DOCSLIB.ORG

RASAL2 CRISPR/Cas9 KO Plasmid (M): Sc-432636

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
RASAL2 CRISPR/Cas9 KO Plasmid (M): Sc-432636 SANTA CRUZ BIOTECHNOLOGY, INC. RASAL2 CRISPR/Cas9 KO Plasmid (m): sc-432636 BACKGROUND APPLICATIONS The Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) and RASAL2 CRISPR/Cas9 KO Plasmid (m) is recommended for the disruption of CRISPR-associated protein (Cas9) system is an adaptive immune response gene expression in mouse cells. defense mechanism used by archea and bacteria for the degradation of foreign genetic material (4,6). This mechanism can be repurposed for other 20 nt non-coding RNA sequence: guides Cas9 functions, including genomic engineering for mammalian systems, such as to a specific target location in the genomic DNA gene knockout (KO) (1,2,3,5). CRISPR/Cas9 KO Plasmid products enable the U6 promoter: drives gRNA scaffold: helps Cas9 identification and cleavage of specific genes by utilizing guide RNA (gRNA) expression of gRNA bind to target DNA sequences derived from the Genome-scale CRISPR Knock-Out (GeCKO) v2 library developed in the Zhang Laboratory at the Broad Institute (3,5). Termination signal Green Fluorescent Protein: to visually REFERENCES verify transfection CRISPR/Cas9 Knockout Plasmid CBh (chicken β-Actin 1. Cong, L., et al. 2013. Multiplex genome engineering using CRISPR/Cas hybrid) promoter: drives expression of Cas9 systems. Science 339: 819-823. 2A peptide: allows production of both Cas9 and GFP from the 2. Mali, P., et al. 2013. RNA-guided human genome engineering via Cas9. same CBh promoter Science 339: 823-826. Nuclear localization signal 3. Ran, F.A., et al. 2013. Genome engineering using the CRISPR-Cas9 system. Nuclear localization signal SpCas9 ribonuclease Nat. Protoc. 8: 2281-2308. 4. Van der Oost, J., et al. 2014. Unraveling the structural and mechanistic gRNA gRNA gRNA basis of CRISPR-Cas systems. Nat. Rev. Microbiol. 7: 479-492. Plasmid Plasmid Plasmid 1 2 3 5. Shalem, O., et al. 2014. Genome-scale CRISPR-Cas9 knockout screening in human cells. Science 343: 84-87. 6. Hsu, P., et al. 2014. Development and applications of CRISPR-Cas9 for Targeted DNA genome editing. Cell 157: 1262-1278. SUPPORT REAGENTS CHROMOSOMAL LOCATION For optimal reaction efficiency with CRISPR/Cas9 KO Plasmids, Santa Cruz Genetic locus: Rasal2 (mouse) mapping to 1 H1. Biotechnology’s UltraCruz® Transfection Reagent: sc-395739 (0.2 ml) and Plasmid Transfection Medium: sc-108062 (20 ml) are recommended. Control PRODUCT CRISPR/Cas9 Plasmid: sc-418922 (20 µg) negative control is also available. RASAL2 CRISPR/Cas9 KO Plasmid (m) is designed to disrupt gene expression by causing a double-strand break (DSB) in a 5' constitutive exon within the GENE EXPRESSION MONITORING Rasal2 (mouse) gene. RASAL2 (B-11): sc-390605 is recommended as a control antibody for moni- RASAL2 CRISPR/Cas9 KO Plasmid (m) consists of a pool of 3 plasmids, each toring of Rasal2 (mouse) gene expression prior to and after knockout by encoding the Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) Western blotting (starting dilution 1:200, dilution range 1:100-1:1000) or designed for maximum knockout efficiency. Each vial contains 20 µg of immunofluorescence (starting dilution 1:50, dilution range 1:50-1:500). lyophilized CRISPR/Cas9 Plasmid DNA. Suitable for up to 20 transfections. Also see RASAL2 HDR Plasmid (m): sc-432636-HDR for selection of cells RESEARCH USE containing a DSB induced by RASAL2 CRISPR/Cas9 KO Plasmid (m). The CRISPR/Cas9 KO Plasmids are considered “Licensed Products” and are to be used in accordance with the Limited License stated on STORAGE AND RESUSPENSION www.scbt.com/limitedlicense. Store lyophilized plasmid DNA at 4° C with desiccant. Stable for at least one The purchase of this product conveys to the buyer the nontransferable right year from the date of shipment. Once resuspended, store at 4° C for short term to use the purchased amount of the product and all replicates and derivatives storage or -20° C for long-term storage. Avoid repeated freeze thaw cycles. for research purposes conducted by the buyer in his laboratory only (whether Resuspend lyophilized plasmid DNA in 200 µl of the provided ultrapure, sterile, the buyer is an academic or for-profit entity). The buyer cannot sell or other- DNase-free water. Resuspension of the plasmid DNA makes a 0.1 µg/µl wise transfer (a) this product (b) its components or (c) materials made using solution in a 10 mM TRIS EDTA, 1 mM EDTA buffered solution. this product or its components to a third party, or otherwise use this product or its components or materials made using this product or its components for Commercial Purposes. Santa Cruz Biotechnology, Inc. 1.800.457.3801 831.457.3800 fax 831.457.3801 Europe +00800 4573 8000 49 6221 4503 0 www.scbt.com.
