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  • 1
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    Nature Publishing Group (NPG)
    Publication Date: 2010-06-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chi, Kelly Rae -- England -- Nature. 2010 May 13;465(7295):256-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20549837" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Genome/genetics ; Genomics/economics/instrumentation/*manpower/*trends ; Humans ; Sequence Analysis, DNA/economics/instrumentation/statistics & numerical ; data/trends ; Software ; Viruses/genetics/isolation & purification
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
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    Nature Publishing Group (NPG)
    Publication Date: 2010-05-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chi, Kelly Rae -- England -- Nature. 2010 Apr 15;464(7291):1090-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20503480" target="_blank"〉PubMed〈/a〉
    Keywords: Breast Neoplasms/genetics/metabolism/pathology/therapy ; Computational Biology/education/manpower/trends ; Female ; Genetic Heterogeneity ; Humans ; Models, Biological ; Neoplasms/genetics/*metabolism/*pathology/therapy ; Research Personnel/education ; Systems Biology/education/manpower/*trends
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
    Publication Date: 2010-10-12
    Description: Gastrointestinal stromal tumour (GIST) is the most common human sarcoma and is primarily defined by activating mutations in the KIT or PDGFRA receptor tyrosine kinases. KIT is highly expressed in interstitial cells of Cajal (ICCs)-the presumed cell of origin for GIST-as well as in haematopoietic stem cells, melanocytes, mast cells and germ cells. Yet, families harbouring germline activating KIT mutations and mice with knock-in Kit mutations almost exclusively develop ICC hyperplasia and GIST, suggesting that the cellular context is important for KIT to mediate oncogenesis. Here we show that the ETS family member ETV1 is highly expressed in the subtypes of ICCs sensitive to oncogenic KIT mediated transformation, and is required for their development. In addition, ETV1 is universally highly expressed in GISTs and is required for growth of imatinib-sensitive and resistant GIST cell lines. Transcriptome profiling and global analyses of ETV1-binding sites suggest that ETV1 is a master regulator of an ICC-GIST-specific transcription network mainly through enhancer binding. The ETV1 transcriptional program is further regulated by activated KIT, which prolongs ETV1 protein stability and cooperates with ETV1 to promote tumorigenesis. We propose that GIST arises from ICCs with high levels of endogenous ETV1 expression that, when coupled with an activating KIT mutation, drives an oncogenic ETS transcriptional program. This differs from other ETS-dependent tumours such as prostate cancer, melanoma and Ewing sarcoma where genomic translocation or amplification drives aberrant ETS expression. It also represents a novel mechanism of oncogenic transcription factor activation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2955195/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2955195/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chi, Ping -- Chen, Yu -- Zhang, Lei -- Guo, Xingyi -- Wongvipat, John -- Shamu, Tambudzai -- Fletcher, Jonathan A -- Dewell, Scott -- Maki, Robert G -- Zheng, Deyou -- Antonescu, Cristina R -- Allis, C David -- Sawyers, Charles L -- 5F32CA130372/CA/NCI NIH HHS/ -- CA148260/CA/NCI NIH HHS/ -- CA47179/CA/NCI NIH HHS/ -- F32 CA130372/CA/NCI NIH HHS/ -- F32 CA130372-02/CA/NCI NIH HHS/ -- GM40922/GM/NIGMS NIH HHS/ -- K08 CA140946/CA/NCI NIH HHS/ -- K08 CA140946-02/CA/NCI NIH HHS/ -- K08CA140946/CA/NCI NIH HHS/ -- P01 CA047179/CA/NCI NIH HHS/ -- P01 CA047179-169002/CA/NCI NIH HHS/ -- P01CA47179/CA/NCI NIH HHS/ -- R21 MH087840/MH/NIMH NIH HHS/ -- R21 MH087840-01/MH/NIMH NIH HHS/ -- R21MH087840/MH/NIMH NIH HHS/ -- RC2 CA148260-02/CA/NCI NIH HHS/ -- England -- Nature. 2010 Oct 14;467(7317):849-53. doi: 10.1038/nature09409. Epub 2010 Oct 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Memorial Sloan-Kettering Cancer Center, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20927104" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzamides ; Binding Sites ; Biomarkers, Tumor/genetics/metabolism ; Cell Line, Tumor ; *Cell Lineage ; Cell Survival/drug effects ; *Cell Transformation, Neoplastic ; DNA-Binding Proteins/antagonists & inhibitors/genetics/*metabolism ; Disease Progression ; Enhancer Elements, Genetic/genetics ; Gastrointestinal Stromal Tumors/*metabolism/*pathology ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic/genetics ; Humans ; Imatinib Mesylate ; Interstitial Cells of Cajal/metabolism/pathology ; Mice ; Mutant Proteins/genetics/metabolism ; Mutation ; NIH 3T3 Cells ; Oncogenes/genetics/*physiology ; Piperazines/pharmacology ; Protein Stability ; Proto-Oncogene Proteins c-kit/genetics/*metabolism ; Pyrimidines/pharmacology ; Signal Transduction ; Transcription Factors/antagonists & inhibitors/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2008-11-04
