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  1. AU="Ihuegbu, Nnamdi"
  2. AU="Berger, Jacob"
  3. AU="Shea, Martin J"
  4. AU="Vecchié, Alessandra"

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  1. Article ; Online: Fast, sensitive discovery of conserved genome-wide motifs.

    Ihuegbu, Nnamdi E / Stormo, Gary D / Buhler, Jeremy

    Journal of computational biology : a journal of computational molecular cell biology

    2012  Volume 19, Issue 2, Page(s) 139–147

    Abstract: Regulatory sites that control gene expression are essential to the proper functioning of cells, and identifying them is critical for modeling regulatory networks. We have developed Magma (Multiple Aligner of Genomic Multiple Alignments), a software tool ... ...

    Abstract Regulatory sites that control gene expression are essential to the proper functioning of cells, and identifying them is critical for modeling regulatory networks. We have developed Magma (Multiple Aligner of Genomic Multiple Alignments), a software tool for multiple species, multiple gene motif discovery. Magma identifies putative regulatory sites that are conserved across multiple species and occur near multiple genes throughout a reference genome. Magma takes as input multiple alignments that can include gaps. It uses efficient clustering methods that make it about 70 times faster than PhyloNet, a previous program for this task, with slightly greater sensitivity. We ran Magma on all non-coding DNA conserved between Caenorhabditis elegans and five additional species, about 70 Mbp in total, in <4 h. We obtained 2,309 motifs with lengths of 6-20 bp, each occurring at least 10 times throughout the genome, which collectively covered about 566 kbp of the genomes, approximately 0.8% of the input. Predicted sites occurred in all types of non-coding sequence but were especially enriched in the promoter regions. Comparisons to several experimental datasets show that Magma motifs correspond to a variety of known regulatory motifs.
    MeSH term(s) Algorithms ; Animals ; Base Sequence ; Binding Sites ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans Proteins/genetics ; Cluster Analysis ; Computer Simulation ; Conserved Sequence ; DNA, Intergenic/genetics ; Genome, Helminth ; Likelihood Functions ; Models, Genetic ; Promoter Regions, Genetic ; Sequence Alignment ; Software ; Transcription Factors/genetics
    Chemical Substances Caenorhabditis elegans Proteins ; DNA, Intergenic ; Transcription Factors
    Language English
    Publishing date 2012-02-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2030900-4
    ISSN 1557-8666 ; 1066-5277
    ISSN (online) 1557-8666
    ISSN 1066-5277
    DOI 10.1089/cmb.2011.0249
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: ARID1A mutations confer intrinsic and acquired resistance to cetuximab treatment in colorectal cancer.

    Johnson, Radia M / Qu, Xueping / Lin, Chu-Fang / Huw, Ling-Yuh / Venkatanarayan, Avinashnarayan / Sokol, Ethan / Ou, Fang-Shu / Ihuegbu, Nnamdi / Zill, Oliver A / Kabbarah, Omar / Wang, Lisa / Bourgon, Richard / de Sousa E Melo, Felipe / Bolen, Chris / Daemen, Anneleen / Venook, Alan P / Innocenti, Federico / Lenz, Heinz-Josef / Bais, Carlos

    Nature communications

    2022  Volume 13, Issue 1, Page(s) 5478

    Abstract: Most colorectal (CRC) tumors are dependent on EGFR/KRAS/BRAF/MAPK signaling activation. ARID1A is an epigenetic regulator mutated in approximately 5% of non-hypermutated CRC tumors. Here we show that anti-EGFR but not anti-VEGF treatment enriches for ... ...

    Abstract Most colorectal (CRC) tumors are dependent on EGFR/KRAS/BRAF/MAPK signaling activation. ARID1A is an epigenetic regulator mutated in approximately 5% of non-hypermutated CRC tumors. Here we show that anti-EGFR but not anti-VEGF treatment enriches for emerging ARID1A mutations in CRC patients. In addition, we find that patients with ARID1A mutations, at baseline, are associated with worse outcome when treated with cetuximab- but not bevacizumab-containing therapies; thus, this suggests that ARID1A mutations may provide both an acquired and intrinsic mechanism of resistance to anti-EGFR therapies. We find that, ARID1A and EGFR-pathway genetic alterations are mutually exclusive across lung and colorectal cancers, further supporting a functional connection between these pathways. Our results not only suggest that ARID1A could be potentially used as a predictive biomarker for cetuximab treatment decisions but also provide a rationale for exploring therapeutic MAPK inhibition in an unexpected but genetically defined segment of CRC patients.
    MeSH term(s) Antineoplastic Agents, Immunological/adverse effects ; Antineoplastic Agents, Immunological/pharmacology ; Antineoplastic Agents, Immunological/therapeutic use ; Cetuximab/adverse effects ; Cetuximab/pharmacology ; Cetuximab/therapeutic use ; Colorectal Neoplasms/drug therapy ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/pathology ; DNA-Binding Proteins/genetics ; Drug Resistance, Neoplasm/genetics ; Humans ; Mutation ; Proto-Oncogene Proteins B-raf/genetics ; Proto-Oncogene Proteins p21(ras)/genetics ; Transcription Factors/genetics
    Chemical Substances ARID1A protein, human ; Antineoplastic Agents, Immunological ; DNA-Binding Proteins ; Transcription Factors ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2) ; Cetuximab (PQX0D8J21J)
    Language English
    Publishing date 2022-09-19
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-022-33172-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Conserved Motifs and Prediction of Regulatory Modules in Caenorhabditis elegans.

