产品说明

Maricque BB et al. (FEB 2017) Nucleic acids research 45 4 e16

A genome-integrated massively parallel reporter assay reveals DNA sequence determinants of cis-regulatory activity in neural cells.

Recent large-scale genomics efforts to characterize the cis-regulatory sequences that orchestrate genome-wide expression patterns have produced impressive catalogues of putative regulatory elements. Most of these sequences have not been functionally tested,and our limited understanding of the non-coding genome prevents us from predicting which sequences are bona fide cis-regulatory elements. Recently,massively parallel reporter assays (MPRAs) have been deployed to measure the activity of putative cis-regulatory sequences in several biological contexts,each with specific advantages and distinct limitations. We developed LV-MPRA,a novel lentiviral-based,massively parallel reporter gene assay,to study the function of genome-integrated regulatory elements in any mammalian cell type; thus,making it possible to apply MPRAs in more biologically relevant contexts. We measured the activity of 2,600 sequences in U87 glioblastoma cells and human neural progenitor cells (hNPCs) and explored how regulatory activity is encoded in DNA sequence. We demonstrate that LV-MPRA can be applied to estimate the effects of local DNA sequence and regional chromatin on regulatory activity. Our data reveal that primary DNA sequence features,such as GC content and dinucleotide composition,accurately distinguish sequences with high activity from sequences with low activity in a full chromosomal context,and may also function in combination with different transcription factor binding sites to determine cell type specificity. We conclude that LV-MPRA will be an important tool for identifying cis-regulatory elements and stimulating new understanding about how the non-coding genome encodes information. View Publication

产品号#：

05833

05710

05835

05839

产品名：

STEMdiff™神经前体细胞培养基

STEMdiff™ 神经诱导培养基

Swartz EW et al. (NOV 2016) STEM CELLS Translational Medicine 5 11 1461--1472

A Novel Protocol for Directed Differentiation of C9orf72-Associated Human Induced Pluripotent Stem Cells Into Contractile Skeletal Myotubes

Induced pluripotent stem cells (iPSCs) offer an unlimited resource of cells to be used for the study of underlying molecular biology of disease,therapeutic drug screening,and transplant-based regenerative medicine. However,methods for the directed differentiation of skeletal muscle for these purposes remain scarce and incomplete. Here,we present a novel,small molecule-based protocol for the generation of multinucleated skeletal myotubes using eight independent iPSC lines. Through combinatorial inhibition of phosphoinositide 3-kinase (PI3K) and glycogen synthase kinase 3β (GSK3β) with addition of bone morphogenic protein 4 (BMP4) and fibroblast growth factor 2 (FGF2),we report up to 64% conversion of iPSCs into the myogenic program by day 36 as indicated by MYOG+ cell populations. These cells began to exhibit spontaneous contractions as early as 34 days in vitro in the presence of a serum-free medium formulation. We used this protocol to obtain iPSC-derived muscle cells from frontotemporal dementia (FTD) patients harboring C9orf72 hexanucleotide repeat expansions (rGGGGCC),sporadic FTD,and unaffected controls. iPSCs derived from rGGGGCC carriers contained RNA foci but did not vary in differentiation efficiency when compared to unaffected controls nor display mislocalized TDP-43 after as many as 120 days in vitro. This study presents a rapid,efficient,and transgene-free method for generating multinucleated skeletal myotubes from iPSCs and a resource for further modeling the role of skeletal muscle in amyotrophic lateral sclerosis and other motor neuron diseases. SIGNIFICANCE Protocols to produce skeletal myotubes for disease modeling or therapy are scarce and incomplete. The present study efficiently generates functional skeletal myotubes from human induced pluripotent stem cells using a small molecule-based approach. Using this strategy,terminal myogenic induction of up to 64% in 36 days and spontaneously contractile myotubes within 34 days were achieved. Myotubes derived from patients carrying the C9orf72 repeat expansion show no change in differentiation efficiency and normal TDP-43 localization after as many as 120 days in vitro when compared to unaffected controls. This study provides an efficient,novel protocol for the generation of skeletal myotubes from human induced pluripotent stem cells that may serve as a valuable tool in drug discovery and modeling of musculoskeletal and neuromuscular diseases. View Publication

