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  1. Book ; Online: Plant Growing Control with Modicon M580

    Won, Brittany M.Y. / Tran, Eileen T.

    Electrical Engineering

    2020  

    Abstract: Currently, the Industrial Power and Controls lab is being developed by the Cal Poly Electrical Engineering department. The lab is equipped with recently donated Modicon M580 Programmable Logic Controllers (PLCs) from Schneider Electric. In addition to ... ...

    Abstract Currently, the Industrial Power and Controls lab is being developed by the Cal Poly Electrical Engineering department. The lab is equipped with recently donated Modicon M580 Programmable Logic Controllers (PLCs) from Schneider Electric. In addition to PLCs, Schneider Electric also donated Human Machine Interfaces (HMI) and input/output modules. This project focuses on the creation of a lab experiment that will give future Cal Poly electrical engineering students hands-on experience with this equipment. To show students the broad range of PLCs and the role that electrical engineering plays in various industries, this experiment focuses on the agriculture industry, but more specifically, an automated indoor gardening system. Originally, the main goals of this project were the complete simulation and hardware test of a possible lab system, along with a corresponding instructional manual for the usage of the HMI in conjunction with the PLCs and input/output modules. Due to COVID-19, the hardware portion of this project was put on hold, along with the full instructional manual. However, a fully functional simulation using one of the PLC programming languages, function block diagram, allows for straightforward hardware testing in the future, when this project is turned into a full lab experiment. Although the hardware components have already been chosen and will appear in the bill of materials, they must still be tested before being put into use for the experiment. In addition, instructions on the HMI setup were also detailed, and will be important for the official lab manual.
    Keywords PLC ; HMI ; FBD ; Automation ; Schneider ; Controls and Control Theory ; covid19
    Subject code 670
    Publishing date 2020-06-01T07:00:00Z
    Publisher DigitalCommons@CalPoly
    Publishing country us
    Document type Book ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Long noncoding RNA GATA2-AS1 augments endothelial hypoxia inducible factor 1-α induction and regulates hypoxic signaling.

    Man, H S Jeffrey / Subramaniam, Noeline / Downs, Tiana / Sukumar, Aravin N / Saha, Aninda D / Nair, Ranju / Chen, Lucy / Teitelbaum, Daniel / Turgeon, Paul J / Ku, Kyung Ha / Tran, Eileen / de Perrot, Marc / Marsden, Philip A

    The Journal of biological chemistry

    2023  Volume 299, Issue 5, Page(s) 103029

    Abstract: Vascular endothelial cells form the inner cellular lining of blood vessels and have myriad physiologic functions including angiogenesis and response to hypoxia. We recently identified a set of endothelial cell (EC)-enriched long noncoding RNAs (lncRNAs) ... ...

    Abstract Vascular endothelial cells form the inner cellular lining of blood vessels and have myriad physiologic functions including angiogenesis and response to hypoxia. We recently identified a set of endothelial cell (EC)-enriched long noncoding RNAs (lncRNAs) in differentiated human primary cell types and described the role of the STEEL lncRNA in angiogenic patterning. We sought to further understand the role of EC-enriched lncRNAs in physiologic adaptation of the vascular endothelium. In this work, we describe an abundant, cytoplasmic, and EC-enriched lncRNA, GATA2-AS1, that is divergently transcribed from the EC-enriched developmental regulator, GATA2. While GATA2-AS1 is largely coexpressed with GATA2 in ECs, GATA2-AS1 and GATA2 appear to be complementary rather than synergistic as they have mostly distinct target genes. Common single nucleotide variants in GATA2-AS1 exons are associated with early-onset coronary artery disease and decreased expression of GATA2-AS1 in endothelial cell lines. In most cells, HIF1-α is central to the transcriptional response to hypoxia, while in ECs, both HIF1-α and HIF2-α are required to coordinate an acute and chronic response, respectively. In this setting, GATA2-AS1 contributes to the "HIF switch" and augments HIF1-α induction in acute hypoxia to regulate HIF1-α/HIF2-α balance. In hypoxia, GATA2-AS1 orchestrates HIF1-α-dependent induction of the glycolytic pathway and HIF1-α-independent maintenance of mitochondrial biogenesis. Similarly, GATA2-AS1 coordinates both metabolism and "tip/stalk" cell signaling to regulate angiogenesis in hypoxic ECs. Furthermore, we find that GATA2-AS1 expression patterns are perturbed in atherosclerotic disease. Together, these results define a role for GATA2-AS1 in the EC-specific response to hypoxia.
    MeSH term(s) Humans ; Endothelial Cells/metabolism ; GATA2 Transcription Factor/genetics ; Hypoxia/metabolism ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism ; Signal Transduction
    Chemical Substances GATA2 protein, human ; GATA2 Transcription Factor ; Hypoxia-Inducible Factor 1, alpha Subunit ; RNA, Long Noncoding ; HIF1A protein, human
    Language English
    Publishing date 2023-02-17
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1016/j.jbc.2023.103029
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  3. Article ; Online: Molecular glue CELMoD compounds are regulators of cereblon conformation.

