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FK506-Binding Protein 12.6/1B, a Negative Regulator of [Ca2+], Rescues Memory and Restores Genomic Regulation in the Hippocampus of Aging Rats
This Accepted Manuscript has not been copyedited and formatted. The final version may differ from this version. A link to any extended data will be provided when the final version is posted online. Research Articles: Neurobiology of Disease FK506-Binding Protein 12.6/1b, a negative regulator of [Ca2+], rescues memory and restores genomic regulation in the hippocampus of aging rats John C. Gant1, Eric M. Blalock1, Kuey-Chu Chen1, Inga Kadish2, Olivier Thibault1, Nada M. Porter1 and Philip W. Landfield1 1Department of Pharmacology & Nutritional Sciences, University of Kentucky, Lexington, KY 40536 2Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL 35294 DOI: 10.1523/JNEUROSCI.2234-17.2017 Received: 7 August 2017 Revised: 10 October 2017 Accepted: 24 November 2017 Published: 18 December 2017 Author contributions: J.C.G. and P.W.L. designed research; J.C.G., E.M.B., K.-c.C., and I.K. performed research; J.C.G., E.M.B., K.-c.C., I.K., and P.W.L. analyzed data; J.C.G., E.M.B., O.T., N.M.P., and P.W.L. wrote the paper. Conflict of Interest: The authors declare no competing financial interests. NIH grants AG004542, AG033649, AG052050, AG037868 and McAlpine Foundation for Neuroscience Research Corresponding author: Philip W. Landfield, [email protected], Department of Pharmacology & Nutritional Sciences, University of Kentucky, 800 Rose Street, UKMC MS 307, Lexington, KY 40536 Cite as: J. Neurosci ; 10.1523/JNEUROSCI.2234-17.2017 Alerts: Sign up at www.jneurosci.org/cgi/alerts to receive customized email alerts when the fully formatted version of this article is published. -
(12) Patent Application Publication (10) Pub. No.: US 2002/0152483 A1 Reue Et Al
US 2002O1524.83A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2002/0152483 A1 Reue et al. (43) Pub. Date: Oct. 17, 2002 (54) NOVEL GENE ASSOCATED WITH Publication Classification REGULATION OF ADPOSITY AND INSULIN RESPONSE (51) Int. Cl." ............................ A01K 67/00; C12O 1/68; C12P 19/34 (75) Inventors: Karen Reue, Torrance, CA (US); (52) U.S. Cl. .................................. 800/9; 435/6; 435/91.2 Miklos Peterfy, Los Angeles, CA (US) (57) ABSTRACT Correspondence Address: This invention pertains to the identification and isolation of LAW OFFICES OF JONATHAN ALAN QUINE a gene implicated in the fatty liver dystrophy (fld) pheno PO BOX 458 type. Mouse and human forms of the novel gene, designated ALAMEDA, CA 94501 herein as Lpin1/LPIN1 (mouse and human genes, respec tively), are identified. This invention additionally provides (73) Assignee: The Regents of the University of Cali methods of Screening for agents that alter adipose tissue fornia development. The methods involve contacting a cell con taining a Lpin1 gene With a test agent, and detecting a (21) Appl. No.: 10/028,056 change in the expression or activity of a Lpin1 gene product, (22) Filed: Dec. 19, 2001 where a difference in the expression or activity of Lpin1 in the contacted cell indicates that the agent alters or is likely Related U.S. Application Data to alter adipose tissue development. Also provided are methods of identifying Lpin1 mutations, and methods of (60) Provisional application No. 60/257,772, filed on Dec. mitigating Symptoms of lipodystrophy, obesity, diabetes, 22, 2000. atherOSclerosis and related pathologies. -
Genome Sequence of the Progenitor of the Wheat D Genome Aegilops Tauschii Ming-Cheng Luo1*, Yong Q
