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632 results on '"Loring, Jeanne"'

151. Circulating melanoma cells isolated from clinical blood samples and characterized by full-length mRNA sequencing at single-cell level.

Author

Wang, Yu-Chieh, primary, Ramskold, Daniel, additional, Luo, Shujun, additional, Li, Robin, additional, Deng, Qiaolin, additional, Daniels, Gregory A., additional, Khrebtukova, Irina, additional, Loring, Jeanne F., additional, Laurent, Louise C., additional, Schroth, Gary P., additional, and Sandberg, Rickard, additional

Published
2012
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152. Recurrent Variations in DNA Methylation in Human Pluripotent Stem Cells and Their Differentiated Derivatives

Author

Nazor, Kristopher L., primary, Altun, Gulsah, additional, Lynch, Candace, additional, Tran, Ha, additional, Harness, Julie V., additional, Slavin, Ileana, additional, Garitaonandia, Ibon, additional, Müller, Franz-Josef, additional, Wang, Yu-Chieh, additional, Boscolo, Francesca S., additional, Fakunle, Eyitayo, additional, Dumevska, Biljana, additional, Lee, Sunray, additional, Park, Hyun Sook, additional, Olee, Tsaiwei, additional, D'Lima, Darryl D., additional, Semechkin, Ruslan, additional, Parast, Mana M., additional, Galat, Vasiliy, additional, Laslett, Andrew L., additional, Schmidt, Uli, additional, Keirstead, Hans S., additional, Loring, Jeanne F., additional, and Laurent, Louise C., additional

Published
2012
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154. Correction: Highly Parallel Genome-Wide Expression Analysis of Single Mammalian Cells

Author

Fan, Jian-Bing, primary, Chen, Jing, additional, April, Craig S., additional, Fisher, Jeffrey S., additional, Klotzle, Brandy, additional, Bibikova, Marina, additional, Kaper, Fiona, additional, Ronaghi, Mostafa, additional, Linnarsson, Sten, additional, Ota, Takayo, additional, Chien, Jeremy, additional, Laurent, Louise C., additional, Loring, Jeanne F., additional, Nisperos, Sean V., additional, Chen, Gina Y., additional, and Zhong, Jiang F., additional

Published
2012
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155. Chromatin Insulator Elements Block Transgene Silencing in Engineered Human Embryonic Stem Cell Lines at a Defined Chromosome 13 Locus

Author

MacArthur, Chad C., primary, Xue, Haipeng, additional, Van Hoof, Dennis, additional, Lieu, Pauline T., additional, Dudas, Miroslav, additional, Fontes, Andrew, additional, Swistowski, Andrzej, additional, Touboul, Thomas, additional, Seerke, Rina, additional, Laurent, Louise C., additional, Loring, Jeanne F., additional, German, Michael S., additional, Zeng, Xianmin, additional, Rao, Mahendra S., additional, Lakshmipathy, Uma, additional, Chesnut, Jonathan D., additional, and Liu, Ying, additional

Published
2012
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156. Spontaneous Single‐Copy Loss of TP53in Human Embryonic Stem Cells Markedly Increases Cell Proliferation and Survival

Author

Amir, Hadar, Touboul, Thomas, Sabatini, Karen, Chhabra, Divya, Garitaonandia, Ibon, Loring, Jeanne F., Morey, Robert, and Laurent, Louise C.

Abstract

Genomic aberrations have been identified in many human pluripotent stem cell (hPSC) cultures. Commonly observed duplications in portions of chromosomes 12p and 17q have been associated with increases in genetic instability and resistance to apoptosis, respectively. However, the phenotypic consequences related to sporadic mutations have not been evaluated to date. Here, we report on the effects of a single‐copy deletion of the chr17p13.1 region, a sporadic mutation that spontaneously arose independently in several subclones of a human embryonic stem cell culture. Compared to cells with two normal copies of chr17p13.1 (“wild‐type”), the cells with a single‐copy deletion of this region (“mutant”) displayed a selective advantage when exposed to stressful conditions, and retained a higher percentage of cells expressing the pluripotency marker POU5F1/OCT4 after 2 weeks of in vitro differentiation. Knockdown of TP53, which is a gene encompassed by the deleted region, in wild‐type cells mimicked the chr17p13.1 deletion phenotype. Thus, sporadic mutations in hPSCs can have phenotypic effects that may impact their utility for clinical applications. StemCells2017;35:872–885 Phenotypes altered by single‐copy deletion of TP53 in human embryonic stem cells.

