Autophagy Dark Genes: Can We Find Them with Machine Learning?
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
OXSR1 (A-4): Sc-271707
SANTA CRUZ BIOTECHNOLOGY, INC. OXSR1 (A-4): sc-271707 BACKGROUND APPLICATIONS Oxidative stress-responsive 1 protein (OXSR1), a protein of 527 amino acids, OXSR1 (A-4) is recommended for detection of OXSR1 of mouse, rat and belongs to the STE20 subfamily. OXSR1 is one of two human homologs of human origin by Western Blotting (starting dilution 1:100, dilution range Fray, a serine/threonine kinase expressed in Drosophila. OXSR1 binds to and 1:100-1:1000), immunoprecipitation [1-2 µg per 100-500 µg of total protein phosphorylates p21-activated protein kinase (PAK1) and regulates downstream (1 ml of cell lysate)], immunofluorescence (starting dilution 1:50, dilution kinases in response to environmental stress. Endogenous OXSR1 is activated range 1:50-1:500) and solid phase ELISA (starting dilution 1:30, dilution only by osmotic stresses, notably sorbitol and to a lesser extent NaCl. OXSR1 range 1:30-1:3000). may also play a role in regulating the Actin cytoskeleton. The chloride channel Suitable for use as control antibody for OXSR1 siRNA (h): sc-61273, OXSR1 proteins SLC12A1, SLC12A2 and SLC12A6 isoform 2 interact with OXSR1, siRNA (m): sc-61274, OXSR1 shRNA Plasmid (h): sc-61273-SH, OXSR1 but SLC12A4 and SLC12A7 do not. The WNK1 and WNK4 protein kinases shRNA Plasmid (m): sc-61274-SH, OXSR1 shRNA (h) Lentiviral Particles: activate OXSR1 by phosphorlating its T-loop. The OXSR1 protein is widely sc-61273-V and OXSR1 shRNA (m) Lentiviral Particles: sc-61274-V. expressed in mammalian tissues. Molecular Weight of OXSR1: 58 kDa. REFERENCES Positive Controls: OXSR1 (h3): 293 Lysate: sc-158793, HeLa whole cell lysate: 1. -
Multiple Activities of Arl1 Gtpase in the Trans-Golgi Network Chia-Jung Yu1,2 and Fang-Jen S
© 2017. Published by The Company of Biologists Ltd | Journal of Cell Science (2017) 130, 1691-1699 doi:10.1242/jcs.201319 COMMENTARY Multiple activities of Arl1 GTPase in the trans-Golgi network Chia-Jung Yu1,2 and Fang-Jen S. Lee3,4,* ABSTRACT typical features of an Arf-family GTPase, including an amphipathic ADP-ribosylation factors (Arfs) and ADP-ribosylation factor-like N-terminal helix and a consensus site for N-myristoylation (Lu et al., proteins (Arls) are highly conserved small GTPases that function 2001; Price et al., 2005). In yeast, recruitment of Arl1 to the Golgi as main regulators of vesicular trafficking and cytoskeletal complex requires a second Arf-like GTPase, Arl3 (Behnia et al., reorganization. Arl1, the first identified member of the large Arl family, 2004; Setty et al., 2003). Yeast Arl3 lacks a myristoylation site and is an important regulator of Golgi complex structure and function in is, instead, N-terminally acetylated; this modification is required for organisms ranging from yeast to mammals. Together with its effectors, its recruitment to the Golgi complex by Sys1. In mammalian cells, Arl1 has been shown to be involved in several cellular processes, ADP-ribosylation-factor-related protein 1 (Arfrp1), a mammalian including endosomal trans-Golgi network and secretory trafficking, lipid ortholog of yeast Arl3, plays a pivotal role in the recruitment of Arl1 droplet and salivary granule formation, innate immunity and neuronal to the trans-Golgi network (TGN) (Behnia et al., 2004; Panic et al., development, stress tolerance, as well as the response of the unfolded 2003b; Setty et al., 2003; Zahn et al., 2006). -
Systematic Screening for Potential Therapeutic Targets in Osteosarcoma Through a Kinome-Wide CRISPR-Cas9 Library