OPEN LETTER doi:10.1038/nature24486 Genome sequence of the progenitor of the wheat D genome Aegilops tauschii Ming-Cheng Luo1*, Yong Q. Gu2*, Daniela Puiu3*, Hao Wang4,5,6*, Sven O. Twardziok7*, Karin R. Deal1, Naxin Huo1,2, Tingting Zhu1, Le Wang1, Yi Wang1,2, Patrick E. McGuire1, Shuyang Liu1, Hai Long1, Ramesh K. Ramasamy1, Juan C. Rodriguez1, Sonny L. Van1, Luxia Yuan1, Zhenzhong Wang1,8, Zhiqiang Xia1, Lichan Xiao1, Olin D. Anderson2, Shuhong Ouyang2,8, Yong Liang2,8, Aleksey V. Zimin3, Geo Pertea3, Peng Qi4,5, Jeffrey L. Bennetzen6, Xiongtao Dai9, Matthew W. Dawson9, Hans-Georg Müller9, Karl Kugler7, Lorena Rivarola-Duarte7, Manuel Spannagl7, Klaus F. X. Mayer7,10, Fu-Hao Lu11, Michael W. Bevan11, Philippe Leroy12, Pingchuan Li13, Frank M. You13, Qixin Sun8, Zhiyong Liu8, Eric Lyons14, Thomas Wicker15, Steven L. Salzberg3,16, Katrien M. Devos4,5 & Jan Dvořák1 Aegilops tauschii is the diploid progenitor of the D genome of We conclude therefore that the size of the Ae. tauschii genome is about hexaploid wheat1 (Triticum aestivum, genomes AABBDD) and 4.3 Gb. an important genetic resource for wheat2–4. The large size and To assess the accuracy of our assembly, sequences of 195 inde- highly repetitive nature of the Ae. tauschii genome has until now pendently sequenced and assembled AL8/78 BAC clones8, which precluded the development of a reference-quality genome sequence5. contained 25,540,177 bp in 2,405 unordered contigs, were aligned to Here we use an array of advanced technologies, including ordered- Aet v3.0. Five contigs failed to align and six extended partly into gaps, clone genome sequencing, whole-genome shotgun sequencing, accounting for 0.25% of the total length of the contigs. -
The Small G Protein Arl8 Contributes to Lysosomal Function and Long-Range Axonal Transport in Drosophila
This is a repository copy of The small G protein Arl8 contributes to lysosomal function and long-range axonal transport in Drosophila. White Rose Research Online URL for this paper: https://eprints.whiterose.ac.uk/134948/ Version: Accepted Version Article: Rosa-Ferreira, Cláudia, Sweeney, Sean orcid.org/0000-0003-2673-9578 and Munro, Sean (Accepted: 2018) The small G protein Arl8 contributes to lysosomal function and long- range axonal transport in Drosophila. Biology Open. (In Press) https://doi.org/10.1242/bio.035964 Reuse Items deposited in White Rose Research Online are protected by copyright, with all rights reserved unless indicated otherwise. They may be downloaded and/or printed for private study, or other acts as permitted by national copyright laws. The publisher or other rights holders may allow further reproduction and re-use of the full text version. This is indicated by the licence information on the White Rose Research Online record for the item. Takedown If you consider content in White Rose Research Online to be in breach of UK law, please notify us by emailing [email protected] including the URL of the record and the reason for the withdrawal request. [email protected] https://eprints.whiterose.ac.uk/ The small G protein Arl8 contributes to lysosomal function and long-range axonal transport in Drosophila Cláudia Rosa-Ferreira1 , Sean T. Sweeney2 and Sean Munro1* 1: MRC Laboratory of Molecular Biology Francis Crick Avenue Cambridge CB2 0QH UK 2: Department of Biology University of York York YO10 5DD UK *: Corresponding author. Email: [email protected] © 2018. -
Targeting MYCN in Neuroblastoma by BET Bromodomain Inhibition