产品号#：

05832

72302

72304

72307

72308

78006

78006.1

78006.2

78005

78005.1

78005.2

78005.3

34811

34815

34850

34821

34825

34860

05835

05839

100-1044

产品名：

STEMdiff™ 神经花环选择试剂

Y-27632（二盐酸盐）

重组人EGF

重组人BDNF

AggreWell™ 800 24孔板，1个

AggreWell™ 800 24孔板，5个

AggreWell™ 800 24孔板启动套装

AggreWell™ 800 6孔板，1个

AggreWell™ 800 6孔板，5个

AggreWell™ 800 6孔板启动套装

STEMdiff™ 神经诱导培养基

Y-27632（二盐酸盐）

Jackson TC et al. (FEB 2018) Experimental Neurology 300 232--246

BrainPhys increases neurofilament levels in CNS cultures, and facilitates investigation of axonal damage after a mechanical stretch-injury in vitro

Neurobasal®/B27 is a gold standard culture media used to study primary neurons in vitro. An alternative media (BrainPhys®/SM1) was recently developed which robustly enhances neuronal activity vs. Neurobasal® or DMEM. To the best of our knowledge BrainPhys® has not been explored in the setting of neuronal injury. Here we characterized the utility of BrainPhys® in a model of in vitro mechanical-stretch injury. METHODS/RESULTSPrimary rat cortical neurons were maintained in classic Neurobasal®,or sequentially maintained in Neurocult® followed by BrainPhys® (hereafter simply referred to as BrainPhys® maintained neurons?). The levels of axonal markers and proteins involved in neurotransmission were compared on day in vitro 10 (DIV10). BrainPhys® maintained neurons had higher levels of GluN2B,GluR1,Neurofilament light/heavy chain (NF-L & NF-H),and protein phosphatase 2 A (PP2A) vs. neurons in Neurobasal®. Mechanical stretch-injury (50ms/54% biaxial stretch) to BrainPhys® maintained neurons modestly (albeit significantly) increased 24h lactate dehydrogenase (LDH) levels but markedly decreased axonal NF-L levels post-injury vs. uninjured controls or neurons given a milder 38% stretch-injury. Furthermore,two 54% stretch-injuries (in tandem) exacerbated 24h LDH release,increased α-spectrin breakdown products (SBDPs),and decreased Tau levels. Also,BrainPhys® maintained cultures had decreased markers of cell damage 24h after a single 54% stretch-injury vs. neurons in Neurobasal®. Finally,we tested the hypothesis that lentivirus mediated overexpression of the pro-death protein RBM5 exacerbates neuronal and/or axonal injury in primary CNS cultures. RBM5 overexpression vs. empty-vector controls increased 24h LDH release,and SBDP levels,after a single 54% stretch-injury but did not affect NF-L levels or Tau. CONCLUSIONBrainPhys® is a promising new reagent which facilities the investigation of molecular targets involved in axonal and/or neuronal injury in vitro. View Publication

产品号#：

05790

05792

05793

05794

05795

产品名：

BrainPhys™神经元培养基

BrainPhys™神经元培养基和SM1试剂盒

BrainPhys™ 神经元培养基N2-A和SM1试剂盒

BrainPhys™原代神经元试剂盒

BrainPhys™ hPSC 神经元试剂盒

Werner A et al. (SEP 2015) Nature 525 7570 523--527

Cell-fate determination by ubiquitin-dependent regulation of translation

Metazoan development depends on the accurate execution of differentiation programs that allow pluripotent stem cells to adopt specific fates. Differentiation requires changes to chromatin architecture and transcriptional networks,yet whether other regulatory events support cell-fate determination is less well understood. Here we identify the ubiquitin ligase CUL3 in complex with its vertebrate-specific substrate adaptor KBTBD8 (CUL3(KBTBD8)) as an essential regulator of human and Xenopus tropicalis neural crest specification. CUL3(KBTBD8) monoubiquitylates NOLC1 and its paralogue TCOF1,the mutation of which underlies the neurocristopathy Treacher Collins syndrome. Ubiquitylation drives formation of a TCOF1-NOLC1 platform that connects RNA polymerase I with ribosome modification enzymes and remodels the translational program of differentiating cells in favour of neural crest specification. We conclude that ubiquitin-dependent regulation of translation is an important feature of cell-fate determination. View Publication

产品号#：

05872

05873

07920

07922

05210

05215

34811

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100-0483

100-0484

产品名：

ACCUTASE™

AggreWell™ 800 24孔板，1个

AggreWell™ 800 24孔板，5个

AggreWell™ 800 24孔板启动套装

AggreWell™ 800 6孔板，1个

AggreWell™ 800 6孔板，5个

AggreWell™ 800 6孔板启动套装

STEMdiff™ 神经诱导培养基

Hausser Scientificᵀᴹ 明线血球计数板

ReLeSR™

M. Ortiz-Virumbrales et al. (dec 2017) Acta neuropathologica communications 5 1 77

CRISPR/Cas9-Correctable mutation-related molecular and physiological phenotypes in iPSC-derived Alzheimer's PSEN2 N141I neurons.