Cancer Biol Med 2020. doi: 10.20892/j.issn.2095-3941.2020.0162 ORIGINAL ARTICLE Systematic screening for potential therapeutic targets in osteosarcoma through a kinome-wide CRISPR-Cas9 library Yuanzhong Wu*, Liwen Zhou*, Zifeng Wang, Xin Wang, Ruhua Zhang, Lisi Zheng, Tiebang Kang Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou 510060, China ABSTRACT Objective: Osteosarcoma is the most common primary malignant bone tumor. However, the survival of patients with osteosarcoma has remained unchanged during the past 30 years, owing to a lack of efficient therapeutic targets. Methods: We constructed a kinome-targeting CRISPR-Cas9 library containing 507 kinases and 100 nontargeting controls and screened the potential kinase targets in osteosarcoma. The CRISPR screening sequencing data were analyzed with the Model-based Analysis of Genome-wide CRISPR/Cas9 Knockout (MAGeCK) Python package. The functional data were applied in the 143B cell line through lenti-CRISPR-mediated gene knockout. The clinical significance of kinases in the survival of patients with osteosarcoma was analyzed in the R2: Genomics Analysis and Visualization Platform. Results: We identified 53 potential kinase targets in osteosarcoma. Among these targets, we analyzed 3 kinases, TRRAP, PKMYT1, and TP53RK, to validate their oncogenic functions in osteosarcoma. PKMYT1 and TP53RK showed higher expression in osteosarcoma than in normal bone tissue, whereas TRRAP showed no significant difference. High expression of all 3 kinases was associated with relatively poor prognosis in patients with osteosarcoma. Conclusions: Our results not only offer potential therapeutic kinase targets in osteosarcoma but also provide a paradigm for functional genetic screening by using a CRISPR-Cas9 library, including target design, library construction, screening workflow, data analysis, and functional validation. -
Significant Shortest Paths for the Detection of Putative Disease Modules
bioRxiv preprint doi: https://doi.org/10.1101/2020.04.01.019844; this version posted April 2, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. SIGNIFICANT SHORTEST PATHS FOR THE DETECTION OF PUTATIVE DISEASE MODULES Daniele Pepe1 1Department of Oncology, KU Leuven, LKI–Leuven Cancer Institute, Leuven, Belgium Email address: DP: [email protected] bioRxiv preprint doi: https://doi.org/10.1101/2020.04.01.019844; this version posted April 2, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. Keywords Structural equation modeling, significant shortest paths, pathway analysis, disease modules. Abstract Background The characterization of diseases in terms of perturbated gene modules was recently introduced for the analysis of gene expression data. Some approaches were proposed in literature, but many times they are inductive approaches. This means that starting directly from data, they try to infer key gene networks potentially associated to the biological phenomenon studied. However they ignore the biological information already available to characterize the gene modules. Here we propose the detection of perturbed gene modules using the combination of data driven and hypothesis-driven approaches relying on biological metabolic pathways and significant shortest paths tested by structural equation modeling. -
Atg4b Antibody A
Revision 1 C 0 2 - t Atg4B Antibody a e r o t S Orders: 877-616-CELL (2355) [email protected] Support: 877-678-TECH (8324) 9 9 Web: [email protected] 2 www.cellsignal.com 5 # 3 Trask Lane Danvers Massachusetts 01923 USA For Research Use Only. Not For Use In Diagnostic Procedures. Applications: Reactivity: Sensitivity: MW (kDa): Source: UniProt ID: Entrez-Gene Id: WB H M R Endogenous 48 Rabbit Q9Y4P1 23192 Product Usage Information 2. Ohsumi, Y. (2001) Nat Rev Mol Cell Biol 2, 211-6. 3. Kabeya, Y. et al. (2000) EMBO J 19, 5720-8. Application Dilution 4. Kabeya, Y. et al. (2004) J Cell Sci 117, 2805-12. 5. Mariño, G. et al. (2003) J Biol Chem 278, 3671-8. Western Blotting 1:1000 6. Sou, Y.S. et al. (2008) Mol Biol Cell 19, 4762-75. 7. Hemelaar, J. et al. (2003) J Biol Chem 278, 51841-50. Storage 8. Kabeya, Y. et al. (2004) J Cell Sci 117, 2805-12. 9. Tanida, I. et al. (2004) J Biol Chem 279, 36268-76. Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% 10. Fujita, N. et al. (2008) Mol Biol Cell 19, 4651-9. glycerol. Store at –20°C. Do not aliquot the antibody. 11. Fujita, N. et al. (2009) Autophagy 5, 88-9. Specificity / Sensitivity Atg4B Antibody detects endogenous levels of total Atg4B protein. This antibody detects a band at ~27 kDa of unknown origin. Species Reactivity: Human, Mouse, Rat Source / Purification Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Ser372 of human Atg4B protein. -