    Description: Protein-RNA interactions have critical roles in all aspects of gene expression. However, applying biochemical methods to understand such interactions in living tissues has been challenging. Here we develop a genome-wide means of mapping protein-RNA binding sites in vivo, by high-throughput sequencing of RNA isolated by crosslinking immunoprecipitation (HITS-CLIP). HITS-CLIP analysis of the neuron-specific splicing factor Nova revealed extremely reproducible RNA-binding maps in multiple mouse brains. These maps provide genome-wide in vivo biochemical footprints confirming the previous prediction that the position of Nova binding determines the outcome of alternative splicing; moreover, they are sufficiently powerful to predict Nova action de novo. HITS-CLIP revealed a large number of Nova-RNA interactions in 3' untranslated regions, leading to the discovery that Nova regulates alternative polyadenylation in the brain. HITS-CLIP, therefore, provides a robust, unbiased means to identify functional protein-RNA interactions in vivo.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2597294/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2597294/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Licatalosi, Donny D -- Mele, Aldo -- Fak, John J -- Ule, Jernej -- Kayikci, Melis -- Chi, Sung Wook -- Clark, Tyson A -- Schweitzer, Anthony C -- Blume, John E -- Wang, Xuning -- Darnell, Jennifer C -- Darnell, Robert B -- MC_U105185858/Medical Research Council/United Kingdom -- R01 NS034389/NS/NINDS NIH HHS/ -- R01 NS034389-09/NS/NINDS NIH HHS/ -- R01 NS034389-10/NS/NINDS NIH HHS/ -- R01 NS034389-11/NS/NINDS NIH HHS/ -- R01 NS034389-12/NS/NINDS NIH HHS/ -- R01 NS034389-13A1/NS/NINDS NIH HHS/ -- R01 NS040955/NS/NINDS NIH HHS/ -- R01 NS040955-05/NS/NINDS NIH HHS/ -- R01 NS34389/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2008 Nov 27;456(7221):464-9. doi: 10.1038/nature07488. Epub 2008 Nov 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Neuro-Oncology and Howard Hughes Medical Institute, The Rockefeller University, 1230 York Avenue, New York, New York 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18978773" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing/*genetics ; Animals ; Antigens, Neoplasm/genetics/*metabolism ; Cell Line ; Cross-Linking Reagents/chemistry/metabolism ; Exons/genetics ; Genome/*genetics ; Genomics ; Humans ; Immunoprecipitation ; Mice ; Neocortex/*cytology ; Neurons/*metabolism ; Organ Specificity ; Polyadenylation/genetics ; RNA, Messenger/genetics/*metabolism ; RNA-Binding Proteins/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Nature Publishing Group (NPG)
    Publication Date: 2009-10-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chi, Kelly Rae -- England -- Nature. 2009 Oct 8;461(7265):712-4. doi: 10.1038/461712a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19812647" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Height/genetics ; Carrier Proteins/genetics ; Fetal Hemoglobin/genetics ; Genetic Predisposition to Disease/*genetics ; *Genetics, Medical/standards ; Genome, Human/genetics ; *Genome-Wide Association Study/standards ; Humans ; Kruppel-Like Transcription Factors/genetics ; Magnetic Resonance Imaging ; Mice ; Multifactorial Inheritance/genetics ; Nuclear Proteins/genetics ; Polymorphism, Single Nucleotide/genetics ; Schizophrenia/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2009-06-19
