Maya Capelson, Ph.D.

Contact Information

The Perelman School of Medicine at the University of Pennsylvania
Department of Cell and Developmental Biology
9-101 Smilow Center for Translational Research
3400 Civic Center Blvd
Philadelphia, PA 19104-6059
Office: 215-898-0550
Lab: 215-573-7548
capelson@pennmedicine.upenn.edu

Robert Babak Faryabi, Ph.D.

Deciphering Mechanisms of Genome Mis-folding In Cancer

Our lab deploys data-rich experimental techniques to elucidate the role of genome mis-folding in controlling oncogenic gene expression programs. Specifically, we are interested in moving beyond the status quo to understand how oncogenic subversion of lineage-determining transcription factors set topology of cancer genome. To tackle this question, we combine genomics and super-resolution imaging and focus on investigating molecular mechanisms of genome mis-folding in breast and blood cancers. These mechanistic studies aim to identify precise epigenetic vulnerabilities of cancer cells and guide treatments disrupting cancer cells’ transcriptional addiction.

Representative Publication:

Oncogenic Notch Promotes Long-Range Regulatory Interactions Within Hyperconnected 3D Cliques. Petrovic J*, Zhou Y*, Fasolino M, Goldman N, Schwartz GW, Mumbach MR, Nguyen SC, Rome KS, Sela Y, Zapataro Z, Blacklow SC, Kruhlak MJ, Shi J, Aster JC, Joyce EF, Little SC, Vahedi G, Pear WS, Faryabi RB Molecular Cell. 2019;73(6):1174-90 e12

Determining Epigenetic Mechanisms Of Resistance To Targeted Therapies

Targeting oncogenic drivers of cancers commonly leads to drug resistance. Mechanisms of acquiring resistance to oncology drugs mostly remain unknown, partly due to the limitations of population-based assays in elucidating heterogeneity of drug-naive and complexity of drug-induced tumor evolution. Using single-cell genomics and imaging, we study how heterogeneity and plasticity of transcriptional dependencies confer resistance to targeted therapeutics such as Notch inhibitors.

Representative Publication

TooManyCells Identifies And Visualizes Relationships Of Single-cell Clades. Schwartz GW, Zhou Y, Petrovic J, Fasolino M, Xu L, Shaffer SM, Pear WS, Vahedi G, Faryabi RB Nature Methods, 2020; 17: 405-413

Innovating Computational Methods To Enable Cancer Discovery

Our lab innovates statistical and machine learning approaches to accelerate discovery of novel therapeutics and biomarkers by elucidating complexity and heterogeneity of tumors. Recently, we have developed a computational ecosystem for mapping molecular and spatial heterogeneity in tumors. As part of the Center for Personalized Diagnostics, we also mine cancer patient genotypic/phenotypic data to improve patient health. patient health.

Representative Publication:

Classes of ITD Predict Outcomes in AML Patients Treated With FLT3 Inhibitors. Schwartz GW, Manning B, Zhou Y, Velu P, Bigdeli A, Astles R, Lehman AW, Morrissette JJD, Perl AE, Li M, Carroll M, Faryabi RB Clinical Cancer Research. 2019;25(2):573-83

Research Interest

Cancer is typically considered a genetic disease. However, recent progress in our understanding of epigenetic aberrations in cancer has challenged this view. Overarching goal of our lab is to understand epigenetic mechanisms of transcriptional addiction in cancer and exploit this information to advance cancer therapeutics.

To pursue this objective, we use cutting-edge chromatin conformation capture, high-content imaging, single-cell epigenomics, functional genomics, and combine these technologies with our expertise in computational sciences to systematically explore: i) how epigenetic control of gene expression is disrupted in cancer, ii) why transcriptional addiction can develop, and iii) how heterogeneity and plasticity of transcriptional dependencies enable drug resistance.

Hongjun Song, Ph.D.