The Role of the Mtor Pathway in Developmental Reprogramming Of
THE ROLE OF THE MTOR PATHWAY IN DEVELOPMENTAL REPROGRAMMING OF HEPATIC LIPID METABOLISM AND THE HEPATIC TRANSCRIPTOME AFTER EXPOSURE TO 2,2',4,4'- TETRABROMODIPHENYL ETHER (BDE-47) An Honors Thesis Presented By JOSEPH PAUL MCGAUNN Approved as to style and content by: ________________________________________________________** Alexander Suvorov 05/18/20 10:40 ** Chair ________________________________________________________** Laura V Danai 05/18/20 10:51 ** Committee Member ________________________________________________________** Scott C Garman 05/18/20 10:57 ** Honors Program Director ABSTRACT An emerging hypothesis links the epidemic of metabolic diseases, such as non-alcoholic fatty liver disease (NAFLD) and diabetes with chemical exposures during development. Evidence from our lab and others suggests that developmental exposure to environmentally prevalent flame-retardant BDE47 may permanently reprogram hepatic lipid metabolism, resulting in an NAFLD-like phenotype. Additionally, we have demonstrated that BDE-47 alters the activity of both mTOR complexes (mTORC1 and 2) in hepatocytes. The mTOR pathway integrates environmental information from different signaling pathways, and regulates key cellular functions such as lipid metabolism, innate immunity, and ribosome biogenesis. Thus, we hypothesized that the developmental effects of BDE-47 on liver lipid metabolism are mTOR-dependent. To assess this, we generated mice with liver-specific deletions of mTORC1 or mTORC2 and exposed these mice and their respective controls perinatally to -
Nuclear Receptor Binding Protein 1 Regulates Intestinal Progenitor Cell Homeostasis and Tumour Formation
Edinburgh Research Explorer Nuclear receptor binding protein 1 regulates intestinal progenitor cell homeostasis and tumour formation Citation for published version: Wilson, CH, Crombie, C, van der Weyden, L, Poulogiannis, G, Rust, AG, Pardo, M, Gracia, T, Yu, L, Choudhary, J, Poulin, GB, McIntyre, RE, Winton, DJ, March, HN, Arends, MJ, Fraser, AG & Adams, DJ 2012, 'Nuclear receptor binding protein 1 regulates intestinal progenitor cell homeostasis and tumour formation', EMBO Journal, vol. 31, no. 11, pp. 2486-97. https://doi.org/10.1038/emboj.2012.91 Digital Object Identifier (DOI): 10.1038/emboj.2012.91 Link: Link to publication record in Edinburgh Research Explorer Document Version: Publisher's PDF, also known as Version of record Published In: EMBO Journal Publisher Rights Statement: This is an openaccess article distributed under the terms of the Creative Commons Attribution License, which permits distribution, and reproduction in any medium, provided the original author and source are credited. This license does not permit commercial exploitation without specific permission. General rights Copyright for the publications made accessible via the Edinburgh Research Explorer is retained by the author(s) and / or other copyright owners and it is a condition of accessing these publications that users recognise and abide by the legal requirements associated with these rights. Take down policy The University of Edinburgh has made every reasonable effort to ensure that Edinburgh Research Explorer content complies with UK legislation. If you believe that the public display of this file breaches copyright please contact [email protected] providing details, and we will remove access to the work immediately and investigate your claim. -
(MMP-9) in Oral Cancer Squamous Cells—Are There Therapeutical Hopes?