    Watson, Edmond R / Novick, Scott / Matyskiela, Mary E / Chamberlain, Philip P / H de la Peña, Andres / Zhu, Jinyi / Tran, Eileen / Griffin, Patrick R / Wertz, Ingrid E / Lander, Gabriel C

    Science (New York, N.Y.)

    2022  Volume 378, Issue 6619, Page(s) 549–553

    Abstract: Cereblon (CRBN) is a ubiquitin ligase (E3) substrate receptor protein co-opted by CRBN E3 ligase modulatory drug (CELMoD) agents that target therapeutically relevant proteins for degradation. Prior crystallographic studies defined the drug-binding site ... ...

    Abstract Cereblon (CRBN) is a ubiquitin ligase (E3) substrate receptor protein co-opted by CRBN E3 ligase modulatory drug (CELMoD) agents that target therapeutically relevant proteins for degradation. Prior crystallographic studies defined the drug-binding site within CRBN's thalidomide-binding domain (TBD), but the allostery of drug-induced neosubstrate binding remains unclear. We performed cryo-electron microscopy analyses of the DNA damage-binding protein 1 (DDB1)-CRBN apo complex and compared these structures with DDB1-CRBN in the presence of CELMoD compounds alone and complexed with neosubstrates. Association of CELMoD compounds to the TBD is necessary and sufficient for triggering CRBN allosteric rearrangement from an open conformation to the canonical closed conformation. The neosubstrate Ikaros only stably associates with the closed CRBN conformation, illustrating the importance of allostery for CELMoD compound efficacy and informing structure-guided design strategies to improve therapeutic efficacy.
    MeSH term(s) Adaptor Proteins, Signal Transducing/chemistry ; Cryoelectron Microscopy ; Thalidomide/chemistry ; Ubiquitin-Protein Ligases/chemistry ; Protein Domains ; Allosteric Regulation
    Chemical Substances Adaptor Proteins, Signal Transducing ; CRBN protein, human ; Thalidomide (4Z8R6ORS6L) ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
    Language English
    Publishing date 2022-11-03
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.add7574
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  4. Article ; Online: In Vivo Function of Flow-Responsive Cis-DNA Elements of eNOS Gene: A Role for Chromatin-Based Mechanisms.

    Ku, Kyung Ha / Dubinsky, Michelle K / Sukumar, Aravin N / Subramaniam, Noeline / Feasson, Manon Y M / Nair, Ranju / Tran, Eileen / Steer, Brent M / Knight, Britta J / Marsden, Philip A

    Circulation

    2021  Volume 144, Issue 5, Page(s) 365–381

    Abstract: Background: eNOS (endothelial nitric oxide synthase) is an endothelial cell (EC)-specific gene predominantly expressed in medium- to large-sized arteries where ECs experience atheroprotective laminar flow with high shear stress. Disturbed flow with ... ...