Basal forebrain cholinergic neurons (BFCNs) are believed to be one of the first cell types to be affected in all forms of AD,and their dysfunction is clinically correlated with impaired short-term memory formation and retrieval. We present an optimized in vitro protocol to generate human BFCNs from iPSCs,using cell lines from presenilin 2 (PSEN2) mutation carriers and controls. As expected,cell lines harboring the PSEN2 N141I mutation displayed an increase in the A$\beta$42/40 in iPSC-derived BFCNs. Neurons derived from PSEN2 N141I lines generated fewer maximum number of spikes in response to a square depolarizing current injection. The height of the first action potential at rheobase current injection was also significantly decreased in PSEN2 N141I BFCNs. CRISPR/Cas9 correction of the PSEN2 point mutation abolished the electrophysiological deficit,restoring both the maximal number of spikes and spike height to the levels recorded in controls. Increased A$\beta$42/40 was also normalized following CRISPR/Cas-mediated correction of the PSEN2 N141I mutation. The genome editing data confirms the robust consistency of mutation-related changes in A$\beta$42/40 ratio while also showing a PSEN2-mutation-related alteration in electrophysiology. View Publication

产品号#：

17854

17854RF

17858

17858RF

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05790

05792

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17754

17861

17877

17877RF

17856

17856RF

100-0694

100-0696

100-1569

85850

85857

产品名：

EasySep™人CD19正选试剂盒II

RoboSep™ 人CD19正选试剂盒II

EasySep™人CD14正选试剂盒II

RoboSep™ 人CD14正选试剂盒II

EasySep™人CD4+ T细胞分选试剂盒

RoboSep™ 人CD4+ T细胞分选试剂盒

BrainPhys™神经元培养基

BrainPhys™神经元培养基和SM1试剂盒

BrainPhys™ 神经元培养基N2-A和SM1试剂盒

BrainPhys™原代神经元试剂盒

BrainPhys™ hPSC 神经元试剂盒

EasySep™ Release人CD19 正选试剂盒

EasySep™人Pan-CD25正选和去除试剂盒

EasySep™人CD138正选试剂盒 II

RoboSep™ 人CD138正选试剂盒 II

EasySep™人CD34正选试剂盒 II

EasySep™人CD14正选试剂盒II

EasySep™人CD4+ T细胞分离试剂盒

EasySep™人CD34正选试剂盒 II

mTeSR™1

Gupta S et al. (DEC 2017) Journal of Neurochemistry

Fibroblast growth factor 2 regulates activity and gene expression of human post-mitotic excitatory neurons

Many neuropsychiatric disorders are thought to result from subtle changes in neural circuit formation. We used human embryonic stem cells and induced pluripotent stem cells (hiPSCs) to model mature,post-mitotic excitatory neurons and examine effects of fibroblast growth factor 2 (FGF2). FGF2 gene expression is known to be altered in brain regions of major depressive disorder (MDD) patients and FGF2 has anti-depressive effects in animal models of depression. We generated stable inducible neurons (siNeurons) conditionally expressing human neurogenin-2 (NEUROG2) to generate a homogenous population of post-mitotic excitatory neurons and study the functional as well as the transcriptional effects of FGF2. Upon induction of NEUROG2 with doxycycline,the vast majority of cells are post-mitotic,and the gene expression profile recapitulates that of excitatory neurons within 6 days. Using hES cell lines that inducibly express NEUROG2 as well as GCaMP6f,we were able to characterize spontaneous calcium activity in these neurons and show that calcium transients increase in the presence of FGF2. The FGF2-responsive genes were determined by RNA-Seq. FGF2-regulated genes previously identified in non-neuronal cell types were up-regulated (EGR1,ETV4,SPRY4,and DUSP6) as a result of chronic FGF2 treatment of siNeurons. Novel neuron-specific genes were also identified that may mediate FGF2-dependent increases in synaptic efficacy including NRXN3,SYT2,and GALR1. Since several of these genes have been implicated in MDD previously,these results will provide the basis for more mechanistic studies of the role of FGF2 in MDD. View Publication