Mechanisms regulating adult hippocampal neural stem cells and neurogenesis.
Adult hippocampal neurogenesis reflects a remarkable form of structural plasticity in the mature mammalian brain. Fully characterizing this phenomenon could have far-reaching implications for understanding hippocampal function and revealing fundamental properties of neural development and the regenerative capacity of the central nervous system. Over the past 14 years, my laboratory has systemically investigated adult hippocampal neurogenesis at the molecular, cellular, and circuit levels and reported a number of key findings that have influenced the field. Via genetic clonal analysis, we conclusively demonstrated, for the first time, the existence of bona fide neural stem cells in the adult mammalian hippocampus, capable of both self-renewal and multipotent fate specification of progeny (Bonaguidi et al., Cell 2011). We also revealed how neural activity and experience can regulate the behavior of these stem cells (Song et al., Nature 2012; Jang et al. Cell Stem Cell 2013). We provided the first detailed characterization of newborn neuron integration into the existing neuronal circuitry and its underlying molecular, cellular and circuitry mechanisms (Ge et al., Nature 2006; Faulkner et al. PNAS 2009; Kang et al. Neuron 2011; Kim et al. Cell 2012; Sun et al. J Neurosci. 2013; Song et al. Nat. Neurosci. 2013). In collaboration with Dr. Guo-li Ming, we have discovered critical roles of DISC1, a psychiatric disorder risk gene, in regulating the development of newborn neurons during adult hippocampal neurogenesis (Duan et al. Cell 2007; Faulkner et al. PNAS 2008, Kim et al Neuron 2009; Kim et al. Cell 2012; Zhou et al. Neuron 2013). We discovered novel circuitry mechanisms whereby local neural activity influences the proliferation and development of newborn neurons in the hippocampus (Ma et al., Science 2009; Song et al., Nature 2012; Song et al., Nat Neurosci 2013).

Duan, X., Chang, J.H., Ge, S-y., Faulkner, R.L., Kim, J.Y., Kitabatake, Y., Liu, X-b., Yang, C-h., Jordan, J.D., Ma, D.K., Liu, C.Y., Ganesan, S., Cheng, H.J., Ming, G-l.*, Lu, B.* and Song, H-j.* (2007). Disrupted-In-Schizophrenia 1 regulates integration of new neurons in the adult brain. Cell 130, 1146-1158.
Bonaguidi, M.A., Wheeler, M., Shapiro, J.S., Stadel, R., Sun, G.J., Ming, G-l.*, and Song, H*. (2011). In vivo clonal analysis reveals self-renew and multipotent adult neural stem cell characteristics. Cell 145, 1142-55.
Song, J., Zhong, C., Bonaguidi, M.A., Sun, G.J., Hsu1, D., Gu, Y., Meletis, K., Huang, Z.J., Ge, S., Enikolopov, G., Deisseroth, K., Luscher, B., Christian, K., Ming, G-l., and Song, H. (2012). Neuronal circuitry mechanism regulating adult quiescent neural stem cell fate decision. Nature 489, 150-4.
Sun, G.J., Zhou, Y., Ito, S., Bonaguidi, M.A., Stein-O’Brien, G., Kawasaki, N., Modak, N., Zhu, Y., Ming, G-l., and Song, H. (2015). Latent tri-lineage potential of adult neural stem cells in the hippocampus revealed by Nf1 inactivation. Nature Neuroscience 18, 1722-4.

Neuroepigenetics and Neuroepitranscriptomics. Contrary to the long-held dogma that DNA methylation is a stable epigenetic mark in post-mitotic neurons, it is now recognized to be a robust form of plasticity in the adult nervous system. We have made significant contributions to the current understanding of epigenetic DNA modifications in the adult nervous system. My laboratory identified the first molecular mechanism regulating active DNA demethylation in mature neurons in vivo (Ma et al. Science 2009) and subsequently delineated molecular pathways mediating this process (Guo et al. Cell 2011). More recently, we showed that the neuronal DNA demethylation pathway plays fundamental roles in neuronal function, including regulation of basal levels of synaptic transmission and homeostatic synaptic plasticity (Yu et al. Nat. Neurosci. 2015). My laboratory has established a pipeline for high-throughput sequencing analysis, including RNA-seq, Chip-seq, Bisulfite-seq, ATAC-seq and single-cell RNA-seq and we have designed custom software programs for bioinformatic analyses. We published the first single-base resolution genome-wide DNA methylation profiles in neurons in vivo and showed large scale neuronal activity-induced dynamic methylation changes (Guo et al. Nat. Neurosci, 2011). Via single-base methylome analysis, we also demonstrated the presence of prominent nonCpG methylation in mature neurons in vivo and identified MeCP2 as the first nonCpG DNA methylation binding protein in the field (Guo et al. Nat. Neurosci. 2014). More recently, we have started to explore how methylation of mRNA can affect neurogenesis, axon regeneration and plasticity (Yoon et al. Cell 2017; Weng et al. Neuron 2018).