materials Article Lutein Treatment Effects on the Redox Status and Metalloproteinase-9 (MMP-9) in Oral Cancer Squamous Cells—Are There Therapeutical Hopes? 1 2,3 4 1 Dan Alexandru Enăs, escu , Mihaela Georgeta Moisescu , Marina Imre , Maria Greabu , Alexandra Ripszky Totan 1,* , Iulia Stanescu-Spinu 1, Marian Burcea 5, Crenguta Albu 6,* and Daniela Miricescu 1 1 Department of Biochemistry, Faculty of Dental Medicine, University of Medicine and Pharmacy Carol Davila, 8 Eroii Sanitari Blvd., Sector 5, 050474 Bucharest, Romania; [email protected] (D.A.E.); [email protected] (M.G.); [email protected] (I.S.-S.); [email protected] (D.M.) 2 Department Biophysics and Cellular Biotechnology, University of Medicine and Pharmacy Carol Davila, 8 Eroii Sanitari Blvd., Sector 5, 050474 Bucharest, Romania; [email protected] 3 Excellence Centre for Research in Biophysics and Cellular Biotechnology, University of Medicine and Pharmacy Carol Davila, 8 Eroii Sanitari Blvd., Sector 5, 050474 Bucharest, Romania 4 Department of Complete Denture, Faculty of Dental Medicine, Carol Davila University of Medicine and Pharmacy, 8 Eroii Sanitari Blvd., Sector 5, 050474 Bucharest, Romania; [email protected] 5 Department of Ophthalmology, Faculty of General Medicine, University of Medicine and Pharmacy Carol Davila, 8 Eroilor Sanitari Blvd., 050474 Bucharest, Romania; [email protected] 6 Department of Genetics, Faculty of General Medicine, University of Medicine and Pharmacy Carol Davila, 8 Eroilor Sanitari Blvd., 050474 Bucharest, Romania * Correspondence: [email protected] (A.R.T.); [email protected] (C.A.) Citation: En˘as, escu, D.A.; Moisescu, M.G.; Imre, M.; Greabu, M.; Ripszky Totan, A.; Stanescu-Spinu, I.; Burcea, Abstract: Carotenoids loaded in nanoparticles should be regarded as a promising way to increase M.; Albu, C.; Miricescu, D. -
A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated. -
Datasheet: AHP2440 Product Details
Datasheet: AHP2440 Description: RABBIT ANTI ATG4B Specificity: ATG4B Format: Purified Product Type: Polyclonal Antibody Isotype: Polyclonal IgG Quantity: 50 µl Product Details Applications This product has been reported to work in the following applications. This information is derived from testing within our laboratories, peer-reviewed publications or personal communications from the originators. Please refer to references indicated for further information. For general protocol recommendations, please visit www.bio- rad-antibodies.com/protocols. Yes No Not Determined Suggested Dilution Western Blotting 1/500 - 1/2000 Where this product has not been tested for use in a particular technique this does not necessarily exclude its use in such procedures. Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own system using appropriate negative/positive controls. Target Species Human Product Form Purified IgG - liquid Antiserum Preparation Antiserum to ATG4B was raised by repeated immunization of rabbits with highly purified antigen. Purified IgG was prepared from whole serum by affinity chromatography. Buffer Solution Phosphate buffered saline Preservative 0.02% Sodium Azide Stabilisers 50% Glycerol Immunogen Recombinant human ATG4B External Database Links UniProt: Q9Y4P1 Related reagents Entrez Gene: 23192 ATG4B Related reagents Page 1 of 2 Synonyms APG4B, AUTL1, KIAA0943 Specificity Rabbit anti ATG4B antibody recognizes the cysteine protease ATG4B, also known as AUT-like 1 cysteine endopeptidase, autophagin-1, autophagy-related cysteine endopeptidase 1 or autophagy-related protein 4 homolog B. ATG4B is a member of the cysteine protease family. ATG4B plays an important role in autophagosome formation. Western Blotting Rabbit anti ATG4B antibody detects a band of approximately 44 kDa in cell lysates under reducing conditions Storage Store at -20oC Storage in frost-free freezers is not recommended. -