Published OnlineFirst February 21, 2013; DOI: 10.1158/2159-8290.CD-12-0418 RESEARCH ARTICLE Targeting MYCN in Neuroblastoma by BET Bromodomain Inhibition Alexandre Puissant1,3, Stacey M. Frumm1,3, Gabriela Alexe1,3,5,6, Christopher F. Bassil1,3, Jun Qi2, Yvan H. Chanthery8, Erin A. Nekritz8, Rhamy Zeid2, William Clay Gustafson8, Patricia Greninger7, Matthew J. Garnett10, Ultan McDermott10, Cyril H. Benes7, Andrew L. Kung1,3, William A. Weiss8,9, James E. Bradner2,4, and Kimberly Stegmaier1,3,6 Downloaded from cancerdiscovery.aacrjournals.org on October 2, 2021. © 2013 American Association for Cancer Research. 15-CD-12-0418_p308-323.indd 1 22/02/13 12:15 AM Published OnlineFirst February 21, 2013; DOI: 10.1158/2159-8290.CD-12-0418 A BSTRACT Bromodomain inhibition comprises a promising therapeutic strategy in cancer, particularly for hematologic malignancies. To date, however, genomic biomarkers to direct clinical translation have been lacking. We conducted a cell-based screen of genetically defined cancer cell lines using a prototypical inhibitor of BET bromodomains. Integration of genetic features with chemosensitivity data revealed a robust correlation between MYCN amplification and sensitivity to bromodomain inhibition. We characterized the mechanistic and translational significance of this finding in neuroblastoma, a childhood cancer with frequent amplification of MYCN. Genome-wide expression analysis showed downregulation of the MYCN transcriptional program accompanied by suppression of MYCN transcription. Functionally, bromodomain-mediated inhibition of MYCN impaired growth and induced apoptosis in neuroblastoma. BRD4 knockdown phenocopied these effects, establishing BET bromodomains as transcriptional regulators of MYCN. BET inhibition conferred a significant survival advantage in 3 in vivo neuroblastoma models, providing a compelling rationale for developing BET bro- modomain inhibitors in patients with neuroblastoma. -
1 First Presentation of LPIN1 Acute Rhabdomyolysis in Adolescence and Adulthood
Manuscript File Click here to view linked References 1 First presentation of LPIN1 acute rhabdomyolysis in adolescence and adulthood 2 3 Chiara Pizzamiglioa, Nayana Lahirib, Niranjanan Nirmalananthanc, Bhrigu Soodd, Subash 4 Somalankad, Philip Ostrowskie, Rahul Phadkef, Dominic Gerard O’Donovang, Francesco 5 Muntonih, Rosaline Quinlivana 6 7 a. MRC Centre for Neuromuscular Diseases, UCL Institute of Neurology and National Hospital for 8 Neurology and Neurosurgery, Queen Square, London, United Kingdom 9 10 b. Clinical Genetics Department, St George's University Hospitals NHS Foundation Trust, London, 11 United Kingdom 12 13 c. Departments of Neurology and Neuroradiology, Atkinson Morley Regional Neurosciences 14 Centre, St George's Hospital, London, United Kingdom 15 16 d. South West Thames Renal & Transplantation Unit and South West Thames Institute for Renal 17 Research, Saint Helier Hospital, Carshalton, Surrey, United Kingdom 18 19 e. South West Thames Regional Genetics Service, St George's University NHS Foundation Trust, 20 London, United Kingdom 21 22 f. Division of Neuropathology, Dubowitz Neuromuscular Centre, UCL Great Ormond Street 23 Hospital for Children, United Kingdom; Division of Neuropathology, National Hospital for 24 Neurology and Neurosurgery, Queen Square, London, United Kingdom 25 1 26 g. Neuropathology, Department of Histopathology, Addenbrooke’s Hospital, Cambridge University 27 Hospitals NHS Foundation Trust, Cambridge, United Kingdom 28 29 h. Paediatric Neurology, Dubowitz Neuromuscular Centre, UCL Institute of Child Health and Great 30 Ormond Street Hospital for Children, London, United Kingdom 31 32 Corresponding author: Chiara Pizzamiglio ([email protected]) 33 34 Abstract: LPIN1 mutations are a known common cause of autosomal recessive, recurrent and life- 35 threatening acute rhabdomyolysis of childhood-onset. -
A Yeast Phenomic Model for the Influence of Warburg Metabolism on Genetic Buffering of Doxorubicin Sean M