产品号#：

05790

05792

05793

05794

05795

85850

85857

85870

85875

05835

05839

产品名：

BrainPhys™神经元培养基

BrainPhys™神经元培养基和SM1试剂盒

BrainPhys™ 神经元培养基N2-A和SM1试剂盒

BrainPhys™原代神经元试剂盒

BrainPhys™ hPSC 神经元试剂盒

mTeSR™1

STEMdiff™ 神经诱导培养基

Robinson M et al. (AUG 2016) Stem Cell Reviews and Reports 12 4 476--483

Functionalizing Ascl1 with Novel Intracellular Protein Delivery Technology for Promoting Neuronal Differentiation of Human Induced Pluripotent Stem Cells

Pluripotent stem cells can become any cell type found in the body. Accordingly,one of the major challenges when working with pluripotent stem cells is producing a highly homogenous population of differentiated cells,which can then be used for downstream applications such as cell therapies or drug screening. The transcription factor Ascl1 plays a key role in neural development and previous work has shown that Ascl1 overexpression using viral vectors can reprogram fibroblasts directly into neurons. Here we report on how a recombinant version of the Ascl1 protein functionalized with intracellular protein delivery technology (Ascl1-IPTD) can be used to rapidly differentiate human induced pluripotent stem cells (hiPSCs) into neurons. We first evaluated a range of Ascl1-IPTD concentrations to determine the most effective amount for generating neurons from hiPSCs cultured in serum free media. Next,we looked at the frequency of Ascl1-IPTD supplementation in the media on differentiation and found that one time supplementation is sufficient enough to trigger the neural differentiation process. Ascl1-IPTD was efficiently taken up by the hiPSCs and enabled rapid differentiation into TUJ1-positive and NeuN-positive populations with neuronal morphology after 8 days. After 12 days of culture,hiPSC-derived neurons produced by Ascl1-IPTD treatment exhibited greater neurite length and higher numbers of branch points compared to neurons derived using a standard neural progenitor differentiation protocol. This work validates Ascl1-IPTD as a powerful tool for engineering neural tissue from pluripotent stem cells. View Publication

产品号#：

05832

05833

05838

05872

05873

05940

07174

07180

07183

07190

27147

07191

36254

07930

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07940

07955

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07954

27845

27945

27840

27865

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27965

05835

05839

08581

08582

100-0483

100-0484

100-1061

07952

100-0763

100-0485

100-1077

产品名：

STEMdiff™ 神经花环选择试剂

STEMdiff™神经前体细胞培养基

STEMdiff™神经祖细胞冻存液

Vitronectin XF™

CellAdhere™ 稀释缓冲液

DMEM/F-12 with 15 mM HEPES

CryoStor® CS10

STEMdiff™ 神经诱导培养基

STEMdiff™SMADi神经诱导试剂盒

STEMdiff™SMADi神经诱导试剂盒，2套

Hausser Scientificᵀᴹ 明线血球计数板

ReLeSR™

CryoStor® CS10

Vitronectin XF™

温和细胞解离试剂

ReLeSR™

Belle K et al. (JAN 2017) Neuroscience letters 637 201--206

Generation of disease-specific autopsy-confirmed iPSCs lines from postmortem isolated Peripheral Blood Mononuclear Cells

Understanding the molecular mechanisms that underlie neurodegenerative disorders has been hampered by a lack of readily available model systems that replicate the complexity of the human disease. Recent advances in stem cell technology have facilitated the derivation of patient-specific stem cells from a variety of differentiated cell types. These induced pluripotent stem cells (iPSCs) are attractive disease models since they can be grown and differentiated to produce large numbers of disease-relevant cell types. However,most iPSC lines are derived in advance of,and without the benefit of,neuropathological confirmation of the donor - the gold standard for many disease classifications and measurement of disease severity. While others have reported the generation of autopsy-confirmed iPSC lines from patient explants,these methods require outgrowth of cadaver tissue,which require additional time and is often only successul 50% of the time. Here we report the rapid generation of autopsy-confirmed iPSC lines from peripheral blood mononuclear cells (PBMCs) drawn postmortem. Since this approach doesn't require the propagation of previously frozen cadaver tissue,iPSC can be rapidly and efficiently produced from patients with autopsy-confirmed pathology. These matched iPSC-derived patient-specific neurons and postmortem brain tissue will support studies of specific mechanisms that drive the pathogenesis of neurodegenerative diseases. View Publication