Load more

Recommended publications
  • Snotarget Shows That Human Orphan Snorna Targets Locate Close to Alternative Splice Junctions
    Available online at www.sciencedirect.com Gene 408 (2008) 172–179 www.elsevier.com/locate/gene snoTARGET shows that human orphan snoRNA targets locate close to alternative splice junctions Peter S. Bazeley a, Valery Shepelev b, Zohreh Talebizadeh c, Merlin G. Butler c, Larisa Fedorova d, ⁎ Vadim Filatov e, Alexei Fedorov a,d, a Program in Bioinformatics and Proteomics/Genomics, University of Toledo Health Science Campus, Toledo, OH 43614, USA b Department of Bioinformatics, Institute of Molecular Genetics, RAS, Moscow 123182, Russia c Section of Medical Genetics and Molecular Medicine, Children's Mercy Hospitals and Clinics and University of Missouri, Kansas City School of Medicine, Kansas City, MO, USA d Department of Medicine, University of Toledo Health Science Campus, Toledo, OH 43614, USA e Dinom LLC, 8/44 Pedagogicheskaya st., Moscow 115404, Russia Received 31 July 2007; received in revised form 19 October 2007; accepted 24 October 2007 Available online 21 November 2007 Received by Takashi Gojobori Abstract Among thousands of non-protein-coding RNAs which have been found in humans, a significant group represents snoRNA molecules that guide other types of RNAs to specific chemical modifications, cleavages, or proper folding. Yet, hundreds of mammalian snoRNAs have unknown function and are referred to as “orphan” molecules. In 2006, for the first time, it was shown that a particular orphan snoRNA (HBII-52) plays an important role in the regulation of alternative splicing of the serotonin receptor gene in humans and other mammals. In order to facilitate the investigation of possible involvement of snoRNAs in the regulation of pre-mRNA processing, we developed a new computational web resource, snoTARGET, which searches for possible guiding sites for snoRNAs among the entire set of human and rodent exonic and intronic sequences.