Ma, D.K., Jang, M.H., Guo, J.U., Kitabatake, Y., Chang, M.L., Pow-Anpongkul, N., Flavell, R.A., Lu, B., Ming, G.L., and Song, H-j. (2009). Neuronal activity-induced Gadd45b promotes epigenetic DNA demethylation and adult neurogenesis. Science 323, 1074-7.
Guo, J.U., Su, Y., Zhong, C., Ming, G.L., and Song, H. (2011). Hydroxylation of 5-methylcytosine by TET1 promotes active DNA demethylation in the adult brain. Cell 145, 423-34.
Yu, H., Su, Y., Shin, J., Zhong, C., Guo, J.U., Weng, Y-l., Gao, F., Geschwind, D.H., Coppola, G., Ming, G-l., and Song, H. (2015). Tet3 regulates synaptic transmission and homeostatic plasticity via DNA oxidation and repair. Nature Neuroscience 18, 836-843.
Yoon, K.J., Ringeling, F.R., Vissers, C., Jacob, F., Pokrass, M., Jimenez-Cyrus, D., Su, Y., Kim, N.S., Zhu, Y., Zheng, L., Kim, S., Wang, X., Doré, L.C., Jin, P., Regot, S., Zhuang, X., Canzar, S., He, C., Ming, G.L., and Song, H. (2017). Temporal control of mammalian cortical neurogenesis by m6A methylation. Cell 171(4):877-889.

Single-cell biology. A complete understanding of the structure and function of neural systems will require integrated analyses at multiple levels. A daunting obstacles to reaching this goal is the technical challenge of characterizing the behavior of single cells in vivo. Many neural processes can be described at the population level, but there are several domains where it is critical to identify molecular and functional properties at the single cell level. My laboratory has developed a “single cell genetic” approach to manipulate target genes in newborn neurons using retroviruses that led to a number of critical discoveries (Ge et al. Nature 2006; Duan et al, Cell 2007; Kim et al. Neuron 2009; Kang et al. Neuron 2011; Kim et al. Cell 2011; Jang et al. Cell Stem Cell 2013; Song et al. Nat. Neurosci. 2013). Our identification of bona fide neural stem cells in the adult brain required clonal analysis to determine whether radial glial-like cells were capable of both self-renewal and giving rise to multiple cell types, thus settling a debate in the field over whether neurons and glia were generated from lineage-restricted progenitors, as opposed to true stem cells (Bonaguidi et al. Cell 2011). To visualize dendritic and axonal growth over development, we devised a new strategy to allow us to reconstruct complete cellular processes of individual cells, revealing a stereotyped pattern of axonal targeting that further suggests the existence of guidance cues in the adult hippocampus (Sun et al., J Neurosci 2013). We have recent developed a single-cell RNA-seq technology and a bioinformatics pipeline to investigate transcriptomes of hundreds to thousands of heterogeneous cell types (Shin et al. Cell Stem Cell, 2015).

Ge, S-y., Goh. E.L.K., Sailor, K.A., Kitabatake, Y., Ming, G-l*. and Song, H-j*. (2006). GABA regulates synaptic integration of newly generated neurons in the adult brain. Nature 439, 589-593.
Bonaguidi, M.A., Wheeler, M., Shapiro, J.S., Stadel, R., Sun, G.J., Ming, G-l.*, and Song, H*. (2011). In vivo clonal analysis reveals self-renew and multipotent adult neural stem cell characteristics. Cell 145, 1142-55.
Jang, M., Bonaguidi, M.A., Kitabatake, Y., Sun, J., Song, J., Kang, E., Jun, H., Zhong, C., Su, Y., Guo, J.U., Wang, M.X., Sailor, K.A., Kim, J.Y., Gao, Y., Christian, K.M., Ming, G-l., and Song, H. (2013). Secreted frizzled-related protein 3 regulates activity-dependent adult hippocampal neurogenesis. Cell Stem Cell 12, 215-23.
Shin, J., Berg, D.A., Zhu, Y., Shin, J.Y., Song, J., Bonaguidi, M.A., Enikolopov, G., Nauen, D.W., Christian, K.M., Ming, G-l., and Song, H. (2015). Single-cell RNA-seq with Waterfall reveals molecular cascades underlying adult neurogenesis. Cell Stem Cell 17, 360-72.