    Abstract Background: eNOS (endothelial nitric oxide synthase) is an endothelial cell (EC)-specific gene predominantly expressed in medium- to large-sized arteries where ECs experience atheroprotective laminar flow with high shear stress. Disturbed flow with lower average shear stress decreases eNOS transcription, which leads to the development of atherosclerosis, especially at bifurcations and curvatures of arteries. This prototypic arterial EC gene contains 2 distinct flow-responsive cis-DNA elements in the promoter, the shear stress response element (SSRE) and the KLF (Krüppel-like factor) element. Previous in vitro studies suggested their positive regulatory functions on flow-induced transcription of EC genes including eNOS. However, the in vivo function of these cis-DNA elements remains unknown.
    Methods: Insertional transgenic mice with a mutation at each flow-responsive cis-DNA element were generated using a murine eNOS promoter-β-galactosidase reporter by linker-scanning mutagenesis and compared with episomal-based mutations in vitro. DNA methylation at the eNOS proximal promoter in mouse ECs was assessed by bisulfite sequencing or pyrosequencing.
    Results: Wild type mice with a functional eNOS promoter-reporter transgene exhibited reduced endothelial reporter expression in the atheroprone regions of disturbed flow (n=5). It is surprising that the SSRE mutation abrogated reporter expression in ECs and was associated with aberrant hypermethylation at the eNOS proximal promoter (n=7). Reporter gene silencing was independent of transgene copy number and integration position, indicating that the SSRE is a critical cis-element necessary for eNOS transcription in vivo. The KLF mutation demonstrated an integration site-specific decrease in eNOS transcription, again with marked promoter methylation (n=8), suggesting that the SSRE alone is not sufficient for eNOS transcription in vivo. In wild type mice, the native eNOS promoter was significantly hypermethylated in ECs from the atheroprone regions where eNOS expression was markedly repressed by chronic disturbed flow, demonstrating that eNOS expression is regulated by flow-dependent DNA methylation that is region-specific in the arterial endothelium in vivo.
    Conclusions: We report, for the first time, that the SSRE and KLF elements are critical flow sensors necessary for a transcriptionally permissive, hypomethylated eNOS promoter in ECs under chronic shear stress in vivo. Moreover, eNOS expression is regulated by flow-dependent epigenetic mechanisms, which offers novel mechanistic insight on eNOS gene regulation in atherogenesis.
    MeSH term(s) Animals ; Biomarkers ; Blood Flow Velocity ; Chromatin/genetics ; Chromatin/metabolism ; DNA Methylation ; Disease Models, Animal ; Disease Susceptibility ; Endothelial Cells/metabolism ; Epigenesis, Genetic ; Gene Dosage ; Gene Expression Regulation ; Gene Silencing ; Genes, Reporter ; Humans ; Kruppel-Like Transcription Factors/metabolism ; Mice ; Mice, Transgenic ; Mutation ; Nitric Oxide Synthase Type III/genetics ; Nitric Oxide Synthase Type III/metabolism ; Promoter Regions, Genetic ; Regulatory Sequences, Nucleic Acid ; Response Elements ; Transcriptional Activation
    Chemical Substances Biomarkers ; Chromatin ; Kruppel-Like Transcription Factors ; NOS3 protein, human (EC 1.14.13.39) ; Nitric Oxide Synthase Type III (EC 1.14.13.39)
    Language English
    Publishing date 2021-04-29
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80099-5
    ISSN 1524-4539 ; 0009-7322 ; 0069-4193 ; 0065-8499
    ISSN (online) 1524-4539
    ISSN 0009-7322 ; 0069-4193 ; 0065-8499
    DOI 10.1161/CIRCULATIONAHA.120.051078
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  5. Article ; Online: Crystal structure of the SALL4-pomalidomide-cereblon-DDB1 complex.

    Matyskiela, Mary E / Clayton, Thomas / Zheng, Xinde / Mayne, Christopher / Tran, Eileen / Carpenter, Aaron / Pagarigan, Barbra / McDonald, Joseph / Rolfe, Mark / Hamann, Lawrence G / Lu, Gang / Chamberlain, Philip P

    Nature structural & molecular biology

    2020  Volume 27, Issue 4, Page(s) 319–322

    Abstract: Thalidomide-dependent degradation of the embryonic transcription factor SALL4 by the ... ...