Santos and Hartman Cancer & Metabolism (2019) 7:9 https://doi.org/10.1186/s40170-019-0201-3 RESEARCH Open Access A yeast phenomic model for the influence of Warburg metabolism on genetic buffering of doxorubicin Sean M. Santos and John L. Hartman IV* Abstract Background: The influence of the Warburg phenomenon on chemotherapy response is unknown. Saccharomyces cerevisiae mimics the Warburg effect, repressing respiration in the presence of adequate glucose. Yeast phenomic experiments were conducted to assess potential influences of Warburg metabolism on gene-drug interaction underlying the cellular response to doxorubicin. Homologous genes from yeast phenomic and cancer pharmacogenomics data were analyzed to infer evolutionary conservation of gene-drug interaction and predict therapeutic relevance. Methods: Cell proliferation phenotypes (CPPs) of the yeast gene knockout/knockdown library were measured by quantitative high-throughput cell array phenotyping (Q-HTCP), treating with escalating doxorubicin concentrations under conditions of respiratory or glycolytic metabolism. Doxorubicin-gene interaction was quantified by departure of CPPs observed for the doxorubicin-treated mutant strain from that expected based on an interaction model. Recursive expectation-maximization clustering (REMc) and Gene Ontology (GO)-based analyses of interactions identified functional biological modules that differentially buffer or promote doxorubicin cytotoxicity with respect to Warburg metabolism. Yeast phenomic and cancer pharmacogenomics data were integrated to predict differential gene expression causally influencing doxorubicin anti-tumor efficacy. Results: Yeast compromised for genes functioning in chromatin organization, and several other cellular processes are more resistant to doxorubicin under glycolytic conditions. Thus, the Warburg transition appears to alleviate requirements for cellular functions that buffer doxorubicin cytotoxicity in a respiratory context. -
Anti-ARL8B Antibody (ARG43276)
Product datasheet [email protected] ARG43276 Package: 50 μg anti-ARL8B antibody Store at: -20°C Summary Product Description Rabbit Polyclonal antibody recognizes ARL8B Tested Reactivity Hu, Ms Tested Application IHC-P, WB Host Rabbit Clonality Polyclonal Isotype IgG Target Name ARL8B Antigen Species Human Immunogen Recombinant protein corresponding to aa. 20-186 of Human ARL8B. Conjugation Un-conjugated Alternate Names Novel small G protein indispensable for equal chromosome segregation 1; ARL10C; ADP-ribosylation factor-like protein 8B; Gie1; ADP-ribosylation factor-like protein 10C Application Instructions Application table Application Dilution IHC-P 1:100 WB 4 µg/ml Application Note * The dilutions indicate recommended starting dilutions and the optimal dilutions or concentrations should be determined by the scientist. Positive Control Mouse brain, NIH/3T3 and Jurkat Calculated Mw 22 kDa Observed Size ~ 22 kDa Properties Form Liquid Purification Caprylic acid ammonium sulfate precipitation purified. Buffer 0.01 M PBS (pH 7.4), 0.03% Proclin 300 and 50% Glycerol. Preservative 0.03% Proclin 300 Stabilizer 50% Glycerol Storage instruction For continuous use, store undiluted antibody at 2-8°C for up to a week. For long-term storage, aliquot and store at -20°C. Storage in frost free freezers is not recommended. Avoid repeated freeze/thaw cycles. Suggest spin the vial prior to opening. The antibody solution should be gently mixed before use. www.arigobio.com 1/2 Note For laboratory research only, not for drug, diagnostic or other use. Bioinformation Gene Symbol ARL8B Gene Full Name ADP-ribosylation factor-like 8B Function Plays a role in lysosome motility (PubMed:16537643, PubMed:25898167). -