4-6 Weeks Old Female C57BL/6 Mice Obtained from Jackson Labs Were Used for Cell Isolation
Methods Mice: 4-6 weeks old female C57BL/6 mice obtained from Jackson labs were used for cell isolation. Female Foxp3-IRES-GFP reporter mice (1), backcrossed to B6/C57 background for 10 generations, were used for the isolation of naïve CD4 and naïve CD8 cells for the RNAseq experiments. The mice were housed in pathogen-free animal facility in the La Jolla Institute for Allergy and Immunology and were used according to protocols approved by the Institutional Animal Care and use Committee. Preparation of cells: Subsets of thymocytes were isolated by cell sorting as previously described (2), after cell surface staining using CD4 (GK1.5), CD8 (53-6.7), CD3ε (145- 2C11), CD24 (M1/69) (all from Biolegend). DP cells: CD4+CD8 int/hi; CD4 SP cells: CD4CD3 hi, CD24 int/lo; CD8 SP cells: CD8 int/hi CD4 CD3 hi, CD24 int/lo (Fig S2). Peripheral subsets were isolated after pooling spleen and lymph nodes. T cells were enriched by negative isolation using Dynabeads (Dynabeads untouched mouse T cells, 11413D, Invitrogen). After surface staining for CD4 (GK1.5), CD8 (53-6.7), CD62L (MEL-14), CD25 (PC61) and CD44 (IM7), naïve CD4+CD62L hiCD25-CD44lo and naïve CD8+CD62L hiCD25-CD44lo were obtained by sorting (BD FACS Aria). Additionally, for the RNAseq experiments, CD4 and CD8 naïve cells were isolated by sorting T cells from the Foxp3- IRES-GFP mice: CD4+CD62LhiCD25–CD44lo GFP(FOXP3)– and CD8+CD62LhiCD25– CD44lo GFP(FOXP3)– (antibodies were from Biolegend). In some cases, naïve CD4 cells were cultured in vitro under Th1 or Th2 polarizing conditions (3, 4). -
Interactions Between the Parasite Philasterides Dicentrarchi and the Immune System of the Turbot Scophthalmus Maximus.A Transcriptomic Analysis
biology Article Interactions between the Parasite Philasterides dicentrarchi and the Immune System of the Turbot Scophthalmus maximus.A Transcriptomic Analysis Alejandra Valle 1 , José Manuel Leiro 2 , Patricia Pereiro 3 , Antonio Figueras 3 , Beatriz Novoa 3, Ron P. H. Dirks 4 and Jesús Lamas 1,* 1 Department of Fundamental Biology, Institute of Aquaculture, Campus Vida, University of Santiago de Compostela, 15782 Santiago de Compostela, Spain; [email protected] 2 Department of Microbiology and Parasitology, Laboratory of Parasitology, Institute of Research on Chemical and Biological Analysis, Campus Vida, University of Santiago de Compostela, 15782 Santiago de Compostela, Spain; [email protected] 3 Institute of Marine Research, Consejo Superior de Investigaciones Científicas-CSIC, 36208 Vigo, Spain; [email protected] (P.P.); antoniofi[email protected] (A.F.); [email protected] (B.N.) 4 Future Genomics Technologies, Leiden BioScience Park, 2333 BE Leiden, The Netherlands; [email protected] * Correspondence: [email protected]; Tel.: +34-88-181-6951; Fax: +34-88-159-6904 Received: 4 September 2020; Accepted: 14 October 2020; Published: 15 October 2020 Simple Summary: Philasterides dicentrarchi is a free-living ciliate that causes high mortality in marine cultured fish, particularly flatfish, and in fish kept in aquaria. At present, there is still no clear picture of what makes this ciliate a fish pathogen and what makes fish resistant to this ciliate. In the present study, we used transcriptomic techniques to evaluate the interactions between P. dicentrarchi and turbot leucocytes during the early stages of infection. The findings enabled us to identify some parasite genes/proteins that may be involved in virulence and host resistance, some of which may be good candidates for inclusion in fish vaccines.