Published
2017
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157. New Monoclonal Antibodies to Defined Cell Surface Proteins on Human Pluripotent Stem Cells

Author

O'Brien, Carmel M., Chy, Hun S., Zhou, Qi, Blumenfeld, Shiri, Lambshead, Jack W., Liu, Xiaodong, Kie, Joshua, Capaldo, Bianca D., Chung, Tung‐Liang, Adams, Timothy E., Phan, Tram, Bentley, John D., McKinstry, William J., Oliva, Karen, McMurrick, Paul J., Wang, Yu‐Chieh, Rossello, Fernando J., Lindeman, Geoffrey J., Chen, Di, Jarde, Thierry, Clark, Amander T., Abud, Helen E., Visvader, Jane E., Nefzger, Christian M., Polo, Jose M., Loring, Jeanne F., and Laslett, Andrew L.

Abstract

The study and application of human pluripotent stem cells (hPSCs) will be enhanced by the availability of well‐characterized monoclonal antibodies (mAbs) detecting cell‐surface epitopes. Here, we report generation of seven new mAbs that detect cell surface proteins present on live and fixed human ES cells (hESCs) and human iPS cells (hiPSCs), confirming our previous prediction that these proteins were present on the cell surface of hPSCs. The mAbs all show a high correlation with POU5F1 (OCT4) expression and other hPSC surface markers (TRA‐160 and SSEA‐4) in hPSC cultures and detect rare OCT4 positive cells in differentiated cell cultures. These mAbs are immunoreactive to cell surface protein epitopes on both primed and naive state hPSCs, providing useful research tools to investigate the cellular mechanisms underlying human pluripotency and states of cellular reprogramming. In addition, we report that subsets of the seven new mAbs are also immunoreactive to human bone marrow‐derived mesenchymal stem cells (MSCs), normal human breast subsets and both normal and tumorigenic colorectal cell populations. The mAbs reported here should accelerate the investigation of the nature of pluripotency, and enable development of robust cell separation and tracing technologies to enrich or deplete for hPSCs and other human stem and somatic cell types. StemCells2017;35:626–640 We describe the generation of novel monoclonal antibodies (mAbs) for the detection and viable characterization of human pluripotent cell (hPSC) cultures and their derivative cells. To select mAb targets we used previously published transcriptional and bioinformatic data that predicts cell surface proteins correlating with the CD9/GCTM‐2 gradient identified for hPSCs cultured in multiple conditions. A large number of novel hybridomas were produced that detected cell surface proteins for known gene targets on live hPSC by flow cytometry. Here, we show detailed immunostaining and flow cytometric analyses of hPSC cultures using a panel of seven new mAbs detecting epitopes corresponding to GPR64, CDCP1, hF11R, DSG2, CDH3, NLGN4X, and PCDH1. We have analyzed the immunoreactivity of these epitopes on hPSCs cultured in a lineage primed state, during early differentiation and in three culture conditions reported to support a naive state of pluripotency. We further examined the detection of these proteins in somatic cell types relevant to the study of breast and colorectal cancers. These mAbs provide a new resource for application in the study of human pluripotency, cell reprogramming and oncogenesis.

Published
2017
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158. Teratoma Generation in the Testis Capsule

Author

Peterson, Suzanne E., primary, Tran, Ha T., primary, Garitaonandia, Ibon, primary, Han, Sangyoon, primary, Nickey, Kyle S., primary, Leonardo, Trevor, primary, Laurent, Louise C., primary, and Loring, Jeanne F., primary

Published
2011
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160. Specific lectin biomarkers for isolation of human pluripotent stem cells identified through array-based glycomic analysis

Author

Wang, Yu-Chieh, primary, Nakagawa, Masato, additional, Garitaonandia, Ibon, additional, Slavin, Ileana, additional, Altun, Gulsah, additional, Lacharite, Robert M, additional, Nazor, Kristopher L, additional, Tran, Ha T, additional, Lynch, Candace L, additional, Leonardo, Trevor R, additional, Liu, Ying, additional, Peterson, Suzanne E, additional, Laurent, Louise C, additional, Yamanaka, Shinya, additional, and Loring, Jeanne F, additional

Published
2011
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161. Induced pluripotent stem cells from highly endangered species

Author

Friedrich Ben-Nun, Inbar, primary, Montague, Susanne C, additional, Houck, Marlys L, additional, Tran, Ha T, additional, Garitaonandia, Ibon, additional, Leonardo, Trevor R, additional, Wang, Yu-Chieh, additional, Charter, Suellen J, additional, Laurent, Louise C, additional, Ryder, Oliver A, additional, and Loring, Jeanne F, additional