产品号#：

05833

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05857

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07801

07811

07851

07861

85450

85460

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85857

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05835

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18061

产品名：

STEMdiff™神经前体细胞培养基

Lymphoprep™

SepMate™-50 (IVD)

mTeSR™1

SepMate™-50 (RUO)

STEMdiff™ 神经诱导培养基

Lymphoprep™

Rajasingh S et al. (AUG 2015) PloS one 10 8 e0134093

Generation of Functional Cardiomyocytes from Efficiently Generated Human iPSCs and a Novel Method of Measuring Contractility.

Human induced pluripotent stem cells (iPSCs) derived cardiomyocytes (iCMCs) would provide an unlimited cell source for regenerative medicine and drug discoveries. The objective of our study is to generate functional cardiomyocytes from human iPSCs and to develop a novel method of measuring contractility of CMCs. In a series of experiments,adult human skin fibroblasts (HSF) and human umbilical vein endothelial cells (HUVECs) were treated with a combination of pluripotent gene DNA and mRNA under specific conditions. The iPSC colonies were identified and differentiated into various cell lineages,including CMCs. The contractile activity of CMCs was measured by a novel method of frame-by-frame cross correlation (particle image velocimetry-PIV) analysis. Our treatment regimen transformed 4% of HSFs into iPSC colonies at passage 0,a significantly improved efficiency compared with use of either DNA or mRNA alone. The iPSCs were capable of differentiating both in vitro and in vivo into endodermal,ectodermal and mesodermal cells,including CMCs with<88% of cells being positive for troponin T (CTT) and Gata4 by flow cytometry. We report a highly efficient combination of DNA and mRNA to generate iPSCs and functional iCMCs from adult human cells. We also report a novel approach to measure contractility of iCMCs. View Publication

产品号#：

05832

05833

05835

05839

产品名：

STEMdiff™ 神经花环选择试剂

STEMdiff™神经前体细胞培养基

STEMdiff™ 神经诱导培养基

Tagliafierro L et al. (NOV 2017) Alzheimer's & dementia : the journal of the Alzheimer's Association 13 11 1237--1250

Genetic analysis of α-synuclein 3' untranslated region and its corresponding microRNAs in relation to Parkinson's disease compared to dementia with Lewy bodies.

INTRODUCTION The α-synuclein (SNCA) gene has been implicated in the etiology of Parkinson's disease (PD) and dementia with Lewy bodies (DLB). METHODS A computational analysis of SNCA 3' untranslated region to identify potential microRNA (miRNA) binding sites and quantitative real-time polymerase chain reaction (PCR) to determine their expression in isogenic induced pluripotent stem cell-derived dopaminergic and cholinergic neurons as a model of PD and DLB,respectively,were performed. In addition,we performed a deep sequencing analysis of the SNCA 3' untranslated region of autopsy-confirmed cases of PD,DLB,and normal controls,followed by genetic association analysis of the identified variants. RESULTS We identified four miRNA binding sites and observed a neuronal-type-specific expression profile for each miRNA in the different isogenic induced pluripotent stem cell-derived dopaminergic and cholinergic neurons. Furthermore,we found that the short structural variant rs777296100-polyT was moderately associated with DLB but not with PD. DISCUSSION We suggest that the regulation of SNCA expression through miRNAs is neuronal-type-specific and possibly plays a part in the phenotypic heterogeneity of synucleinopathies. Furthermore,genetic variability in the SNCA gene may contribute to synucleinopathies in a pathology-specific manner. View Publication

产品号#：

05790

05792

05793

05794

05795

产品名：

BrainPhys™神经元培养基

BrainPhys™神经元培养基和SM1试剂盒

BrainPhys™ 神经元培养基N2-A和SM1试剂盒

BrainPhys™原代神经元试剂盒

BrainPhys™ hPSC 神经元试剂盒

Xia G et al. (JUN 2015) Stem cells (Dayton,Ohio) 33 6 1829--38

Genome modification leads to phenotype reversal in human myotonic dystrophy type 1 induced pluripotent stem cell-derived neural stem cells.