Research Interest

Research in Dr. Hongjun Song’s laboratory focuses on two core topics: (1) neural stem cell regulation and neurogenesis in the developing and adult mammalian brain and how these processes affect neural function; (2) epigenetic and epitranscriptomic mechanisms and their functions in the mammalian nervous system. The lab is also interested in addressing how dysfunction of these mechanisms may be involved in brain disorders.

Brian C. Capell, M.D., Ph.D.

Demonstrated the importance of the KMT2D-LSD1-H3K4 methylation axis in epithelial homeostasis:Epithelial tissues rely on a highly coordinated balance between self-renewal, proliferation and differentiation; disruption of which may drive carcinogenesis. Here we established the first known role of the epigenetic regulatorKMT2D (MLL4) in epithelial enhancer control, including the regulation of p63-target genes involved in epithelial development, differentiation and stratification. Additionally, we have now shown that LSD1 serves to oppose the role of KMT2D by repressing major fate-determining transcription factors that drive epithelial differentiation and may serve as an effective therapeutic target for cutaneous squamous cell carcinoma.

Lin-Shiao E, Lan Y, Coradin M, Anderson A, Donahue G, Simpson CL, Sen P, Saffie R, Busino L, Garcia BA, Berger SL, Capell BC. “KMT2D regulates p63 target enhancers to coordinate epithelial homeostasis.” Genes Dev.32(2): 2018. PMID: 29440247
Egolf S, Aubert Y, Doepner M, Anderson A, Maldonado-Lopez A, Pacella G, Lan Y, Simpson CL, Ridky T, Capell BC. “LSD1 inhibition promotes epithelial differentiation through derepression of fate-determining transcription factors.” Cell Reports. 28(8): 2019. PMID: 31433976
Aubert Y, Egolf S, Capell BC. “The Unexpected Noncatalytic Roles of Histone Modifiers in Development and Disease.” Trends in Genetics. 35(9): 2019. PMID: 31301850
Egolf S, Capell BC. “LSD1: a viable therapeutic target in cutaneous squamous cell carcinoma?” Expert Opin Ther Targets. Online ahead of print: 2020. PMID: 32379508

Demonstrated the role of MLL1 and chromatin alterations in senescence and DNA damage-induced inflammation: We have shown that senescent cells possess large-scale alterations in the epigenome (Shah, et al. 2013; Dou, et al. 2015), and that MLL1, a known H3K4me3 methyltransferase and oncogene, is critical for the expression of DNA-damage response (DDR)-induced inflammation (Capell, et al. 2016), also known as the senescence-associated secretory phenotype (SASP) in the context of senescence (Ghosh and Capell, et al. 2016). MLL1 inhibition can dramatically attenuate the expression and secretion of the SASP, and ameliorate the pro-carcinogenic effects of the SASP, while having no effects on the expression of tumor suppressors or the senescence growth arrest. Together this work suggests that epigenetic abnormalities in senescence can be targeted to prevent its pro-cancer and pro-aging effects.

Shah PP, Donahue G, Otte G, Capell BC, Nelson DM, Cao K, Aggarwala V, Cruickshanks HA, Singh Rai T, McBryan T, Gregory BD, Adams PD, Berger SL. “Lamin B1 depletion in senescent cells triggers large-scale changes in gene expression and in the chromatin landscape” Genes Dev. 27(16): 2013. PMID: 23934658
Dou Z, Xu C, Donahue G, Ivanov A, Pan J, Zhu J, Capell BC, Catanzaro JM, Ricketts MD, Shimi T, Adam SA, Mamorstein R, Zong WX, Goldman RD, Johansen T, Adams PD, Berger SL. “Autophagy mediates degradation of nuclear lamina.” Nature. 527(7576): 2015. PMID: 26524528
Capell BC, Drake A, Shah PP, Dorsey J, Simola DF, Dou Z, Zhu J, Sammons M, Donahue G, Singh Rai T, Natale C, Ridky TW, Adams PD, Berger SL. “MLL1 epigenetically regulates expression of ATM and the senescence-associated secretory phenotype” Genes Dev. 30(3): 2016. PMID: 26833731
Dou Z, Ghosh K, Vizioli MG, Zhu J, Sen P, Wangensteen KJ, Simithy J, Lan Y, Lin Y, Zhou Z, Capell BC, Xu C, Xu M, Kieckhaefer JE, Jiang T, Shoshkes-Carmel M, Tanim KM, Barber G, Seykora JT, Millar SE, Kaestner KH, Garcia BA, Adams PD, Berger SL. “Cytoplasmic chromatin triggers inflammation in senescence and cancer”. Nature. 550(7676): 2017. PMID: 28976970

