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  1. AU="Knott, Simon Rv"
  2. AU="King, A Paden"
  3. AU="Akons, Kfir"
  4. AU="Tannista Banerjee"

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  1. Article ; Online: Strategies for analyzing highly enriched IP-chip datasets

    Tavaré Simon / Aparicio Oscar M / Viggiani Christopher J / Knott Simon RV

    BMC Bioinformatics, Vol 10, Iss 1, p

    2009  Volume 305

    Abstract: Abstract Background Chromatin immunoprecipitation on tiling arrays (ChIP-chip) has been employed to examine features such as protein binding and histone modifications on a genome-wide scale in a variety of cell types. Array data from the latter studies ... ...

    Abstract Abstract Background Chromatin immunoprecipitation on tiling arrays (ChIP-chip) has been employed to examine features such as protein binding and histone modifications on a genome-wide scale in a variety of cell types. Array data from the latter studies typically have a high proportion of enriched probes whose signals vary considerably (due to heterogeneity in the cell population), and this makes their normalization and downstream analysis difficult. Results Here we present strategies for analyzing such experiments, focusing our discussion on the analysis of Bromodeoxyruridine (BrdU) immunoprecipitation on tiling array (BrdU-IP-chip) datasets. BrdU-IP-chip experiments map large, recently replicated genomic regions and have similar characteristics to histone modification/location data. To prepare such data for downstream analysis we employ a dynamic programming algorithm that identifies a set of putative unenriched probes, which we use for both within-array and between-array normalization. We also introduce a second dynamic programming algorithm that incorporates a priori knowledge to identify and quantify positive signals in these datasets. Conclusion Highly enriched IP-chip datasets are often difficult to analyze with traditional array normalization and analysis strategies. Here we present and test a set of analytical tools for their normalization and quantification that allows for accurate identification and analysis of enriched regions.
    Keywords Computer applications to medicine. Medical informatics ; R858-859.7 ; Biology (General) ; QH301-705.5
    Subject code 006
    Language English
    Publishing date 2009-09-01T00:00:00Z
    Publisher BMC
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: COP1/DET1/ETS axis regulates ERK transcriptome and sensitivity to MAPK inhibitors.

    Xie, Yuanyuan / Cao, Zhen / Wong, Elissa Wp / Guan, Youxin / Ma, Wenfu / Zhang, Jenny Q / Walczak, Edward G / Murphy, Devan / Ran, Leili / Sirota, Inna / Wang, Shangqian / Shukla, Shipra / Gao, Dong / Knott, Simon Rv / Chang, Kenneth / Leu, Justin / Wongvipat, John / Antonescu, Cristina R / Hannon, Gregory /
    Chi, Ping / Chen, Yu

    The Journal of clinical investigation

    2018  Volume 128, Issue 4, Page(s) 1442–1457

    Abstract: Aberrant activation of MAPK signaling leads to the activation of oncogenic transcriptomes. How MAPK signaling is coupled with the transcriptional response in cancer is not fully understood. In 2 MAPK-activated tumor types, gastrointestinal stromal tumor ... ...