Bioinformatics Integrated Analysis to Investigate Candidate Biomarkers and Associated Metabolites in Osteosarcoma
Wang et al. Journal of Orthopaedic Surgery and Research (2021) 16:432 https://doi.org/10.1186/s13018-021-02578-0 RESEARCH ARTICLE Open Access Bioinformatics integrated analysis to investigate candidate biomarkers and associated metabolites in osteosarcoma Jun Wang, Mingzhi Gong, Zhenggang Xiong, Yangyang Zhao and Deguo Xing* Abstract Background: This study hoped to explore the potential biomarkers and associated metabolites during osteosarcoma (OS) progression based on bioinformatics integrated analysis. Methods: Gene expression profiles of GSE28424, including 19 human OS cell lines (OS group) and 4 human normal long bone tissue samples (control group), were downloaded. The differentially expressed genes (DEGs) in OS vs. control were investigated. The enrichment investigation was performed based on DEGs, followed by protein–protein interaction network analysis. Then, the feature genes associated with OS were explored, followed by survival analysis to reveal prognostic genes. The qRT-PCR assay was performed to test the expression of these genes. Finally, the OS- associated metabolites and disease-metabolic network were further investigated. Results: Totally, 357 DEGs were revealed between the OS vs. control groups. These DEGs, such as CXCL12, were mainly involved in functions like leukocyte migration. Then, totally, 38 feature genes were explored, of which 8 genes showed significant associations with the survival of patients. High expression of CXCL12, CEBPA, SPARCL1, CAT, TUBA1A, and ALDH1A1 was associated with longer survival time, while high expression of CFLAR and STC2 was associated with poor survival. Finally, a disease-metabolic network was constructed with 25 nodes including two disease-associated metabolites cyclophosphamide and bisphenol A (BPA). BPA showed interactions with multiple prognosis-related genes, such as CXCL12 and STC2. -
Transcriptional Profiling of Long Non-Coding Rnas and Novel
Brunner et al. Genome Biology 2012, 13:R75 http://genomebiology.com/2012/13/8/R75 RESEARCH Open Access Transcriptional profiling of long non-coding RNAs and novel transcribed regions across a diverse panel of archived human cancers Alayne L Brunner1, Andrew H Beck1,2, Badreddin Edris1,3, Robert T Sweeney1, Shirley X Zhu1, Rui Li1, Kelli Montgomery1, Sushama Varma1, Thea Gilks1, Xiangqian Guo1, Joseph W Foley3, Daniela M Witten4, Craig P Giacomini1,5, Ryan A Flynn6, Jonathan R Pollack1, Robert Tibshirani7,8, Howard Y Chang6, Matt van de Rijn1 and Robert B West1* Abstract Background: Molecular characterization of tumors has been critical for identifying important genes in cancer biology and for improving tumor classification and diagnosis. Long non-coding RNAs, as a new, relatively unstudied class of transcripts, provide a rich opportunity to identify both functional drivers and cancer-type-specific biomarkers. However, despite the potential importance of long non-coding RNAs to the cancer field, no comprehensive survey of long non-coding RNA expression across various cancers has been reported. Results: We performed a sequencing-based transcriptional survey of both known long non-coding RNAs and novel intergenic transcripts across a panel of 64 archival tumor samples comprising 17 diagnostic subtypes of adenocarcinomas, squamous cell carcinomas and sarcomas. We identified hundreds of transcripts from among the known 1,065 long non-coding RNAs surveyed that showed variability in transcript levels between the tumor types and are therefore potential biomarker candidates. We discovered 1,071 novel intergenic transcribed regions and demonstrate that these show similar patterns of variability between tumor types. -
