyses and blood samples. A subset of the cohort is asked to provide oral and vaginal swabs, and fecal samples. Questionnaire and electronic health record data gather information about residential address history during pregnancy, pregnancy history and prenatal care, sociodemographic and lifestyle factors, experiences of discrimination and stress, and sources of social support. Using information on where a participant lived during their pregnancy, features of their neighborhood environment are characterized. We provide summaries of key individual- and neighborhood-level features of the entire cohort, as well as for Black and white participants separately. Results: Between April 2021 and February 2023, 1,244 pregnant people were recruited. Nearly all participants provided urine samples and slightly less than half provided blood samples. PAH exposure patterns as assessed on 47% of participants thus far showed varying levels depending on metabolite as compared to previous studies. Additionally, analyses suggest differences between Black and white pregnant people in experiences of discrimination, stress, and levels of social support, as well as in neighborhood characteristics. Discussion: Our findings to date highlight racial differences in experiences of discrimination, stress, and levels of support, as well as neighborhood characteristics. Recruitment of the cohort is ongoing and additional neighborhood metrics are being constructed. Biospecimens will be analyzed for metals and PAH metabolites (urine samples), miRNAs (plasma samples) and the microbiome (oral swabs). Once enrollment ends, formal assessments are planned to elucidate individual- and neighborhood-level features in the environmental riskscape that contribute to Black-White disparities in perinatal health.
Language	English
Publishing date	2024-04-22
Publishing country	Switzerland
Document type	Journal Article
ISSN	2673-3153
ISSN (online)	2673-3153
DOI	10.3389/frph.2024.1304717
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article: Molecular hallmarks of renal medullary carcinoma: more to c-MYC than meets the eye.

Msaouel, Pavlos / Walker, Cheryl L / Genovese, Giannicola / Tannir, Nizar M

Molecular & cellular oncology

2020 Volume 7, Issue 5, Page(s) 1777060

Abstract: Renal medullary carcinoma (RMC) is a lethal disease that predominantly afflicts young individuals with sickle cell trait. Our recently reported molecular profiling of primary untreated RMC tissues elucidated distinct genomic and immune hallmarks of RMC, ... ...

Abstract	Renal medullary carcinoma (RMC) is a lethal disease that predominantly afflicts young individuals with sickle cell trait. Our recently reported molecular profiling of primary untreated RMC tissues elucidated distinct genomic and immune hallmarks of RMC, and identified MYC-induced replication stress as a targetable vulnerability for this disease.
Language	English
Publishing date	2020-06-23
Publishing country	United States
Document type	Journal Article
ISSN	2372-3556
ISSN	2372-3556
DOI	10.1080/23723556.2020.1777060
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article: TGFβ signaling links early-life endocrine-disrupting chemicals exposure to suppression of nucleotide excision repair in rat myometrial stem cells.

Bariani, Maria Victoria / Cui, Yan-Hong / Ali, Mohamed / Bai, Tao / Grimm, Sandra L / Coarfa, Cristian / Walker, Cheryl L / He, Yu-Ying / Yang, Qiwei / Al-Hendy, Ayman

Research square

2023

Abstract: Environmental exposure to endocrine-disrupting chemicals (EDCs) is linked to the development of uterine fibroids (UFs) in women. UFs, non-cancerous tumors, are thought to originate from abnormal myometrial stem cells (MMSCs). Defective DNA repair ... ...

Abstract	Environmental exposure to endocrine-disrupting chemicals (EDCs) is linked to the development of uterine fibroids (UFs) in women. UFs, non-cancerous tumors, are thought to originate from abnormal myometrial stem cells (MMSCs). Defective DNA repair capacity may contribute to the emergence of mutations that promote tumor growth. The multifunctional cytokine TGFβ1 is associated with UF progression and DNA damage repair pathways. To investigate the impact of EDC exposure on TGFβ1 and nucleotide excision repair (NER) pathways, we isolated MMSCs from 5-months old Eker rats exposed neonatally to Diethylstilbestrol (DES), an EDC, or to vehicle (VEH). EDC-MMSCs exhibited overactivated TGFβ1 signaling and reduced mRNA and protein levels of NER pathway components compared to VEH-MMSCs. EDC-MMSCs also demonstrated impaired NER capacity. Exposing VEH-MMSCs to TGFβ1 decreased NER capacity while inhibiting TGFβ signaling in EDC-MMSCs restored it. RNA-seq analysis and further validation revealed decreased expression of Uvrag, a tumor suppressor gene involved in DNA damage recognition, in VEH-MMSCs treated with TGFβ1, but increased expression in EDC-MMSCs after TGFβ signaling inhibition. Overall, we demonstrated that the overactivation of the TGFβ pathway links early-life exposure to EDCs with impaired NER capacity, which would lead to increased genetic instability, arise of mutations, and fibroid tumorigenesis. We demonstrated that the overactivation of the TGFβ pathway links early-life exposure to EDCs with impaired NER capacity, which would lead to increased fibroid incidence.
Language	English
Publishing date	2023-06-07
Publishing country	United States
Document type	Preprint
DOI	10.21203/rs.3.rs-3001855/v1
Database	MEDical Literature Analysis and Retrieval System OnLINE