    Abstract Aberrant activation of MAPK signaling leads to the activation of oncogenic transcriptomes. How MAPK signaling is coupled with the transcriptional response in cancer is not fully understood. In 2 MAPK-activated tumor types, gastrointestinal stromal tumor and melanoma, we found that ETV1 and other Pea3-ETS transcription factors are critical nuclear effectors of MAPK signaling that are regulated through protein stability. Expression of stabilized Pea3-ETS factors can partially rescue the MAPK transcriptome and cell viability after MAPK inhibition. To identify the players involved in this process, we performed a pooled genome-wide RNAi screen using a fluorescence-based ETV1 protein stability sensor and identified COP1, DET1, DDB1, UBE3C, PSMD4, and COP9 signalosome members. COP1 or DET1 loss led to decoupling between MAPK signaling and the downstream transcriptional response, where MAPK inhibition failed to destabilize Pea3 factors and fully inhibit the MAPK transcriptome, thus resulting in decreased sensitivity to MAPK pathway inhibitors. We identified multiple COP1 and DET1 mutations in human tumors that were defective in the degradation of Pea3-ETS factors. Two melanoma patients had de novo DET1 mutations arising after vemurafenib treatment. These observations indicate that MAPK signaling-dependent regulation of Pea3-ETS protein stability is a key signaling node in oncogenesis and therapeutic resistance to MAPK pathway inhibition.
    MeSH term(s) Adenovirus E1A Proteins/genetics ; Adenovirus E1A Proteins/metabolism ; Animals ; Carrier Proteins/genetics ; Carrier Proteins/metabolism ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Extracellular Signal-Regulated MAP Kinases/antagonists & inhibitors ; Extracellular Signal-Regulated MAP Kinases/genetics ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Humans ; MAP Kinase Signaling System/drug effects ; MAP Kinase Signaling System/genetics ; Melanoma/drug therapy ; Melanoma/genetics ; Melanoma/metabolism ; Melanoma/pathology ; Mice ; Mice, SCID ; Mutation ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism ; Proto-Oncogene Proteins c-ets/genetics ; Proto-Oncogene Proteins c-ets/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Transcriptome/drug effects ; Transcriptome/genetics ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism ; Vemurafenib/pharmacology ; Xenograft Model Antitumor Assays
    Chemical Substances Adenovirus E1A Proteins ; Carrier Proteins ; DET1 protein, human ; DNA-Binding Proteins ; ETV1 protein, human ; ETV4 protein, human ; Proto-Oncogene Proteins ; Proto-Oncogene Proteins c-ets ; Transcription Factors ; Vemurafenib (207SMY3FQT) ; COP1 protein, human (EC 2.3.2.27) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Extracellular Signal-Regulated MAP Kinases (EC 2.7.11.24)
    Language English
    Publishing date 2018-03-05
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI94840
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: lncRNA requirements for mouse acute myeloid leukemia and normal differentiation.

    Delás, M Joaquina / Sabin, Leah R / Dolzhenko, Egor / Knott, Simon Rv / Munera Maravilla, Ester / Jackson, Benjamin T / Wild, Sophia A / Kovacevic, Tatjana / Stork, Eva Maria / Zhou, Meng / Erard, Nicolas / Lee, Emily / Kelley, David R / Roth, Mareike / Barbosa, Inês Am / Zuber, Johannes / Rinn, John L / Smith, Andrew D / Hannon, Gregory J

    eLife

    2017  Volume 6

    Abstract: A substantial fraction of the genome is transcribed in a cell-type-specific manner, producing long non-coding RNAs (lncRNAs), rather than protein-coding transcripts. Here, we systematically characterize transcriptional dynamics during hematopoiesis and ... ...

    Abstract A substantial fraction of the genome is transcribed in a cell-type-specific manner, producing long non-coding RNAs (lncRNAs), rather than protein-coding transcripts. Here, we systematically characterize transcriptional dynamics during hematopoiesis and in hematological malignancies. Our analysis of annotated and de novo assembled lncRNAs showed many are regulated during differentiation and mis-regulated in disease. We assessed lncRNA function via an in vivo RNAi screen in a model of acute myeloid leukemia. This identified several lncRNAs essential for leukemia maintenance, and found that a number act by promoting leukemia stem cell signatures. Leukemia blasts show a myeloid differentiation phenotype when these lncRNAs were depleted, and our data indicates that this effect is mediated via effects on the MYC oncogene. Bone marrow reconstitutions showed that a lncRNA expressed across all progenitors was required for the myeloid lineage, whereas the other leukemia-induced lncRNAs were dispensable in the normal setting.
    MeSH term(s) Animals ; Cell Differentiation ; Disease Models, Animal ; Gene Expression Profiling ; Gene Expression Regulation ; Hematopoiesis ; Leukemia, Myeloid, Acute/pathology ; Mice ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism
    Chemical Substances RNA, Long Noncoding
    Language English
    Publishing date 2017-09-06
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2687154-3
    ISSN 2050-084X ; 2050-084X
    ISSN (online) 2050-084X
    ISSN 2050-084X
    DOI 10.7554/eLife.25607
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Dynamic, mating-induced gene expression changes in female head and brain tissues of Drosophila melanogaster

    Stirling Emma J / Sanders Laura E / Nishitani Allison / Lebo Matthew S / Knott Simon RV / Kacheria Tanvi S / Dalton Justin E / Winbush Ari / Arbeitman Michelle N

    BMC Genomics, Vol 11, Iss 1, p

    2010  Volume 541

    Abstract: Abstract Background Drosophila melanogaster females show changes in behavior and physiology after mating that are thought to maximize the number of progeny resulting from the most recent copulation. Sperm and seminal fluid proteins induce post-mating ... ...