Established farnesyltransferase inhibitors as a potential therapy for Hutchinson-Gilford progeria syndrome (HGPS): We have demonstrated both in vitro and in vivo that farnesyltransferase inhbitors (FTIs) are efficacious in improving phenotypes in model systems of the most dramatic form of human premature aging, HGPS. This work was proof of principle that FTIs may be effective for the cardiovascular disease which is the major cause of mortality in HGPS. This work has been replicated by numerous other labs, and FTIs have now been shown to improve patient phenotypes in the very first clinical trial of human HGPS patients, providing the first therapeutic option for these patients.

Capell BC, Erdos MR, Madigan JP, Fiordalisi JJ, Varga R, Conneely KN, Gordon LB, Der CJ, Cox AD, Collins FS. “Inhibiting the farnesylation of progerin prevents the characteristic nuclear blebbing of Hutchinson-Gilford progeria syndrome”. Proc Natl Acad Sci USA. 102(36): 2005. PMID: 16129833
Varga R, Eriksson M, Erdos MR, Olive M, Harten I, Kolodgie F, Capell BC, Cheng J, Faddah D, Perkins S, Avallone H, San H, Qu X, Ganesh S, Gordon LB, Virmani R, Wight TN, Nabel EG, Collins FS. “Progressive vascular smooth muscle cell defects in a mouse model of Hutchinson-Gilford progeria syndrome”. Proc Natl Acad Sci USA. 103(9): 2006. PMID: 16492728
“Farnesyltransferase inhibitors for treatment of laminopathies, cellular aging and atherosclerosis.” Filed with the United States Patent and Trademark Office, European Patent Office, international patent number: 06733984.6-2123-US2006002977 (USPTO#: 20080131375 – Class: 424 92 USPTO). Publication Number: WO/2006/081444 with the World Intellectual Property Organization: 2007.
Capell BC, Olive M, Erdos MR, Cao K, Faddah DA, Whipperman M, San H, Qu X, Ganesh SK, Chen X, Avallone H, Kolodgie F, Virmani R, Nabel EG, Collins FS. “A farnesyltransferase inhibitor prevents the onset and late progression of cardiovascular disease in a progeria mouse model”. Proc Natl Acad Sci USA. 105(41): 2008. PMID: 18838683

Demonstrated links between mechanisms of premature aging in Hutchinson-Gilford progeria syndrome (HGPS) and the normal human aging process: We have shown that in normal human aging, cells also produce small but increasing amounts of the mutant protein, progerin, which directly causes premature aging in HGPS. These increases in progerin lead to abnormalities in nuclear architecture with aging in both HGPS and normal cells. Furthermore, we have demonstrated that variations in the LMNA gene, which when mutated can cause HGPS as well as other diseases of premature aging, may in fact serve a protective function, as a particular form (haplotype) of this gene was overrepresented in centenarian populations.

Cao K, Capell BC, Erdos MR, Djabali K, Collins FS. “A lamin A protein isoform overexpressed in Hutchinson-Gilford progeria syndrome interferes with mitosis in both progeria and normal cells”. Proc Natl Acad Sci USA. 104(12): 2007. PMID: 17360355
Capell BC, Collins FS. “Human laminopathies: nuclei gone genetically awry”. Nat Rev Genet. 7(12): 2006. PMID: 17139325
Capell BC, Tlougan BE, Orlow SJ. “From the rarest to the most common: insights from progeroid syndromes into skin cancer and aging.” J Invest Dermatol. 129(10): 2009. PMID: 19387478
Conneely KN, Capell BC, Erdos MR, Sebastiani P, Timofeev N, Terry DF, Baldwin CT, Budagov T, Atzmon G, Barzalai N, Thomas GA, Puca AA, Perls TT, Geesaman BJ, Boehnke M, Collins FS. “Human longevity and common variations in the LMNA gene: a meta-analysis.” Aging Cell. 11(3): 2012. PMID: 22340368