    Abstract Thalidomide-dependent degradation of the embryonic transcription factor SALL4 by the CRL4
    MeSH term(s) Adaptor Proteins, Signal Transducing/chemistry ; Adaptor Proteins, Signal Transducing/genetics ; Crystallography, X-Ray ; DNA-Binding Proteins/chemistry ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/ultrastructure ; Humans ; Multiprotein Complexes/chemistry ; Multiprotein Complexes/genetics ; Multiprotein Complexes/ultrastructure ; Protein Binding ; Protein Conformation ; Proteolysis/drug effects ; Substrate Specificity ; Thalidomide/analogs & derivatives ; Thalidomide/chemistry ; Thalidomide/pharmacology ; Transcription Factors/chemistry ; Transcription Factors/genetics ; Transcription Factors/ultrastructure ; Ubiquitin-Protein Ligases/chemistry ; Ubiquitin-Protein Ligases/ultrastructure ; Ubiquitination/genetics
    Chemical Substances Adaptor Proteins, Signal Transducing ; CRBN protein, human ; DDB1 protein, human ; DNA-Binding Proteins ; Multiprotein Complexes ; SALL4 protein, human ; Transcription Factors ; Thalidomide (4Z8R6ORS6L) ; pomalidomide (D2UX06XLB5) ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
    Language English
    Publishing date 2020-04-06
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2126708-X
    ISSN 1545-9985 ; 1545-9993
    ISSN (online) 1545-9985
    ISSN 1545-9993
    DOI 10.1038/s41594-020-0405-9
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  6. Article ; Online: Chemoproteomic discovery of a covalent allosteric inhibitor of WRN helicase.

    Baltgalvis, Kristen A / Lamb, Kelsey N / Symons, Kent T / Wu, Chu-Chiao / Hoffman, Melissa A / Snead, Aaron N / Song, Xiaodan / Glaza, Thomas / Kikuchi, Shota / Green, Jason C / Rogness, Donald C / Lam, Betty / Rodriguez-Aguirre, Maria E / Woody, David R / Eissler, Christie L / Rodiles, Socorro / Negron, Seth M / Bernard, Steffen M / Tran, Eileen /
    Pollock, Jonathan / Tabatabaei, Ali / Contreras, Victor / Williams, Heather N / Pastuszka, Martha K / Sigler, John J / Pettazzoni, Piergiorgio / Rudolph, Markus G / Classen, Moritz / Brugger, Doris / Claiborne, Christopher / Plancher, Jean-Marc / Cuartas, Isabel / Seoane, Joan / Burgess, Laurence E / Abraham, Robert T / Weinstein, David S / Simon, Gabriel M / Patricelli, Matthew P / Kinsella, Todd M

    Nature

    2024  Volume 629, Issue 8011, Page(s) 435–442

    Abstract: WRN helicase is a promising target for treatment of cancers with microsatellite instability (MSI) due to its essential role in resolving deleterious non-canonical DNA structures that accumulate in cells with faulty mismatch repair ... ...

    Abstract WRN helicase is a promising target for treatment of cancers with microsatellite instability (MSI) due to its essential role in resolving deleterious non-canonical DNA structures that accumulate in cells with faulty mismatch repair mechanisms
    MeSH term(s) Humans ; Werner Syndrome Helicase/metabolism ; Werner Syndrome Helicase/chemistry ; Animals ; Mice ; Allosteric Regulation/drug effects ; Cell Line, Tumor ; Female ; Xenograft Model Antitumor Assays ; Colorectal Neoplasms/drug therapy ; Colorectal Neoplasms/pathology ; Colorectal Neoplasms/metabolism ; Colorectal Neoplasms/enzymology ; Proteomics ; DNA Breaks, Double-Stranded ; Microsatellite Instability ; Drug Discovery ; Enzyme Inhibitors/pharmacology ; Enzyme Inhibitors/chemistry ; Models, Molecular ; Male ; Cysteine/metabolism ; Cysteine/chemistry
    Chemical Substances Werner Syndrome Helicase (EC 3.6.4.12) ; WRN protein, human (EC 3.6.4.12) ; Enzyme Inhibitors ; Cysteine (K848JZ4886)
    Language English
    Publishing date 2024-04-24
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 120714-3
    ISSN 1476-4687 ; 0028-0836
    ISSN (online) 1476-4687
    ISSN 0028-0836
    DOI 10.1038/s41586-024-07318-y
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  7. Article ; Online: CC-90009, a novel cereblon E3 ligase modulator, targets acute myeloid leukemia blasts and leukemia stem cells.