Published
2011
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163. Normal Human Pluripotent Stem Cell Lines Exhibit Pervasive Mosaic Aneuploidy

Author

Peterson, Suzanne E., primary, Westra, Jurjen W., additional, Rehen, Stevens K., additional, Young, Holly, additional, Bushman, Diane M., additional, Paczkowski, Christine M., additional, Yung, Yun C., additional, Lynch, Candace L., additional, Tran, Ha T., additional, Nickey, Kyle S., additional, Wang, Yu-Chieh, additional, Laurent, Louise C., additional, Loring, Jeanne F., additional, Carpenter, Melissa K., additional, and Chun, Jerold, additional

Published
2011
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164. Targeted Gene Correction of Laminopathy-Associated LMNA Mutations in Patient-Specific iPSCs

Author

Liu, Guang-Hui, primary, Suzuki, Keiichiro, additional, Qu, Jing, additional, Sancho-Martinez, Ignacio, additional, Yi, Fei, additional, Li, Mo, additional, Kumar, Sachin, additional, Nivet, Emmanuel, additional, Kim, Jessica, additional, Soligalla, Rupa Devi, additional, Dubova, Ilir, additional, Goebl, April, additional, Plongthongkum, Nongluk, additional, Fung, Ho-Lim, additional, Zhang, Kun, additional, Loring, Jeanne F., additional, Laurent, Louise C., additional, and Izpisua Belmonte, Juan Carlos, additional

Published
2011
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165. A Call for Standardized Naming and Reporting of Human ESC and iPSC Lines

Author

Luong, Mai X., primary, Auerbach, Jonathan, additional, Crook, Jeremy M., additional, Daheron, Laurence, additional, Hei, Derek, additional, Lomax, Geoffrey, additional, Loring, Jeanne F., additional, Ludwig, Tenneille, additional, Schlaeger, Thorsten M., additional, Smith, Kelly P., additional, Stacey, Glyn, additional, Xu, Ren-He, additional, and Zeng, Fanyi, additional

Published
2011
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167. A bioinformatic assay for pluripotency in human cells

Author

Müller, Franz-Josef, primary, Schuldt, Bernhard M, additional, Williams, Roy, additional, Mason, Dylan, additional, Altun, Gulsah, additional, Papapetrou, Eirini P, additional, Danner, Sandra, additional, Goldmann, Johanna E, additional, Herbst, Arne, additional, Schmidt, Nils O, additional, Aldenhoff, Josef B, additional, Laurent, Louise C, additional, and Loring, Jeanne F, additional

Published
2011
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169. Dynamic Changes in the Copy Number of Pluripotency and Cell Proliferation Genes in Human ESCs and iPSCs during Reprogramming and Time in Culture

Author

Laurent, Louise C., primary, Ulitsky, Igor, additional, Slavin, Ileana, additional, Tran, Ha, additional, Schork, Andrew, additional, Morey, Robert, additional, Lynch, Candace, additional, Harness, Julie V., additional, Lee, Sunray, additional, Barrero, Maria J., additional, Ku, Sherman, additional, Martynova, Marina, additional, Semechkin, Ruslan, additional, Galat, Vasiliy, additional, Gottesfeld, Joel, additional, Belmonte, Juan Carlos Izpisua, additional, Murry, Chuck, additional, Keirstead, Hans S., additional, Park, Hyun-Sook, additional, Schmidt, Uli, additional, Laslett, Andrew L., additional, Muller, Franz-Josef, additional, Nievergelt, Caroline M., additional, Shamir, Ron, additional, and Loring, Jeanne F., additional

Published
2011
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176. Restricted ethnic diversity in human embryonic stem cell lines

Author

Laurent, Louise C, primary, Nievergelt, Caroline M, additional, Lynch, Candace, additional, Fakunle, Eyitayo, additional, Harness, Julie V, additional, Schmidt, Uli, additional, Galat, Vasiliy, additional, Laslett, Andrew L, additional, Otonkoski, Timo, additional, Keirstead, Hans S, additional, Schork, Andrew, additional, Park, Hyun-Sook, additional, and Loring, Jeanne F, additional

Published
2010
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182. A panel of induced pluripotent stem cells from chimpanzees: a resource for comparative functional genomics.