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Details ▾

Article ; Online: TGFβ signaling links early life endocrine-disrupting chemicals exposure to suppression of nucleotide excision repair in rat myometrial stem cells.

Bariani, Maria Victoria / Cui, Yan-Hong / Ali, Mohamed / Bai, Tao / Grimm, Sandra L / Coarfa, Cristian / Walker, Cheryl L / He, Yu-Ying / Yang, Qiwei / Al-Hendy, Ayman

Cellular and molecular life sciences : CMLS

2023 Volume 80, Issue 10, Page(s) 288

Abstract	Environmental exposure to endocrine-disrupting chemicals (EDCs) is linked to the development of uterine fibroids (UFs) in women. UFs, non-cancerous tumors, are thought to originate from abnormal myometrial stem cells (MMSCs). Defective DNA repair capacity may contribute to the emergence of mutations that promote tumor growth. The multifunctional cytokine TGFβ1 is associated with UF progression and DNA damage repair pathways. To investigate the impact of EDC exposure on TGFβ1 and nucleotide excision repair (NER) pathways, we isolated MMSCs from 5-month-old Eker rats exposed neonatally to diethylstilbestrol (DES), an EDC, or to vehicle (VEH). EDC-MMSCs exhibited overactivated TGFβ1 signaling and reduced mRNA and protein levels of NER pathway components compared to VEH-MMSCs. EDC-MMSCs also demonstrated impaired NER capacity. Exposing VEH-MMSCs to TGFβ1 decreased NER capacity while inhibiting TGFβ signaling in EDC-MMSCs restored it. RNA-seq analysis and further validation revealed decreased expression of Uvrag, a tumor suppressor gene involved in DNA damage recognition, in VEH-MMSCs treated with TGFβ1, but increased expression in EDC-MMSCs after TGFβ signaling inhibition. Overall, we demonstrated that the overactivation of the TGFβ pathway links early life exposure to EDCs with impaired NER capacity, which would lead to increased genetic instability, arise of mutations, and fibroid tumorigenesis. We demonstrated that the overactivation of the TGFβ pathway links early life exposure to EDCs with impaired NER capacity, which would lead to increased fibroid incidence.
MeSH term(s)	Female ; Animals ; Rats ; DNA Repair/genetics ; DNA Damage ; Transforming Growth Factor beta/genetics ; Carcinogenesis ; Endocrine Disruptors/toxicity ; Leiomyoma/chemically induced ; Leiomyoma/genetics
Chemical Substances	Transforming Growth Factor beta ; Endocrine Disruptors
Language	English
Publishing date	2023-09-09
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1358415-7
ISSN	1420-9071 ; 1420-682X
ISSN (online)	1420-9071
ISSN	1420-682X
DOI	10.1007/s00018-023-04928-z
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 195: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Endocrine-disrupting chemicals and fatty liver disease.

Foulds, Charles E / Treviño, Lindsey S / York, Brian / Walker, Cheryl L

Nature reviews. Endocrinology

2017 Volume 13, Issue 8, Page(s) 445–457

Abstract: A growing epidemic of nonalcoholic fatty liver disease (NAFLD) is paralleling the increase in the incidence of obesity and diabetes mellitus in countries that consume a Western diet. As NAFLD can lead to life-threatening conditions such as cirrhosis and ... ...