    Surka, Christine / Jin, Liqing / Mbong, Nathan / Lu, Chin-Chun / Jang, In Sock / Rychak, Emily / Mendy, Derek / Clayton, Thomas / Tindall, Elizabeth / Hsu, Christy / Fontanillo, Celia / Tran, Eileen / Contreras, Adrian / Ng, Stanley W K / Matyskiela, Mary / Wang, Kai / Chamberlain, Philip / Cathers, Brian / Carmichael, James /
    Hansen, Joshua / Wang, Jean C Y / Minden, Mark D / Fan, Jinhong / Pierce, Daniel W / Pourdehnad, Michael / Rolfe, Mark / Lopez-Girona, Antonia / Dick, John E / Lu, Gang

    Blood

    2020  Volume 137, Issue 5, Page(s) 661–677

    Abstract: A number of clinically validated drugs have been developed by repurposing the CUL4-DDB1-CRBN-RBX1 (CRL4CRBN) E3 ubiquitin ligase complex with molecular glue degraders to eliminate disease-driving proteins. Here, we present the identification of a first- ... ...

    Abstract A number of clinically validated drugs have been developed by repurposing the CUL4-DDB1-CRBN-RBX1 (CRL4CRBN) E3 ubiquitin ligase complex with molecular glue degraders to eliminate disease-driving proteins. Here, we present the identification of a first-in-class GSPT1-selective cereblon E3 ligase modulator, CC-90009. Biochemical, structural, and molecular characterization demonstrates that CC-90009 coopts the CRL4CRBN to selectively target GSPT1 for ubiquitination and proteasomal degradation. Depletion of GSPT1 by CC-90009 rapidly induces acute myeloid leukemia (AML) apoptosis, reducing leukemia engraftment and leukemia stem cells (LSCs) in large-scale primary patient xenografting of 35 independent AML samples, including those with adverse risk features. Using a genome-wide CRISPR-Cas9 screen for effectors of CC-90009 response, we uncovered the ILF2 and ILF3 heterodimeric complex as a novel regulator of cereblon expression. Knockout of ILF2/ILF3 decreases the production of full-length cereblon protein via modulating CRBN messenger RNA alternative splicing, leading to diminished response to CC-90009. The screen also revealed that the mTOR signaling and the integrated stress response specifically regulate the response to CC-90009 in contrast to other cereblon modulators. Hyperactivation of the mTOR pathway by inactivation of TSC1 and TSC2 protected against the growth inhibitory effect of CC-90009 by reducing CC-90009-induced binding of GSPT1 to cereblon and subsequent GSPT1 degradation. On the other hand, GSPT1 degradation promoted the activation of the GCN1/GCN2/ATF4 pathway and subsequent apoptosis in AML cells. Collectively, CC-90009 activity is mediated by multiple layers of signaling networks and pathways within AML blasts and LSCs, whose elucidation gives insight into further assessment of CC-90009s clinical utility. These trials were registered at www.clinicaltrials.gov as #NCT02848001 and #NCT04336982).
    MeSH term(s) Acetamides/pharmacology ; Acetamides/therapeutic use ; Adaptor Proteins, Signal Transducing/antagonists & inhibitors ; Animals ; CRISPR-Cas Systems ; Cell Line, Tumor ; Humans ; Isoindoles/pharmacology ; Isoindoles/therapeutic use ; Leukemia, Myeloid, Acute/pathology ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Models, Molecular ; Molecular Targeted Therapy ; Neoplasm Proteins/antagonists & inhibitors ; Neoplastic Stem Cells/drug effects ; Neoplastic Stem Cells/enzymology ; Nuclear Factor 45 Protein/physiology ; Nuclear Factor 90 Proteins/physiology ; Peptide Termination Factors/metabolism ; Piperidones/pharmacology ; Piperidones/therapeutic use ; Proteasome Endopeptidase Complex/metabolism ; Protein Conformation ; Protein Processing, Post-Translational/drug effects ; Proteolysis ; Small Molecule Libraries ; Stress, Physiological ; TOR Serine-Threonine Kinases/physiology ; U937 Cells ; Ubiquitin-Protein Ligases/antagonists & inhibitors ; Ubiquitination/drug effects ; Xenograft Model Antitumor Assays
    Chemical Substances Acetamides ; Adaptor Proteins, Signal Transducing ; CC-90009 ; CRBN protein, human ; IL17RB protein, human ; ILF2 protein, human ; ILF3 protein, human ; Isoindoles ; Neoplasm Proteins ; Nuclear Factor 45 Protein ; Nuclear Factor 90 Proteins ; Peptide Termination Factors ; Piperidones ; Small Molecule Libraries ; peptide-chain-release factor 3 ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
    Language English
    Publishing date 2020-10-23
    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 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2020008676
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