Author

Romero, Irene Gallego, Pavlovic, Bryan J., Hernando-Herraez, Irene, Xiang Zhou, Ward, Michelle C., Banovich, Nicholas E., Kagan, Courtney L., Burnett, Jonathan E., Huang, Constance H., Mitrano, Amy, Chavarria, Claudia I., Ben-Nun, Inbar Friedrich, Yingchun Li, Sabatini, Karen, Leonardo, Trevor R., Parast, Mana, Marques-Bonet, Tomas, Laurent, Louise C., Loring, Jeanne F., and Gilad, Yoav

Subjects
PLURIPOTENT stem cells, DNA methylation, RNA sequencing
Abstract

The article presents a study that determines the pluripotent stem cells (iPSC) lines derived from healthy chimpanzees through the collection of RNA-sequencing and DNA methylation data from the source lines.

Published
2015
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183. HDAC inhibition imparts beneficial transgenerational effects in Huntington's disease mice via altered DNA and histone methylation.

Author

Haiqun Jia, Morris, Charles D., Williams, Roy M., Loring, Jeanne F., and Thomas, Elizabeth A.

Subjects
HUNTINGTON disease, DEOXYRIBOSE, MURIDAE, DNA, AMPLIFIED fragment length polymorphism, METHYLATION
Abstract

Increasing evidence has demonstrated that epigenetic factors can profoundly influence gene expression and, in turn, influence resistance or susceptibility to disease. Epigenetic drugs, such as histone deacetylase (HDAC) inhibitors, are finding their way into clinical practice, although their exact mechanisms of action are unclear. To identify mechanisms associated with HDAC inhibition, we performed microarray analysis on brain and muscle samples treated with the HDAC1/3-targeting inhibitor, HDACi 4b. Pathways analyses of microarray datasets implicate DNA methylation as significantly associated with HDAC inhibition. Further assessment of DNA methylation changes elicited by HDACi 4b in human fibroblasts from normal controls and patients with Huntington's disease (HD) using the Infinium HumanMethylation450 BeadChip revealed a limited, but overlapping, subset of methylated CpG sites that were altered by HDAC inhibition in both normal and HD cells. Among the altered loci of Y chromosome-linked genes, KDM5D, which encodes Lys (K)-specific demethylase 5D, showed increased methylation at several CpG sites in both normal and HD cells, as well as in DNA isolated from sperm from drug-treated male mice. Further, we demonstrate that first filial generation (F1) offspring from drug-treated male HD transgenic mice show significantly improved HD disease phenotypes compared with F1 offspring from vehicle-treated male HD transgenic mice, in association with increased Kdm5d expression, and decreased histone H3 Lys4 (K4) (H3K4) methylation in the CNS of male offspring. Additionally, we show that overexpression of Kdm5d in mutant HD striatal cells significantly improves metabolic deficits. These findings indicate that HDAC inhibitors can elicit transgenerational effects, via cross-talk between different epigenetic mechanisms, to have an impact on disease phenotypes in a beneficial manner. [ABSTRACT FROM AUTHOR]

Published
2015
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184. 6. Cryobiology for stem cell therapy: Research overview

Author

Katkov, Igor I., primary, Kim, Min S., additional, Karpova, Natalia S., additional, Lulat, Ayub G.M., additional, Cao, Calvin, additional, Levine, Fred, additional, Terskikh, Alexey V., additional, Loring, Jeanne F., additional, and Snyder, Evan Y., additional

Published
2006
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188. Genome wide profiling of human embryonic stem cells (hESCs), their derivatives and embryonal carcinoma cells to develop base profiles of U.S. Federal government approved hESC lines

Author

Liu, Ying, primary, Shin, Soojung, additional, Zeng, Xianmin, additional, Zhan, Ming, additional, Gonzalez, Rodolfo, additional, Mueller, Franz-Josef, additional, Schwartz, Catherine M, additional, Xue, Haipeng, additional, Li, Huai, additional, Baker, Shawn C, additional, Chudin, Eugene, additional, Barker, David L, additional, McDaniel, Timothy K, additional, Oeser, Steffen, additional, Loring, Jeanne F, additional, Mattson, Mark P, additional, and Rao, Mahendra S, additional

Published
2006
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194. NTera2: A Model System to Study Dopaminergic Differentiation of Human Embryonic Stem Cells

Author

Schwartz, Catherine M., primary, Spivak, Charles E., additional, Baker, Shawn C., additional, McDaniel, Timothy K., additional, Loring, Jeanne F., additional, Nguyen, Cuong, additional, Chrest, Francis J., additional, Wersto, Robert, additional, Arenas, Ernest, additional, Zeng, Xianmin, additional, Freed, William J., additional, and Rao, Mahendra S., additional

Published
2005
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197. Designing Microarray Experiments for Neurobiology.

Author

Boulton, Alan A., Baker, Glen B., LeBlanc, Andréa C., Scott Eastman, P., and Loring, Jeanne F.