Myotonic dystrophy type 1 (DM1) is caused by expanded CTG repeats in the 3'-untranslated region (3' UTR) of the DMPK gene. Correcting the mutation in DM1 stem cells would be an important step toward autologous stem cell therapy. The objective of this study is to demonstrate in vitro genome editing to prevent production of toxic mutant transcripts and reverse phenotypes in DM1 stem cells. Genome editing was performed in DM1 neural stem cells (NSCs) derived from human DM1 induced pluripotent stem (iPS) cells. An editing cassette containing SV40/bGH polyA signals was integrated upstream of the CTG repeats by TALEN-mediated homologous recombination (HR). The expression of mutant CUG repeats transcript was monitored by nuclear RNA foci,the molecular hallmarks of DM1,using RNA fluorescence in situ hybridization. Alternative splicing of microtubule-associated protein tau (MAPT) and muscleblind-like (MBNL) proteins were analyzed to further monitor the phenotype reversal after genome modification. The cassette was successfully inserted into DMPK intron 9 and this genomic modification led to complete disappearance of nuclear RNA foci. MAPT and MBNL 1,2 aberrant splicing in DM1 NSCs were reversed to normal pattern in genome-modified NSCs. Genome modification by integration of exogenous polyA signals upstream of the DMPK CTG repeat expansion prevents the production of toxic RNA and leads to phenotype reversal in human DM1 iPS-cells derived stem cells. Our data provide proof-of-principle evidence that genome modification may be used to generate genetically modified progenitor cells as a first step toward autologous cell transfer therapy for DM1. View Publication

产品号#：

05833

05835

05839

产品名：

STEMdiff™神经前体细胞培养基

STEMdiff™ 神经诱导培养基

Burbulla LF et al. (AUG 2016) Advanced Healthcare Materials 5 15 1894--1903

Micropatterning Facilitates the Long-Term Growth and Analysis of iPSC-Derived Individual Human Neurons and Neuronal Networks

The discovery of induced pluripotent stem cells (iPSCs) and their application to patient-specific disease models offers new opportunities for studying the pathophysiology of neurological disorders. However,current methods for culturing iPSC-derived neuronal cells result in clustering of neurons,which precludes the analysis of individual neurons and defined neuronal networks. To address this challenge,cultures of human neurons on micropatterned surfaces are developed that promote neuronal survival over extended periods of time. This approach facilitates studies of neuronal development,cellular trafficking,and related mechanisms that require assessment of individual neurons and specific network connections. Importantly,micropatterns support the long-term stability of cultured neurons,which enables time-dependent analysis of cellular processes in living neurons. The approach described in this paper allows mechanistic studies of human neurons,both in terms of normal neuronal development and function,as well as time-dependent pathological processes,and provides a platform for testing of new therapeutics in neuropsychiatric disorders. View Publication

产品号#：

05711

100-1281

产品名：

NeuroCult™ SM1 神经添加物

A genome-integrated massively parallel reporter assay reveals DNA sequence determinants of cis-regulatory activity in neural cells.

A Novel Protocol for Directed Differentiation of C9orf72-Associated Human Induced Pluripotent Stem Cells Into Contractile Skeletal Myotubes

BrainPhys increases neurofilament levels in CNS cultures, and facilitates investigation of axonal damage after a mechanical stretch-injury in vitro

Cell-fate determination by ubiquitin-dependent regulation of translation

CRISPR/Cas9-Correctable mutation-related molecular and physiological phenotypes in iPSC-derived Alzheimer's PSEN2 N141I neurons.

Fibroblast growth factor 2 regulates activity and gene expression of human post-mitotic excitatory neurons

Functionalizing Ascl1 with Novel Intracellular Protein Delivery Technology for Promoting Neuronal Differentiation of Human Induced Pluripotent Stem Cells

Generation of disease-specific autopsy-confirmed iPSCs lines from postmortem isolated Peripheral Blood Mononuclear Cells

Generation of Functional Cardiomyocytes from Efficiently Generated Human iPSCs and a Novel Method of Measuring Contractility.

Genetic analysis of α-synuclein 3' untranslated region and its corresponding microRNAs in relation to Parkinson's disease compared to dementia with Lewy bodies.

Genome modification leads to phenotype reversal in human myotonic dystrophy type 1 induced pluripotent stem cell-derived neural stem cells.

Micropatterning Facilitates the Long-Term Growth and Analysis of iPSC-Derived Individual Human Neurons and Neuronal Networks

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