    Zhao, Guoyan / Ihuegbu, Nnamdi / Lee, Mo / Schriefer, Larry / Wang, Ting / Stormo, Gary D

    G3 (Bethesda, Md.)

    2012  Volume 2, Issue 4, Page(s) 469–481

    Abstract: Transcriptional regulation, a primary mechanism for controlling the development of multicellular organisms, is carried out by transcription factors (TFs) that recognize and bind to their cognate binding sites. In Caenorhabditis elegans, our knowledge of ... ...

    Abstract Transcriptional regulation, a primary mechanism for controlling the development of multicellular organisms, is carried out by transcription factors (TFs) that recognize and bind to their cognate binding sites. In Caenorhabditis elegans, our knowledge of which genes are regulated by which TFs, through binding to specific sites, is still very limited. To expand our knowledge about the C. elegans regulatory network, we performed a comprehensive analysis of the C. elegans, Caenorhabditis briggsae, and Caenorhabditis remanei genomes to identify regulatory elements that are conserved in all genomes. Our analysis identified 4959 elements that are significantly conserved across the genomes and that each occur multiple times within each genome, both hallmarks of functional regulatory sites. Our motifs show significant matches to known core promoter elements, TF binding sites, splice sites, and poly-A signals as well as many putative regulatory sites. Many of the motifs are significantly correlated with various types of experimental data, including gene expression patterns, tissue-specific expression patterns, and binding site location analysis as well as enrichment in specific functional classes of genes. Many can also be significantly associated with specific TFs. Combinations of motif occurrences allow us to predict the location of cis-regulatory modules and we show that many of them significantly overlap experimentally determined enhancers. We provide access to the predicted binding sites, their associated motifs, and the predicted cis-regulatory modules across the whole genome through a web-accessible database and as tracks for genome browsers.
    Language English
    Publishing date 2012-04-01
    Publishing country England
    Document type Journal Article
    ZDB-ID 2629978-1
    ISSN 2160-1836 ; 2160-1836
    ISSN (online) 2160-1836
    ISSN 2160-1836
    DOI 10.1534/g3.111.001081
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Innate host defense requires TFEB-mediated transcription of cytoprotective and antimicrobial genes.

    Visvikis, Orane / Ihuegbu, Nnamdi / Labed, Sid A / Luhachack, Lyly G / Alves, Anna-Maria F / Wollenberg, Amanda C / Stuart, Lynda M / Stormo, Gary D / Irazoqui, Javier E

    Immunity

    2014  Volume 40, Issue 6, Page(s) 896–909

    Abstract: Animal host defense against infection requires the expression of defense genes at the right place and the right time. Understanding such tight control of host defense requires the elucidation of the transcription factors involved. By using an unbiased ... ...

    Abstract Animal host defense against infection requires the expression of defense genes at the right place and the right time. Understanding such tight control of host defense requires the elucidation of the transcription factors involved. By using an unbiased approach in the model Caenorhabditis elegans, we discovered that HLH-30 (known as TFEB in mammals) is a key transcription factor for host defense. HLH-30 was activated shortly after Staphylococcus aureus infection, and drove the expression of close to 80% of the host response, including antimicrobial and autophagy genes that were essential for host tolerance of infection. TFEB was also rapidly activated in murine macrophages upon S. aureus infection and was required for proper transcriptional induction of several proinflammatory cytokines and chemokines. Thus, our data suggest that TFEB is a previously unappreciated, evolutionarily ancient transcription factor in the host response to infection.
    MeSH term(s) Animals ; Autophagy/genetics ; Autophagy/immunology ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/genetics ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/immunology ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Basic Helix-Loop-Helix Transcription Factors/immunology ; Caenorhabditis elegans/immunology ; Caenorhabditis elegans/microbiology ; Caenorhabditis elegans Proteins/genetics ; Caenorhabditis elegans Proteins/immunology ; Enterococcus faecalis/immunology ; Immunity, Innate ; Macrophages/immunology ; Mice ; Pseudomonas Infections/immunology ; Pseudomonas aeruginosa/immunology ; RNA Interference ; RNA, Small Interfering ; Salmonella Infections/immunology ; Salmonella enterica/immunology ; Signal Transduction/immunology ; Staphylococcal Infections/immunology ; Staphylococcus aureus/immunology ; Transcriptional Activation/genetics ; Transcriptional Activation/immunology
    Chemical Substances Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; Basic Helix-Loop-Helix Transcription Factors ; Caenorhabditis elegans Proteins ; HLH-30 protein, C elegans ; RNA, Small Interfering ; Tcfeb protein, mouse
    Language English
    Publishing date 2014-05-29
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1217235-2
    ISSN 1097-4180 ; 1074-7613
    ISSN (online) 1097-4180
    ISSN 1074-7613
    DOI 10.1016/j.immuni.2014.05.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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