    [Show full text]
  • Genetic and Genomic Analysis of Hyperlipidemia, Obesity and Diabetes Using (C57BL/6J × TALLYHO/Jngj) F2 Mice
    University of Tennessee, Knoxville TRACE: Tennessee Research and Creative Exchange Nutrition Publications and Other Works Nutrition 12-19-2010 Genetic and genomic analysis of hyperlipidemia, obesity and diabetes using (C57BL/6J × TALLYHO/JngJ) F2 mice Taryn P. Stewart Marshall University Hyoung Y. Kim University of Tennessee - Knoxville, [email protected] Arnold M. Saxton University of Tennessee - Knoxville, [email protected] Jung H. Kim Marshall University Follow this and additional works at: https://trace.tennessee.edu/utk_nutrpubs Part of the Animal Sciences Commons, and the Nutrition Commons Recommended Citation BMC Genomics 2010, 11:713 doi:10.1186/1471-2164-11-713 This Article is brought to you for free and open access by the Nutrition at TRACE: Tennessee Research and Creative Exchange. It has been accepted for inclusion in Nutrition Publications and Other Works by an authorized administrator of TRACE: Tennessee Research and Creative Exchange. For more information, please contact [email protected]. Stewart et al. BMC Genomics 2010, 11:713 http://www.biomedcentral.com/1471-2164/11/713 RESEARCH ARTICLE Open Access Genetic and genomic analysis of hyperlipidemia, obesity and diabetes using (C57BL/6J × TALLYHO/JngJ) F2 mice Taryn P Stewart1, Hyoung Yon Kim2, Arnold M Saxton3, Jung Han Kim1* Abstract Background: Type 2 diabetes (T2D) is the most common form of diabetes in humans and is closely associated with dyslipidemia and obesity that magnifies the mortality and morbidity related to T2D. The genetic contribution to human T2D and related metabolic disorders is evident, and mostly follows polygenic inheritance. The TALLYHO/ JngJ (TH) mice are a polygenic model for T2D characterized by obesity, hyperinsulinemia, impaired glucose uptake and tolerance, hyperlipidemia, and hyperglycemia.
    [Show full text]
  • Rabbit Anti-RASAL2/FITC Conjugated Antibody-SL21160R-FITC
    SunLong Biotech Co.,LTD Tel: 0086-571- 56623320 Fax:0086-571- 56623318 E-mail:[email protected] www.sunlongbiotech.com Rabbit Anti-RASAL2/FITC Conjugated antibody SL21160R-FITC Product Name: Anti-RASAL2/FITC Chinese Name: FITC标记的RASAL2蛋白抗体 nGAP; NGAP_HUMAN; Ras GTPase-activating protein nGAP; Ras protein activator Alias: like 1; RAS protein activator-like 2; RASAL2. Organism Species: Rabbit Clonality: Polyclonal React Species: Human, ICC=1:50-200IF=1:50-200 Applications: not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. Molecular weight: 129kDa Form: Lyophilized or Liquid Concentration: 2mg/1ml immunogen: KLH conjugated synthetic peptide derived from human RASAL2 Lsotype: IgG Purification: affinity purified by Protein A Storage Buffer: 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol. Storewww.sunlongbiotech.com at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year Storage: when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C. background: This gene encodes a protein that contains the GAP-related domain (GRD), a characteristic domain of GTPase-activating proteins (GAPs). GAPs function as activators of Ras superfamily of small GTPases. The protein encoded by this gene is Product Detail: able to complement the defective RasGAP function in a yeast system. Two alternatively spliced transcript variants of this gene encoding distinct isoforms have been reported.
    [Show full text]
  • Article Characterization of HMGB1/2 Interactome in Prostate Cancer by Yeast Two Hybrid Approach: Potential Pathobiological Implications