Research Interest

Epithelial tissues rely on a highly coordinated balance between self-renewal, proliferation, and differentiation. Epigenetic mechanisms provide this precise control through the regulation of gene enhancer and transcriptional networks that establish and maintain cell fate and identity. Disruption of these pathways can lead to a loss of proliferative control, ultimately driving cancer.
Consistent with this, chromatin regulators are amongst the most frequently mutated genes in all of cancer, with an exceptionally high incidence of mutations in cancers of self-renewing epithelial tissues, such as squamous cell carcinoma (SCC). SCC is the most common type of cancer worldwide, affecting numerous epithelial tissues ranging from the skin and eyes to the lung, esophagus, and oropharynx. Despite this, precisely how disruption of epigenetic homeostasis may drive epithelial cancers such as SCC is poorly understood.
In the Capell Lab, we combine cutting-edge epigenetic technologies, human patient samples, primary cells, and mouse models in order to solve several fundamental unanswered questions:

  • How is the skin epigenome altered by intrinsic (i.e. aging) and extrinsic (i.e. ultraviolet radiation) environmental influences, and how do these changes contribute to disease?
  • How do chromatin regulatory enzymes function in both normal and diseased skin, particularly during carcinogenesis?
  • Can we target the epigenome with precision to treat disease?

Through this, we hope to identify new epigenetic targets for prevention and treatment of these potentially deadly cancers.

Montserrat Anguera, Ph.D.

Mechanisms of X-chromosome Inactivation: We are investigating the molecular mechanisms of X-Chromosome Inactivation, and how altered dosage of X-linked genes affects early embryonic development and contributes to sex-biased disease. We focus on the autoimmune disorder lupus, which has a strong female-bias, exhibits overexpression of X-linked immune-related genes, and involves lymphocytes. We study the epigenetic status of the inactive X in female lymphocytes from humans and mice, and have made the remarkable discovery that these cells do not maintain X-Chromosome Inactivation in the same way as other female somatic cells. We were the first to discover that the inactive X has euchromatic features in female lymphocytes, which may explain the female bias in autoimmune disorders such as lupus. We also study the dynamic mechanisms of Xist RNA localization and heterochromatin mark recruitment to the inactive X following lymphocyte activation.

Jianle Wang, Camille Syrett, Marianne Kramer, Arindam Basu, Michael Atchison, and Montserrat C. Anguera. (2016). “Unusual maintenance of X-chromosome Inactivation predisposes female lymphocytes for increased expression from the inactive X”. Proc Natl Acad Sci, Mar. 21, 2016. PMCID: PMC4833277
Anguera, Montserrat C.., Sadreyev, R., Zhang, Z., Szanto, A., Sheridan, S., Haggerty, S., Jaenisch, R., Gimbelbrandt, A., Mitalipova, M., and Lee, J.T. (2012). “Molecular signatures and epigenetic stability of human induced pluripotent stem cells.” Cell Stem Cell 11(1):75-90. PMCID: PMC3587778
Lessing, D., Anguera, Montserrat C., and Lee, J.T. (2013). “X Chromosome Inactivation and Epigenetic Responses to Cellular Reprogramming.” Annu Rev Genomics Hum Genet. 14:85-110. PMID: 23662665.
Anguera, Montserrat C., Sun, B.K., Xu, N., and Lee, J.T. (2006). “X-Chromosome Kiss and Tell: How the Xs Go Their Separate Ways.” Cold Spring Harb Symp Quant Biol. 71:429-37.

Long noncoding RNAs during early human development: We are also investigating sex-specific differences during human placental development using in vitro model systems. We discovered a novel X-linked long noncoding RNA specifically expressed in human placental progenitor cells that regulates the innate immune response.

Ian Penkala, Camille Syrett, Jianle Wang, and Montserrat C. Anguera. (2016). “LNCRHOXF1: a long noncoding RNA from the X-chromosome that suppresses viral response genes during development of the early human placenta”. Mol Cell Biol.  Apr 11, 2016, PMID: 27066803. PMCID: PMC4907097.
Jianle Wang, Montserrat C. Anguera. “In Vitro Differentiation of Human Pluripotent Stem Cells into Trophoblastic Cells”. J Vis Exp. 2017 Mar 16;(121). doi: 10.3791/55268. PMID: 28362386

Research Interest

The research in the Anguera laboratory focuses on maintenance of X-chromosome Inactivation in the immune system and in stem cells.  They also study epigenetic mechanisms involving long noncoding RNAs during early human development and placental progenitors.

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