    Description: MicroRNAs (miRNAs) have critical roles in the regulation of gene expression; however, as miRNA activity requires base pairing with only 6-8 nucleotides of messenger RNA, predicting target mRNAs is a major challenge. Recently, high-throughput sequencing of RNAs isolated by crosslinking immunoprecipitation (HITS-CLIP) has identified functional protein-RNA interaction sites. Here we use HITS-CLIP to covalently crosslink native argonaute (Ago, also called Eif2c) protein-RNA complexes in mouse brain. This produced two simultaneous data sets-Ago-miRNA and Ago-mRNA binding sites-that were combined with bioinformatic analysis to identify interaction sites between miRNA and target mRNA. We validated genome-wide interaction maps for miR-124, and generated additional maps for the 20 most abundant miRNAs present in P13 mouse brain. Ago HITS-CLIP provides a general platform for exploring the specificity and range of miRNA action in vivo, and identifies precise sequences for targeting clinically relevant miRNA-mRNA interactions.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2733940/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2733940/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chi, Sung Wook -- Zang, Julie B -- Mele, Aldo -- Darnell, Robert B -- R01 NS034389/NS/NINDS NIH HHS/ -- R01 NS034389-14/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2009 Jul 23;460(7254):479-86. doi: 10.1038/nature08170. Epub 2009 Jun 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Neuro-Oncology and Howard Hughes Medical Institute, The Rockefeller University, 1230 York Avenue, New York, New York 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19536157" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cross-Linking Reagents/chemistry/metabolism ; *Gene Expression Regulation ; HeLa Cells ; Humans ; Immunoprecipitation/*methods ; Mice ; MicroRNAs/*metabolism ; Protein Interaction Mapping ; Reproducibility of Results
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2007-09-29
    Description: Structural variation of the genome involves kilobase- to megabase-sized deletions, duplications, insertions, inversions, and complex combinations of rearrangements. We introduce high-throughput and massive paired-end mapping (PEM), a large-scale genome-sequencing method to identify structural variants (SVs) approximately 3 kilobases (kb) or larger that combines the rescue and capture of paired ends of 3-kb fragments, massive 454 sequencing, and a computational approach to map DNA reads onto a reference genome. PEM was used to map SVs in an African and in a putatively European individual and identified shared and divergent SVs relative to the reference genome. Overall, we fine-mapped more than 1000 SVs and documented that the number of SVs among humans is much larger than initially hypothesized; many of the SVs potentially affect gene function. The breakpoint junction sequences of more than 200 SVs were determined with a novel pooling strategy and computational analysis. Our analysis provided insights into the mechanisms of SV formation in humans.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2674581/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2674581/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Korbel, Jan O -- Urban, Alexander Eckehart -- Affourtit, Jason P -- Godwin, Brian -- Grubert, Fabian -- Simons, Jan Fredrik -- Kim, Philip M -- Palejev, Dean -- Carriero, Nicholas J -- Du, Lei -- Taillon, Bruce E -- Chen, Zhoutao -- Tanzer, Andrea -- Saunders, A C Eugenia -- Chi, Jianxiang -- Yang, Fengtang -- Carter, Nigel P -- Hurles, Matthew E -- Weissman, Sherman M -- Harkins, Timothy T -- Gerstein, Mark B -- Egholm, Michael -- Snyder, Michael -- 077008/Wellcome Trust/United Kingdom -- 077014/Wellcome Trust/United Kingdom -- RR19895/RR/NCRR NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2007 Oct 19;318(5849):420-6. Epub 2007 Sep 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Biophysics and Biochemistry Department, Yale University, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17901297" target="_blank"〉PubMed〈/a〉
    Keywords: Chromosome Inversion ; Chromosome Mapping ; Computational Biology ; Female ; Gene Fusion ; *Genetic Variation ; *Genome, Human ; Humans ; Mutagenesis, Insertional ; *Mutation ; Oligonucleotide Array Sequence Analysis ; Recombination, Genetic ; Repetitive Sequences, Nucleic Acid ; Retroelements ; Sequence Analysis, DNA ; Sequence Deletion
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2004-07-27
    Description: The extent to which large duplications and deletions contribute to human genetic variation and diversity is unknown. Here, we show that large-scale copy number polymorphisms (CNPs) (about 100 kilobases and greater) contribute substantially to genomic variation between normal humans. Representational oligonucleotide microarray analysis of 20 individuals revealed a total of 221 copy number differences representing 76 unique CNPs. On average, individuals differed by 11 CNPs, and the average length of a CNP interval was 465 kilobases. We observed copy number variation of 70 different genes within CNP intervals, including genes involved in neurological function, regulation of cell growth, regulation of