    Abstract Abstract Background Drosophila melanogaster females show changes in behavior and physiology after mating that are thought to maximize the number of progeny resulting from the most recent copulation. Sperm and seminal fluid proteins induce post-mating changes in females, however, very little is known about the resulting gene expression changes in female head and central nervous system tissues that contribute to the post-mating response. Results We determined the temporal gene expression changes in female head tissues 0-2, 24, 48 and 72 hours after mating. Females from each time point had a unique post-mating gene expression response, with 72 hours post-mating having the largest number of genes with significant changes in expression. At most time points, genes expressed in the head fat body that encode products involved in metabolism showed a marked change in expression. Additional analysis of gene expression changes in dissected brain tissues 24 hours post-mating revealed changes in transcript abundance of many genes, notably, the reduced transcript abundance of genes that encode ion channels. Conclusions Substantial changes occur in the regulation of many genes in female head tissues after mating, which might underlie aspects of the female post-mating response. These results provide new insights into the physiological and metabolic changes that accompany changes in female behaviors.
    Keywords Genetics ; QH426-470 ; Biology (General) ; QH301-705.5 ; Science ; Q ; DOAJ:Genetics ; DOAJ:Biology ; DOAJ:Biology and Life Sciences ; Biotechnology ; TP248.13-248.65
    Language English
    Publishing date 2010-10-01T00:00:00Z
    Publisher BioMed Central
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Dynamic, mating-induced gene expression changes in female head and brain tissues of Drosophila melanogaster.

    Dalton, Justin E / Kacheria, Tanvi S / Knott, Simon Rv / Lebo, Matthew S / Nishitani, Allison / Sanders, Laura E / Stirling, Emma J / Winbush, Ari / Arbeitman, Michelle N

    BMC genomics

    2010  Volume 11, Page(s) 541

    Abstract: Background: Drosophila melanogaster females show changes in behavior and physiology after mating that are thought to maximize the number of progeny resulting from the most recent copulation. Sperm and seminal fluid proteins induce post-mating changes in ...

    Abstract Background: Drosophila melanogaster females show changes in behavior and physiology after mating that are thought to maximize the number of progeny resulting from the most recent copulation. Sperm and seminal fluid proteins induce post-mating changes in females, however, very little is known about the resulting gene expression changes in female head and central nervous system tissues that contribute to the post-mating response.
    Results: We determined the temporal gene expression changes in female head tissues 0-2, 24, 48 and 72 hours after mating. Females from each time point had a unique post-mating gene expression response, with 72 hours post-mating having the largest number of genes with significant changes in expression. At most time points, genes expressed in the head fat body that encode products involved in metabolism showed a marked change in expression. Additional analysis of gene expression changes in dissected brain tissues 24 hours post-mating revealed changes in transcript abundance of many genes, notably, the reduced transcript abundance of genes that encode ion channels.
    Conclusions: Substantial changes occur in the regulation of many genes in female head tissues after mating, which might underlie aspects of the female post-mating response. These results provide new insights into the physiological and metabolic changes that accompany changes in female behaviors.
    MeSH term(s) Animals ; Brain/metabolism ; Databases, Genetic ; Dissection ; Drosophila melanogaster/genetics ; Female ; Gene Expression Profiling ; Gene Expression Regulation ; Genes, Insect/genetics ; Head ; Male ; Organ Specificity/genetics ; Sexual Behavior, Animal ; Time Factors
    Language English
    Publishing date 2010-10-06
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ISSN 1471-2164
    ISSN (online) 1471-2164
    DOI 10.1186/1471-2164-11-541
    Database MEDical Literature Analysis and Retrieval System OnLINE

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