ARL8B Sirna (M): Sc-141251
SAN TA C RUZ BI OTEC HNOL OG Y, INC . ARL8B siRNA (m): sc-141251 BACKGROUND STORAGE AND RESUSPENSION ADP-ribosylation factors (ARFs) are highly conserved guanine nucleotide bind - Store lyophilized siRNA duplex at -20° C with desiccant. Stable for at least ing proteins that enhance the ADP-ribosyltransferase activity of Cholera Toxin. one year from the date of shipment. Once resuspended, store at -20° C, ARF’s are important in eukaryotic vesicular trafficking pathways and they play avoid contact with RNAses and repeated freeze thaw cycles. an essential role in the activation of phospholipase D (PC-PLD). ARL8B (ADP- Resuspend lyophilized siRNA duplex in 330 µl of the RNAse-free water ribosylation factor-like protein 8B), also known as ARL10C or GIE1, is a 186 pro vided. Resuspension of the siRNA duplex in 330 µl of RNAse-free water amino acid protein that localizes to the late endosome membrane and belongs makes a 10 µM solution in a 10 µM Tris-HCl, pH 8.0, 20 mM NaCl, 1 mM to the ARL family of ARF-like GTPase proteins. Expressed ubiquitously, ARL8A EDTA buffered solution. interacts with Tubulin and is thought to play a role in lysosome motility, as well as in chromosomal segregation. The gene encoding ARL8B maps to APPLICATIONS human chromosome 3, which houses over 1,100 genes, including a chemokine receptor (CKR) gene cluster and a variety of human cancer-related gene loci. ARL8B siRNA (m) is recommended for the inhibition of ARL8B expression in mouse cells. REFERENCES SUPPORT REAGENTS 1. Secombe, J., et al. 2004. -
Os9) and the Hypoxia Response Gene, Hypoxia Inducible Factor 1 (Hif1) Alpha, in Kidney Tubular Cells
North Carolina Agricultural and Technical State University Aggie Digital Collections and Scholarship Theses Electronic Theses and Dissertations 2013 Meprin Interaction With Osteosarcoma 9 (Os9) And The Hypoxia Response Gene, Hypoxia Inducible Factor 1 (Hif1) Alpha, In Kidney Tubular Cells Barry L. Martin North Carolina Agricultural and Technical State University Follow this and additional works at: https://digital.library.ncat.edu/theses Recommended Citation Martin, Barry L., "Meprin Interaction With Osteosarcoma 9 (Os9) And The Hypoxia Response Gene, Hypoxia Inducible Factor 1 (Hif1) Alpha, In Kidney Tubular Cells" (2013). Theses. 287. https://digital.library.ncat.edu/theses/287 This Thesis is brought to you for free and open access by the Electronic Theses and Dissertations at Aggie Digital Collections and Scholarship. It has been accepted for inclusion in Theses by an authorized administrator of Aggie Digital Collections and Scholarship. For more information, please contact [email protected]. Meprin Interaction with Osteosarcoma 9 (OS9) and the Hypoxia Response Gene, Hypoxia- inducible Factor 1 (HIF1) Alpha, in Kidney Tubular Cells Barry L. Martin North Carolina A&T State University A thesis submitted to the graduate faculty in partial fulfillment of the requirements for the degree of MASTER OF SCIENCE Department: Biology Major: Biology Major Professor: Dr. Elimelda Moige Ongeri Greensboro, North Carolina 2013 i School of Graduate Studies North Carolina Agricultural and Technical State University This is to certify that the Master’s Thesis of Barry L. Martin has met the thesis requirements of North Carolina Agricultural and Technical State University Greensboro, North Carolina 2013 Approved by: Elimelda Moige Ongeri, PhD Jian Han, PhD Major Professor Committee Member Catherine White, PhD Scott Harrison, PhD Committee Member Committee Member Mary Smith, PhD Sanjiv Sarin, PhD Department Chair Dean, The Graduate School ii © Copyright by Barry L.