metabolism, and several genes known to be associated with disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sebat, Jonathan -- Lakshmi, B -- Troge, Jennifer -- Alexander, Joan -- Young, Janet -- Lundin, Par -- Maner, Susanne -- Massa, Hillary -- Walker, Megan -- Chi, Maoyen -- Navin, Nicholas -- Lucito, Robert -- Healy, John -- Hicks, James -- Ye, Kenny -- Reiner, Andrew -- Gilliam, T Conrad -- Trask, Barbara -- Patterson, Nick -- Zetterberg, Anders -- Wigler, Michael -- 5T32 CA069311/CA/NCI NIH HHS/ -- CA078544/CA/NCI NIH HHS/ -- CA81674/CA/NCI NIH HHS/ -- DC004209/DC/NIDCD NIH HHS/ -- GM057070/GM/NIGMS NIH HHS/ -- HG02606/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2004 Jul 23;305(5683):525-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15273396" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Bacterial Proteins/metabolism ; Cell Line, Transformed ; Chromosome Aberrations ; Chromosome Mapping ; Chromosomes, Human/genetics ; Deoxyribonuclease HindIII/metabolism ; Deoxyribonucleases, Type II Site-Specific/metabolism ; Female ; Gene Deletion ; *Gene Dosage ; Gene Duplication ; Gene Frequency ; *Genetic Variation ; *Genome, Human ; Humans ; Male ; Markov Chains ; Oligonucleotide Array Sequence Analysis ; *Polymorphism, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Nature Publishing Group (NPG)
    Publication Date: 2011-03-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chi, Kelly Rae -- England -- Nature. 2011 Mar 24;471(7339):537-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21438188" target="_blank"〉PubMed〈/a〉
    Keywords: Allergy and Immunology/education/manpower ; Biomedical Research/education/*manpower/*trends ; Cancer Vaccines/biosynthesis/*immunology/*therapeutic use ; Clinical Trials as Topic/methods/trends ; Disease Progression ; Fellowships and Scholarships ; Humans ; Medical Oncology/education/manpower ; Neoplasms/immunology/*prevention & control/*therapy ; Precision Medicine/methods ; Research Personnel/education/psychology ; Tissue Extracts/immunology/therapeutic use ; Treatment Outcome
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2011-08-05
    Description: The vertebrate thymus provides an inductive environment for T-cell development. Within the mouse thymus, Notch signals are indispensable for imposing the T-cell fate on multipotential haematopoietic progenitors, but the downstream effectors that impart T-lineage specification and commitment are not well understood. Here we show that a transcription factor, T-cell factor 1 (TCF-1; also known as transcription factor 7, T-cell specific, TCF7), is a critical regulator in T-cell specification. TCF-1 is highly expressed in the earliest thymic progenitors, and its expression is upregulated by Notch signals. Most importantly, when TCF-1 is forcibly expressed in bone marrow (BM) progenitors, it drives the development of T-lineage cells in the absence of T-inductive Notch1 signals. Further characterization of these TCF-1-induced cells revealed expression of many T-lineage genes, including T-cell-specific transcription factors Gata3 and Bcl11b, and components of the T-cell receptor. Our data suggest a model where Notch signals induce TCF-1, and TCF-1 in turn imprints the T-cell fate by upregulating expression of T-cell essential genes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3156435/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3156435/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Weber, Brittany Nicole -- Chi, Anthony Wei-Shine -- Chavez, Alejandro -- Yashiro-Ohtani, Yumi -- Yang, Qi -- Shestova, Olga -- Bhandoola, Avinash -- AI059621/AI/NIAID NIH HHS/ -- R01 AI059621/AI/NIAID NIH HHS/ -- R01 AI059621-09/AI/NIAID NIH HHS/ -- RC1 HL099758/HL/NHLBI NIH HHS/ -- RC1 HL099758-01/HL/NHLBI NIH HHS/ -- T32 AI055428/AI/NIAID NIH HHS/ -- T32 CA009140/CA/NCI NIH HHS/ -- T32AI055428/AI/NIAID NIH HHS/ -- T32CA09140/CA/NCI NIH HHS/ -- England -- Nature. 2011 Aug 3;476(7358):63-8. doi: 10.1038/nature10279.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21814277" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation ; *Cell Lineage ; Female ; Genes, Essential ; HEK293 Cells ; Hepatocyte Nuclear Factor 1-alpha ; Humans ; Lymphoid Enhancer-Binding Factor 1/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Receptor, Notch1/metabolism ; Signal Transduction ; T Cell Transcription Factor 1/deficiency/genetics/*metabolism ; T-Lymphocytes/*cytology/*metabolism ; Up-Regulation
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    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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