Abstract	A growing epidemic of nonalcoholic fatty liver disease (NAFLD) is paralleling the increase in the incidence of obesity and diabetes mellitus in countries that consume a Western diet. As NAFLD can lead to life-threatening conditions such as cirrhosis and hepatocellular carcinoma, an understanding of the factors that trigger its development and pathological progression is needed. Although by definition this disease is not associated with alcohol consumption, exposure to environmental agents that have been linked to other diseases might have a role in the development of NAFLD. Here, we focus on one class of these agents, endocrine-disrupting chemicals (EDCs), and their potential to influence the initiation and progression of a cascade of pathological conditions associated with hepatic steatosis (fatty liver). Experimental studies have revealed several potential mechanisms by which EDC exposure might contribute to disease pathogenesis, including the modulation of nuclear hormone receptor function and the alteration of the epigenome. However, many questions remain to be addressed about the causal link between acute and chronic EDC exposure and the development of NAFLD in humans. Future studies that address these questions hold promise not only for understanding the linkage between EDC exposure and liver disease but also for elucidating the molecular mechanisms that underpin NAFLD, which in turn could facilitate the development of new prevention and treatment opportunities.
MeSH term(s)	Animals ; Endocrine Disruptors/adverse effects ; Humans ; Liver/drug effects ; Liver/metabolism ; Liver/pathology ; Non-alcoholic Fatty Liver Disease/chemically induced ; Non-alcoholic Fatty Liver Disease/metabolism ; Non-alcoholic Fatty Liver Disease/pathology ; Obesity/metabolism ; Obesity/pathology ; Risk Factors
Chemical Substances	Endocrine Disruptors
Language	English
Publishing date	2017-05-19
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	2489381-X
ISSN	1759-5037 ; 1759-5029
ISSN (online)	1759-5037
ISSN	1759-5029
DOI	10.1038/nrendo.2017.42
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 6336: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 93: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Phosphorylation of epigenetic "readers, writers and erasers": Implications for developmental reprogramming and the epigenetic basis for health and disease.

Treviño, Lindsey S / Wang, Quan / Walker, Cheryl L

Progress in biophysics and molecular biology

2015 Volume 118, Issue 1-2, Page(s) 8–13

Abstract: Epigenetic reprogramming that occurs during critical periods of development can increase the susceptibility to many diseases in adulthood. Programming of the epigenome during development occurs via the activity of a variety of epigenetic modifiers, ... ...

Abstract	Epigenetic reprogramming that occurs during critical periods of development can increase the susceptibility to many diseases in adulthood. Programming of the epigenome during development occurs via the activity of a variety of epigenetic modifiers, including "readers, writers and erasers" of histone methyl marks. Posttranslational modification of these programmers can alter their activity, resulting in global or gene-specific changes in histone methylation and gene transcription. This review summarizes what is currently known about phosphorylation of histone methyltransferases ("writers"), demethylases ("erasers") and effector proteins ("readers) that program the epigenome, and the impact of this posttranslational modification on their activity. Understanding how the activity of these epigenetic programmers is perturbed by environmental exposures via changes in phosphorylation is key to understanding mechanisms of developmental reprogramming and the epigenetic basis of health and disease.
MeSH term(s)	Animals ; Carcinogens, Environmental/toxicity ; Disease/genetics ; Epigenesis, Genetic/drug effects ; Growth and Development/drug effects ; Growth and Development/genetics ; Health ; Humans ; Phosphorylation/drug effects
Chemical Substances	Carcinogens, Environmental
Language	English
Publishing date	2015-07
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	209302-9
ISSN	1873-1732 ; 0079-6107
ISSN (online)	1873-1732
ISSN	0079-6107
DOI	10.1016/j.pbiomolbio.2015.02.013
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Uc I Zs.281: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Hypothesis: Activation of rapid signaling by environmental estrogens and epigenetic reprogramming in breast cancer.

Treviño, Lindsey S / Wang, Quan / Walker, Cheryl L

Reproductive toxicology (Elmsford, N.Y.)

2015 Volume 54, Page(s) 136–140

Abstract: Environmental and lifestyle factors are considered significant components of the increasing breast cancer risk in the last 50 years. Specifically, exposure to environmental endocrine disrupting compounds is correlated with cancer susceptibility in a ... ...

