Jennifer L. Martindale mostly deals with Molecular biology, Cell biology, RNA-binding protein, AU-rich element and Protein biosynthesis. Her biological study deals with issues like Translation, which deal with fields such as Polysome. Her studies deal with areas such as Apoptosis, Programmed cell death and microRNA as well as Cell biology.
She interconnects Oxidative stress, Reactive oxygen species and Signal transduction in the investigation of issues within Programmed cell death. Jennifer L. Martindale has included themes like Regulation of gene expression, Ubiquitin, Transcription and Untranslated region in her RNA-binding protein study. Her work in AU-rich element covers topics such as Gene expression which are related to areas like Effector, Adipocyte and Endocrinology.
Jennifer L. Martindale mainly focuses on Cell biology, Molecular biology, RNA-binding protein, Messenger RNA and Gene silencing. Her Cell biology study combines topics from a wide range of disciplines, such as RNA, Cell and microRNA. Jennifer L. Martindale focuses mostly in the field of RNA, narrowing it down to topics relating to Mitochondrion and, in certain cases, Oxidative stress.
Her work deals with themes such as Translation, Three prime untranslated region, Untranslated region and Polysome, which intersect with Molecular biology. Her study in RNA-binding protein is interdisciplinary in nature, drawing from both Regulation of gene expression, Gene expression and RNA interference. Her Messenger RNA research is multidisciplinary, incorporating elements of RNA splicing and Bioinformatics.
Her scientific interests lie mostly in Cell biology, Gene silencing, Gene expression, RNA-binding protein and Messenger RNA. Her biological study spans a wide range of topics, including Cell, Transcription factor, microRNA and Cell growth. Her microRNA study also includes
Her research integrates issues of CCL2, Immune system, Antigen and Tumor necrosis factor alpha in her study of Gene silencing. Her RNA-binding protein research incorporates elements of Translation, Insulin and Autophagy, Autophagosome formation. Her Messenger RNA research includes elements of Biophysics, Distribution and Polysome.
Jennifer L. Martindale spends much of her time researching Cell biology, RNA, Gene silencing, Transcription and Phenotype. Her work carried out in the field of Cell biology brings together such families of science as Polyadenylation and Oxidative stress. While the research belongs to areas of Polyadenylation, Jennifer L. Martindale spends her time largely on the problem of Protein biosynthesis, intersecting her research to questions surrounding Untranslated region.
The various areas that Jennifer L. Martindale examines in her Oxidative stress study include DNA damage, Reactive oxygen species, Proinflammatory cytokine, PI3K/AKT/mTOR pathway and Mitochondrion. Her Phenotype research is multidisciplinary, incorporating perspectives in Interleukin 6, Secretion, Interleukin 8 and Chemokine, CXCL1. Jennifer L. Martindale works mostly in the field of Endoplasmic reticulum, limiting it down to topics relating to Polysome and, in certain cases, Gene expression and Carcinogenesis, as a part of the same area of interest.
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Cellular response to oxidative stress: signaling for suicide and survival.
Jennifer L. Martindale;Nikki J. Holbrook;Nikki J. Holbrook.
Journal of Cellular Physiology (2002)
Gadd153 Sensitizes Cells to Endoplasmic Reticulum Stress by Down-Regulating Bcl2 and Perturbing the Cellular Redox State
Karen D. McCullough;Jennifer L. Martindale;Lars-Oliver Klotz;Tak-Yee Aw.
Molecular and Cellular Biology (2001)
The cellular response to oxidative stress: influences of mitogen-activated protein kinase signalling pathways on cell survival
Xiantao Wang;Jennifer L. Martindale;Yusen Liu;Nikki J. Holbrook.
Biochemical Journal (1998)
LincRNA-p21 Suppresses Target mRNA Translation
Je Hyun Yoon;Kotb Abdelmohsen;Subramanya Srikantan;Xiaoling Yang.
Molecular Cell (2012)
Requirement for ERK Activation in Cisplatin-induced Apoptosis *
Xiantao Wang;Jennifer L. Martindale;Nikki J. Holbrook.
Journal of Biological Chemistry (2000)
HuR recruits let-7/RISC to repress c-Myc expression
Hyeon Ho Kim;Yuki Kuwano;Subramanya Srikantan;Eun Kyung Lee.
Genes & Development (2009)
Complexes containing activating transcription factor (ATF)/cAMP-responsive-element-binding protein (CREB) interact with the CCAAT/enhancer-binding protein (C/EBP)-ATF composite site to regulate Gadd153 expression during the stress response.
Timothy W. Fawcett;Jennifer L. Martindale;Kathryn Z. Guyton;Tsonwin Hai.
Biochemical Journal (1999)
Identification of HuR target circular RNAs uncovers suppression of PABPN1 translation by CircPABPN1.
Kotb Abdelmohsen;Amaresh C. Panda;Rachel Munk;Ioannis Grammatikakis.
RNA Biology (2017)
Concurrent versus individual binding of HuR and AUF1 to common labile target mRNAs
Ashish Lal;Krystyna Mazan-Mamczarz;Tomoko Kawai;Xiaoling Yang.
The EMBO Journal (2004)
RNA-binding protein HuR enhances p53 translation in response to ultraviolet light irradiation
Krystyna Mazan-Mamczarz;Stefanie Galbán;Isabel López de Silanes;Jennifer L. Martindale.
Proceedings of the National Academy of Sciences of the United States of America (2003)
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