Abstract

Microarray technology, while it is no longer in its infancy, is still immature and unpredictable. If it works well, microarray expression analysis is a powerful method for estimating the behavior of 10,000 genes simultaneously. But how often does it work well? Because of the rapid adoption of this young technology, we have to anticipate that one of the consequences will be the occasional publication of incorrect results. Some microarray data are simply wrong. In the course of trying to perfect microarray gene expression experiments in the last few years, we think that we have encountered most of the problems that can lead to erroneous interpretation of microarray data. The goal of this chapter is to offer advice from our experience in the hope that it will increase the odds of obtaining accurate data from microarray experiments in neurobiology. [ABSTRACT FROM AUTHOR]

Published
2002
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198. Designing Animal Models of Alzheimer's Disease with Amyloid Precursor Protein (APP)Transgenes.

Author

Walker, John M., Hooper, Nigel M., and Loring, Jeanne F.

Abstract

Amyloid precursor protein (APP) and Alzheimer's disease are irrevocably linked, as APP is cleaved to form the Aβ peptides that are the major components of amyloid plaques. One of the most resilient hypotheses about the cause of AD centers on the Aβ peptide; all genetic causes and risk factors can be fitted into a general "amyloid cascade hypothesis," which maintains that all pathology is initiated by an abnormal accumulation of Aβ amyloid (1). [ABSTRACT FROM AUTHOR]

Published
2000
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199. Promoting remyelination: utilizing a viral model of demyelination to assess cell-based therapies.

Author

Marro, Brett S, Blanc, Caroline A, Loring, Jeanne F, Cahalan, Michael D, and Lane, Thomas E

Abstract

Multiple sclerosis (MS) is a chronic inflammatory disease of the CNS. While a broad range of therapeutics effectively reduce the incidence of focal white matter inflammation and plaque formation for patients with relapse-remitting forms of MS, a challenge within the field is to develop therapies that allow for axonal protection and remyelination. In the last decade, growing interest has focused on utilizing neural precursor cells (NPCs) to promote remyelination. To understand how NPCs function in chronic demyelinating environments, several excellent pre-clinical mouse models have been developed. One well accepted model is infection of susceptible mice with neurotropic variants of mouse hepatitis virus (MHV) that undergo chronic demyelination exhibiting clinical and histopathologic similarities to MS patients. Combined with the possibility that an environmental agent such as a virus could trigger MS, the MHV model of demyelination presents a relevant mouse model to assess the therapeutic potential of NPCs transplanted into an environment in which inflammatory-mediated demyelination is established. [ABSTRACT FROM AUTHOR]

Published
2014
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200. Neural stem cells genetically-modified to express neprilysin reduce pathology in Alzheimer transgenic models.

Author

Blurton-Jones, Mathew, Spencer, Brian, Michael, Sara, Castello, Nicholas A., Agazaryan, Andranik A., Davis, Joy L., Müller, Franz-Josef, Loring, Jeanne F., Masliah, Eliezer, and LaFerla, Frank M.

Abstract

Introduction: Short-term neural stem cell (NSC) transplantation improves cognition in Alzheimer's disease (AD) transgenic mice by enhancing endogenous synaptic connectivity. However, this approach has no effect on the underlying beta-amyloid (Aβ) and neurofibrillary tangle pathology. Long term efficacy of cell based approaches may therefore require combinatorial approaches. Methods: To begin to examine this question we genetically-modified NSCs to stably express and secrete the Aβ-degrading enzyme, neprilysin (sNEP). Next, we studied the effects of sNEP expression in vitro by quantifying Aβ-degrading activity, NSC multipotency markers, and Aβ-induced toxicity. To determine whether sNEP-expressing NSCs can also modulate AD-pathogenesis in vivo, control-modified and sNEP-NSCs were transplanted unilaterally into the hippocampus of two independent and well characterized transgenic models of AD: 3xTg-AD and Thy1-APP mice. After three months, stem cell engraftment, neprilysin expression, and AD pathology were examined. Results: Our findings reveal that stem cell-mediated delivery of NEP provides marked and significant reductions in Aβ pathology and increases synaptic density in both 3xTg-AD and Thy1-APP transgenic mice. Remarkably, Aβ plaque loads are reduced not only in the hippocampus and subiculum adjacent to engrafted NSCs, but also within the amygdala and medial septum, areas that receive afferent projections from the engrafted region. Conclusions: Taken together, our data suggest that genetically-modified NSCs could provide a powerful combinatorial approach to not only enhance synaptic plasticity but to also target and modify underlying Alzheimer's disease pathology. [ABSTRACT FROM AUTHOR]

Published
2014
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