    Article Characterization of HMGB1/2 Interactome in Prostate Cancer by Yeast Two Hybrid Approach: Potential Pathobiological Implications Aida Barreiro-Alonso 1,†, María Cámara-Quílez 1,†, Martín Salamini-Montemurri 1, Mónica Lamas- Maceiras 1, Ángel Vizoso-Vázquez 1, Esther Rodríguez-Belmonte 1, María Quindós-Varela 2, Olaia Martínez-Iglesias 3, Angélica Figueroa 3 and María-Esperanza Cerdán 1,* Table S1. Association of proteins that interact with Hmgb1 or Hmgb2 to cancer hallmarks. Cancer Hallmark Protein Model Reference MAP1B Colorectal cancers [109] GENOMIC INSTABILITY AND Liver adenocarcinoma (SKHep1) and NOP53 [110] MUTATIONS/ CHANGES IN glioblastoma (T98G) cell lines TELOMERASE ACTIVITY RSF1 Ovarian cells [111] SRSF3 Ovarian cancer [112] C1QBP Breast cancer [54,113] cFOS Bladder cancer [114] cFOS Breast cancer [115] DLAT Gastric Cancer [116] Human melanoma (A7), Prostate cancer FLNA [117] (PC3) cell lines GOLM1 Hepatocellular carcinoma [118] GOLM1 Breast cancer [119] GOLM1 Lung proliferation [120] GOLM1 Prostate cancer [82] SUSTAINING PROLIFERATIVE Hox-A10 Prostate cancer cell line PC-3 [58] SIGNALLING/ CELL Hox-A10 Ovarian cancer cell lines [121,122] PROLIFERATION NOP53 Breast cancer [123] PSMA7 Cervical cancer [124] PTPN2 Epithelial carcinogenesis [125] RASAL2 hepatocellular carcinoma [126] RSF1 Prostate cancer [95] RSF1 Nasopharyngeal carcinoma [127] SPIN1 Glioma [128] TGM3 Esophageal cancer [129] UBE2E3 Retinal pigment epithelial (RPE) [130] Vigilin Hepatocellular carcinomas [131] WNK4 Kidney [100] C1QBP Prostate cancer [48]
    [Show full text]
  • A High-Throughput Approach to Uncover Novel Roles of APOBEC2, a Functional Orphan of the AID/APOBEC Family
    Rockefeller University Digital Commons @ RU Student Theses and Dissertations 2018 A High-Throughput Approach to Uncover Novel Roles of APOBEC2, a Functional Orphan of the AID/APOBEC Family Linda Molla Follow this and additional works at: https://digitalcommons.rockefeller.edu/ student_theses_and_dissertations Part of the Life Sciences Commons A HIGH-THROUGHPUT APPROACH TO UNCOVER NOVEL ROLES OF APOBEC2, A FUNCTIONAL ORPHAN OF THE AID/APOBEC FAMILY A Thesis Presented to the Faculty of The Rockefeller University in Partial Fulfillment of the Requirements for the degree of Doctor of Philosophy by Linda Molla June 2018 © Copyright by Linda Molla 2018 A HIGH-THROUGHPUT APPROACH TO UNCOVER NOVEL ROLES OF APOBEC2, A FUNCTIONAL ORPHAN OF THE AID/APOBEC FAMILY Linda Molla, Ph.D. The Rockefeller University 2018 APOBEC2 is a member of the AID/APOBEC cytidine deaminase family of proteins. Unlike most of AID/APOBEC, however, APOBEC2’s function remains elusive. Previous research has implicated APOBEC2 in diverse organisms and cellular processes such as muscle biology (in Mus musculus), regeneration (in Danio rerio), and development (in Xenopus laevis). APOBEC2 has also been implicated in cancer. However the enzymatic activity, substrate or physiological target(s) of APOBEC2 are unknown. For this thesis, I have combined Next Generation Sequencing (NGS) techniques with state-of-the-art molecular biology to determine the physiological targets of APOBEC2. Using a cell culture muscle differentiation system, and RNA sequencing (RNA-Seq) by polyA capture, I demonstrated that unlike the AID/APOBEC family member APOBEC1, APOBEC2 is not an RNA editor. Using the same system combined with enhanced Reduced Representation Bisulfite Sequencing (eRRBS) analyses I showed that, unlike the AID/APOBEC family member AID, APOBEC2 does not act as a 5-methyl-C deaminase.
    [Show full text]
  • Epigenetic Changes in Fibroblasts Drive Cancer Metabolism and Differentiation
    26 12 Endocrine-Related R Mishra et al. TME based epigenetic targets 26:12 R673–R688 Cancer in cancer REVIEW Epigenetic changes in fibroblasts drive cancer metabolism and differentiation Rajeev Mishra1, Subhash Haldar2, Surabhi Suchanti1 and Neil A Bhowmick3,4 1Department of Biosciences, Manipal University Jaipur, Jaipur, Rajasthan, India 2Department of Biotechnology, Brainware University, Kolkata, India 3Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA 4Department of Research, Greater Los Angeles Veterans Administration, Los Angeles, California, USA Correspondence should be addressed to N A Bhowmick: [email protected] Abstract Genomic changes that drive cancer initiation and progression contribute to the Key Words co-evolution of the adjacent stroma. The nature of the stromal reprogramming involves f endocrine therapy differential DNA methylation patterns and levels that change in response to the tumor resistance and systemic therapeutic intervention. Epigenetic reprogramming in carcinoma- f prostate associated fibroblasts are robust biomarkers for cancer progression and have a f neuroendocrine tumors transcriptional impact that support cancer epithelial progression in a paracrine manner. For prostate cancer, promoter hypermethylation and silencing of the RasGAP, RASAL3 that resulted in the activation of Ras signaling in carcinoma-associated fibroblasts. Stromal Ras activity initiated a process of macropinocytosis that provided prostate cancer epithelia with abundant glutamine for metabolic conversion
    [Show full text]
  • RASAL2 Promotes Tumor Progression Through LATS2/YAP1 Axis of Hippo
    Pan et al. Molecular Cancer (2018) 17:102 https://doi.org/10.1186/s12943-018-0853-6 RESEARCH Open Access RASAL2 promotes tumor progression through LATS2/YAP1 axis of hippo signaling pathway in colorectal cancer Yi Pan1,2,3†, Joanna Hung Man Tong1,2,3†, Raymond Wai Ming Lung1,2,3, Wei Kang1,2,3, Johnny Sheung Him Kwan1,2, Wing Po Chak1,2,3, Ka Yee Tin1,2, Lau Ying Chung1,2,3, Feng Wu1,2,3, Simon Siu Man Ng3,4, Tony Wing Chung Mak4, Jun Yu3,5, Kwok Wai Lo1,2, Anthony Wing Hung Chan1,2* and Ka Fai To1,2,3* Abstract Background: Patients with colorectal cancer (CRC) have a high incidence of regional and distant metastases. Although metastasis is the main cause of CRC-related death, its molecular mechanisms remain largely unknown. Methods: Using array-CGH and expression microarray analyses, changes in DNA copy number and mRNA expression levels were investigated in human CRC samples. The mRNA expression level of RASAL2 was validated by qRT-PCR, and the protein expression was evaluated by western blot as well as immunohistochemistry in CRC cell lines and primary tumors. The functional role of RASAL2 in CRC was determined by MTT proliferation assay, monolayer and soft agar colony formation assays, cell cycle analysis, cell invasion and migration and in vivo study through siRNA/shRNA mediated knockdown and overexpression assays. Identification of RASAL2 involved in hippo pathway was achieved by expression microarray screening, double immunofluorescence staining and co-immunoprecipitation assays. Results: Integrated genomic analysis identified copy number gains and upregulation of RASAL2 in metastatic CRC.
    [Show full text]
  • RASAL2 (B-11): Sc-390605
    SANTA CRUZ BIOTECHNOLOGY, INC. RASAL2 (B-11): sc-390605 BACKGROUND RECOMMENDED SUPPORT REAGENTS RASAL2 (Ras protein activator like 2), also known as nGAP, is a Ras GTPase- To ensure optimal results, the following support reagents are recommended: activating protein. RAS proteins cycle between an active guanosine-triphos- 1) Western Blotting: use m-IgGκ BP-HRP: sc-516102 or m-IgGκ BP-HRP (Cruz phate (GTP) bound form and an inactive, guanosine-diphosphate (GDP) bound Marker): sc-516102-CM (dilution range: 1:1000-1:10000), Cruz Marker™ form. GTPase-activating proteins (GAPs) accelerate the intrinsic rate of GTP Molecular Weight Standards: sc-2035, UltraCruz® Blocking Reagent: hydrolysis of Ras-related proteins, resulting in downregulation of their active sc-516214 and Western Blotting Luminol Reagent: sc-2048. 2) Immunopre- form. RASAL2 functions in the Ras/MAPK/ERK signaling pathway. It contains cipitation: use Protein A/G PLUS-Agarose: sc-2003 (0.5 ml agarose/2.0 ml). a C2 domain, a PH domain and a Ras-GAP domain. The gene encoding RASAL2 3) Immunofluorescence: use m-IgGκ BP-FITC: sc-516140 or m-IgGκ BP-PE: is located on chromosome 1 within the prostate cancer susceptibility locus. sc-516141 (dilution range: 1:50-1:200) with UltraCruz® Mounting Medium: This suggests that a mutation or defect in RASAL2 is implicated in carcino- sc-24941 or UltraCruz® Hard-set Mounting Medium: sc-359850. 4) Immuno- genesis. Two transcript variants exist for RASAL2 due to alternative splicing histochemistry: use m-IgGκ BP-HRP: sc-516102 with DAB, 50X: sc-24982 events. and Immunohistomount: sc-45086, or Organo/Limonene Mount: sc-45087.
    [Show full text]
  • Quantitative Trait Loci Mapping of Macrophage Atherogenic Phenotypes
    QUANTITATIVE TRAIT LOCI MAPPING OF MACROPHAGE ATHEROGENIC PHENOTYPES BRIAN RITCHEY Bachelor of Science Biochemistry John Carroll University May 2009 submitted in partial fulfillment of requirements for the degree DOCTOR OF PHILOSOPHY IN CLINICAL AND BIOANALYTICAL CHEMISTRY at the CLEVELAND STATE UNIVERSITY December 2017 We hereby approve this thesis/dissertation for Brian Ritchey Candidate for the Doctor of Philosophy in Clinical-Bioanalytical Chemistry degree for the Department of Chemistry and the CLEVELAND STATE UNIVERSITY College of Graduate Studies by ______________________________ Date: _________ Dissertation Chairperson, Johnathan D. Smith, PhD Department of Cellular and Molecular Medicine, Cleveland Clinic ______________________________ Date: _________ Dissertation Committee member, David J. Anderson, PhD Department of Chemistry, Cleveland State University ______________________________ Date: _________ Dissertation Committee member, Baochuan Guo, PhD Department of Chemistry, Cleveland State University ______________________________ Date: _________ Dissertation Committee member, Stanley L. Hazen, MD PhD Department of Cellular and Molecular Medicine, Cleveland Clinic ______________________________ Date: _________ Dissertation Committee member, Renliang Zhang, MD PhD Department of Cellular and Molecular Medicine, Cleveland Clinic ______________________________ Date: _________ Dissertation Committee member, Aimin Zhou, PhD Department of Chemistry, Cleveland State University Date of Defense: October 23, 2017 DEDICATION I dedicate this work to my entire family. In particular, my brother Greg Ritchey, and most especially my father Dr. Michael Ritchey, without whose support none of this work would be possible. I am forever grateful to you for your devotion to me and our family. You are an eternal inspiration that will fuel me for the remainder of my life. I am extraordinarily lucky to have grown up in the family I did, which I will never forget.
    [Show full text]
  • Supplementary Table 1 Double Treatment Vs Single Treatment
    Supplementary table 1 Double treatment vs single treatment Probe ID Symbol Gene name P value Fold change TC0500007292.hg.1 NIM1K NIM1 serine/threonine protein kinase 1.05E-04 5.02 HTA2-neg-47424007_st NA NA 3.44E-03 4.11 HTA2-pos-3475282_st NA NA 3.30E-03 3.24 TC0X00007013.hg.1 MPC1L mitochondrial pyruvate carrier 1-like 5.22E-03 3.21 TC0200010447.hg.1 CASP8 caspase 8, apoptosis-related cysteine peptidase 3.54E-03 2.46 TC0400008390.hg.1 LRIT3 leucine-rich repeat, immunoglobulin-like and transmembrane domains 3 1.86E-03 2.41 TC1700011905.hg.1 DNAH17 dynein, axonemal, heavy chain 17 1.81E-04 2.40 TC0600012064.hg.1 GCM1 glial cells missing homolog 1 (Drosophila) 2.81E-03 2.39 TC0100015789.hg.1 POGZ Transcript Identified by AceView, Entrez Gene ID(s) 23126 3.64E-04 2.38 TC1300010039.hg.1 NEK5 NIMA-related kinase 5 3.39E-03 2.36 TC0900008222.hg.1 STX17 syntaxin 17 1.08E-03 2.29 TC1700012355.hg.1 KRBA2 KRAB-A domain containing 2 5.98E-03 2.28 HTA2-neg-47424044_st NA NA 5.94E-03 2.24 HTA2-neg-47424360_st NA NA 2.12E-03 2.22 TC0800010802.hg.1 C8orf89 chromosome 8 open reading frame 89 6.51E-04 2.20 TC1500010745.hg.1 POLR2M polymerase (RNA) II (DNA directed) polypeptide M 5.19E-03 2.20 TC1500007409.hg.1 GCNT3 glucosaminyl (N-acetyl) transferase 3, mucin type 6.48E-03 2.17 TC2200007132.hg.1 RFPL3 ret finger protein-like 3 5.91E-05 2.17 HTA2-neg-47424024_st NA NA 2.45E-03 2.16 TC0200010474.hg.1 KIAA2012 KIAA2012 5.20E-03 2.16 TC1100007216.hg.1 PRRG4 proline rich Gla (G-carboxyglutamic acid) 4 (transmembrane) 7.43E-03 2.15 TC0400012977.hg.1 SH3D19
    [Show full text]
  • Feature Selection for Longitudinal Data by Using Sign Averages to Summarize Gene Expression Values Over Time
    University of Kentucky UKnowledge Biostatistics Faculty Publications Biostatistics 3-19-2019 Feature Selection for Longitudinal Data by Using Sign Averages to Summarize Gene Expression Values over Time Suyan Tian The First Hospital of Jilin University, China, [email protected] Chi Wang University of Kentucky, [email protected] Right click to open a feedback form in a new tab to let us know how this document benefits oy u. Follow this and additional works at: https://uknowledge.uky.edu/biostatistics_facpub Part of the Biostatistics Commons, Computational Biology Commons, Longitudinal Data Analysis and Time Series Commons, and the Microarrays Commons Repository Citation Tian, Suyan and Wang, Chi, "Feature Selection for Longitudinal Data by Using Sign Averages to Summarize Gene Expression Values over Time" (2019). Biostatistics Faculty Publications. 43. https://uknowledge.uky.edu/biostatistics_facpub/43 This Article is brought to you for free and open access by the Biostatistics at UKnowledge. It has been accepted for inclusion in Biostatistics Faculty Publications by an authorized administrator of UKnowledge. For more information, please contact [email protected]. Feature Selection for Longitudinal Data by Using Sign Averages to Summarize Gene Expression Values over Time Notes/Citation Information Published in BioMed Research International, v. 2019, article ID 1724898, p. 1-12. © 2019 Suyan Tian and Chi Wang. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use,
    [Show full text]
  • 82481 RASAL2 (D6K9L) Rabbit Mab
    Revision 1 C 0 2 - t RASAL2 (D6K9L) Rabbit mAb a e r o t S Orders: 877-616-CELL (2355) [email protected] 1 Support: 877-678-TECH (8324) 8 4 Web: [email protected] 2 www.cellsignal.com 8 # 3 Trask Lane Danvers Massachusetts 01923 USA For Research Use Only. Not For Use In Diagnostic Procedures. Applications: Reactivity: Sensitivity: MW (kDa): Source/Isotype: UniProt ID: Entrez-Gene Id: WB, IP H Endogenous 150 Rabbit IgG Q9UJF2 9462 Product Usage Information Application Dilution Western Blotting 1:1000 Immunoprecipitation 1:50 Specificity / Sensitivity RASAL2 (D6K9L) Rabbit mAb recognizes endogenous levels of total RASAL2 protein. Species Reactivity: Human Source / Purification Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro69 of human RASAL2 protein. Background Small GTPases act as molecular switches, regulating processes such as cell migration, adhesion, proliferation and differentiation. They are activated by guanine nucleotide exchange factors (GEFs), which catalyze the exchange of bound GDP for GTP, and inhibited by GTPase activating proteins (GAPs), which catalyze the hydrolysis of GTP to GDP. RASAL2 was initially identified as a GAP for the small GTPase, Ras, and later shown to interact with the Rho-GEF ECT2, and to regulate Rho activity in human astrocytoma cells (1). Researchers have implicated RASAL2 as a suppressor of migration and metastasis in human cancer (2), and have shown that RASAL2 downregulation promotes epithelial- mesenchymal transition and metastasis in ovarian cancer (3) and lung cancer (4). Conversely, other research studies show that RASAL2 can be oncogenic in triple negative breast cancer through activation of Rac1 signaling (5).
    [Show full text]