Abstract	Environmental and lifestyle factors are considered significant components of the increasing breast cancer risk in the last 50 years. Specifically, exposure to environmental endocrine disrupting compounds is correlated with cancer susceptibility in a variety of tissues. In both human and rodent models, the exposure to ubiquitous environmental estrogens during early life has been shown to disrupt normal mammary development and cause permanent adverse effects. Recent studies indicate that environmental estrogens not only have the ability to disrupt estrogen receptor (ER) signaling, but can also reprogram the epigenome by altering DNA and histone methylation through rapid, nongenomic ER actions. We have observed xenoestrogen-mediated activation of several nongenomic signaling pathways and have identified a target for epigenetic reprogramming in MCF-7 breast cancer cells. These observations, in addition to data from the literature, support the hypothesis that activation of rapid signaling by environmental estrogens can lead to epigenetic reprogramming and contribute to the progression of breast cancer.
MeSH term(s)	Age Factors ; Animals ; Breast Neoplasms/chemically induced ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Carcinogens, Environmental/toxicity ; Cell Transformation, Neoplastic/chemically induced ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; Cell Transformation, Neoplastic/pathology ; Cellular Reprogramming/drug effects ; Endocrine Disruptors/toxicity ; Environmental Exposure/adverse effects ; Epigenesis, Genetic/drug effects ; Estrogens/toxicity ; Female ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; MCF-7 Cells ; Risk Assessment ; Risk Factors ; Signal Transduction/drug effects
Chemical Substances	Carcinogens, Environmental ; Endocrine Disruptors ; Estrogens
Language	English
Publishing date	2015-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	639342-1
ISSN	1873-1708 ; 0890-6238
ISSN (online)	1873-1708
ISSN	0890-6238
DOI	10.1016/j.reprotox.2014.12.014
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 2316: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Epigenetic response to hyperoxia in the neonatal lung is sexually dimorphic.

Coarfa, Cristian / Grimm, Sandra L / Katz, Tiffany / Zhang, Yuhao / Jangid, Rahul K / Walker, Cheryl L / Moorthy, Bhagavatula / Lingappan, Krithika

Redox biology

2020 Volume 37, Page(s) 101718

Abstract: Sex as a biological variable plays a critical role both during lung development and in modulating postnatal hyperoxic lung injury and repair. The molecular mechanisms behind these sex-specific differences need to be elucidated. Our objective was to ... ...

Abstract	Sex as a biological variable plays a critical role both during lung development and in modulating postnatal hyperoxic lung injury and repair. The molecular mechanisms behind these sex-specific differences need to be elucidated. Our objective was to determine if the neonatal lung epigenomic landscape reconfiguration has profound effects on gene expression and could underlie sex-biased differences in protection from or susceptibility to diseases. Neonatal male and female mice (C57BL/6) were exposed to hyperoxia (95% FiO, PND 1-5: saccular stage) or room air and euthanized on PND 7 and 21. Pulmonary gene expression was studied using RNA-seq on Illumina HiSeq 2500 platform and quantified. Epigenomic landscape was assessed using Chromatin Immunoprecipitation (ChIP-Seq) of the H3K27ac histone modification mark, associated with active genes, enhancers, and super-enhancers. These data were then integrated, pathways identified and validated. Sex-biased epigenetic modulation of gene expression leads to differential regulation of biological processes in the developing lung at baseline and after exposure to hyperoxia. The female lung exhibits a more robust epigenomic response for the H3K27ac mark in response to hyperoxia. Epigenomic changes distribute over genomic and epigenomic domains in a sex-specific manner. The differential epigenomic responses also enrich for key transcription regulators crucial for lung development. In addition, by utilizing H3K27ac as the target epigenomic change we were also able to identify new epigenomic reprogramming at super-enhancers. Finally, we report for the first time that the upregulation of p21 (Cdkn1a) in the injured neonatal lung could be mediated through gain of H3K27ac. These data demonstrate that modulation of transcription via epigenomic landscape alterations may contribute to the sex-specific differences in preterm neonatal hyperoxic lung injury and repair.
MeSH term(s)	Animals ; Animals, Newborn ; Epigenesis, Genetic ; Epigenomics ; Female ; Hyperoxia/genetics ; Lung ; Male ; Mice ; Mice, Inbred C57BL
Language	English
Publishing date	2020-09-11
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2020.101718
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

To top

More links

Kategorien

Inter-library loan at ZB MED

More links

Kategorien

Inter-library loan at ZB MED

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

Inter-library loan at ZB MED

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito