MRS2 Antibody (N-Term)

Catalog: OM214641 Scan to get more validated information MRS2 Antibody (N-term) Catalog: OM214641 100ug Product profile Product name MRS2 Antibody (N-term) Antibody Type Primary Antibodies Key Feature Clonality Polyclonal Isotype Ig Host Species Rabbit Tested Applications WB ,FC Species Reactivity Human Concentration 1 mg/ml Purification Target Information Gene Synonyms HPT, MRS2L Alternative Names MRS2; HPT; MRS2L; Magnesium transporter MRS2 homolog, mitochondrial; MRS2-like protein Molecular Weight(MW) 50318 Da Function Magnesium transporter that may mediate the influx of magnesium into the mitochondrial matrix Tissue Specificity This MRS2 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide betwe en amino acids 80-110 from the N-terminal region of human MRS2. Cellular Localization Mitochondrion inner membrane; Multi-pass membrane protein (By similarity) Database Links Entrez Gene 57380 Application Application Western blot analysis of MRS2 Antibody (N-term) in mouse liver tissue lysates (35ug/lane). MRS2 (arrow) was detected using the purified Pab. Application MRS2 Antibody (N-term) flow cytometric analysis of MCF-7 cells (right histogram) compared to a negative control cell (left histogram).FITC-conjugated goat-anti- rabbit secondary antibodies were used for the analysis. Application Notes WB~~1:100~500 FC~~1:10~50: Additional Information Form Liquid Storage Instructions For short-term storage, store at 4° C. For long-term storage, aliquot and store at -20ºC or below. Avoid multiple freeze-thaw cycles. Storage Buffer Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified thro ugh a protein A column, followed by peptide affinity purification. Note The product is for research use only,not for use in diagnostic or therapeutic procedures. OmnimAbs.com [email protected] 506 N. GARFIELD AVE # 210 ALHAMBRA, CA 91801 This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.

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(12) Patent Application Publication (10) Pub. No.: US 2005/0010974A1 Milligan Et Al
US 20050010974A1 (19) United States (12) Patent Application Publication (10) Pub. No.: US 2005/0010974A1 Milligan et al. (43) Pub. Date: Jan. 13, 2005 (54) PROMOTERS FOR REGULATION OF GENE Publication Classification EXPRESSION IN PLANT ROOTS (51) Int. Cl." ............................ C12N 15/82; C12O 1/68; (76) Inventors: Stephen B Milligan, Kirkland, WA C12N 15/87; C12N 15/63; (US); Dale Skalla, Research Triangle C12N 15/85; C12N 5/10; Park, NC (US); Kay Lawton, Research C12N 15/09; CO7H 21/04 Triangle Park, NC (US) (52) U.S. Cl. ..................... 800/287; 536/23.6; 435/320.1; 435/455; 435/419; 435/468; Correspondence Address: 800/278; 435/6; 536/24.33 Randee S Schwatz Syngenta Biotechnology 3054 Cornwallis Road (57) ABSTRACT Research Triangle Park, NC 27709 (US) The present invention is directed to promoters isolated from (21) Appl. No.: 10/490,147 maize and functional equivalents thereto. The promoters of the present invention have particular utility in driving root (22) PCT Filed: Nov. 4, 2002 Specific expression of heterologous genes that impart (86) PCT No.: PCT/US02/35374 increased agronomic, horticultural and/or pesticidal charac teristics to a given promoters of the invention and trans (30) Foreign Application Priority Data formed plant tissues containing DNA molecules comprising a promoter of the invention operably linked to a heterolo Nov. 7, 2001 (US)........................................... 60337026 gous gene or genes, and Seeds thereof. US 2005/0010974 A1 Jan. 13, 2005 PROMOTERS FOR REGULATION OF GENE latory Sequences may be short regions of DNA sequence EXPRESSION IN PLANT ROOTS 6-100 base pairs that define the binding sites for trans-acting factors, Such as transcription factors.
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Downloaded and Searched Against the Dbest Database to Identify Ests
BMC Genomics BioMed Central Research article Open Access A transcription map of the 6p22.3 reading disability locus identifying candidate genes Eric R Londin1, Haiying Meng2 and Jeffrey R Gruen*2 Address: 1Graduate Program in Genetics, State University of New York at Stony Brook, NY, USA and 2Yale Child Health Research Center, Department of Pediatrics, Yale University School of Medicine, New Haven, CT, USA Email: Eric R Londin - [email protected]; Haiying Meng - [email protected]; Jeffrey R Gruen* - [email protected] * Corresponding author Published: 30 June 2003 Received: 22 April 2003 Accepted: 30 June 2003 BMC Genomics 2003, 4:25 This article is available from: http://www.biomedcentral.com/1471-2164/4/25 © 2003 Londin et al; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL. reading disabilitydyslexia6p22.3In silicoESTs Abstract Background: Reading disability (RD) is a common syndrome with a large genetic component. Chromosome 6 has been identified in several linkage studies as playing a significant role. A more recent study identified a peak of transmission disequilibrium to marker JA04 (G72384) on chromosome 6p22.3, suggesting that a gene is located near this marker. Results: In silico cloning was used to identify possible candidate genes located near the JA04 marker. The 2 million base pairs of sequence surrounding JA04 was downloaded and searched against the dbEST database to identify ESTs. In total, 623 ESTs from 80 different tissues were identified and assembled into 153 putative coding regions from 19 genes and 2 pseudogenes encoded near JA04.
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Supplementary Data
Supplementary Fig. 1 A B Responder_Xenograft_ Responder_Xenograft_ NON- NON- Lu7336, Vehicle vs Lu7466, Vehicle vs Responder_Xenograft_ Responder_Xenograft_ Sagopilone, Welch- Sagopilone, Welch- Lu7187, Vehicle vs Lu7406, Vehicle vs Test: 638 Test: 600 Sagopilone, Welch- Sagopilone, Welch- Test: 468 Test: 482 Responder_Xenograft_ NON- Lu7860, Vehicle vs Responder_Xenograft_ Sagopilone, Welch - Lu7558, Vehicle vs Test: 605 Sagopilone, Welch- Test: 333 Supplementary Fig. 2 Supplementary Fig. 3 Supplementary Figure S1. Venn diagrams comparing probe sets regulated by Sagopilone treatment (10mg/kg for 24h) between individual models (Welsh Test ellipse p-value<0.001 or 5-fold change). A Sagopilone responder models, B Sagopilone non-responder models. Supplementary Figure S2. Pathway analysis of genes regulated by Sagopilone treatment in responder xenograft models 24h after Sagopilone treatment by GeneGo Metacore; the most significant pathway map representing cell cycle/spindle assembly and chromosome separation is shown, genes upregulated by Sagopilone treatment are marked with red thermometers. Supplementary Figure S3. GeneGo Metacore pathway analysis of genes differentially expressed between Sagopilone Responder and Non-Responder models displaying –log(p-Values) of most significant pathway maps. Supplementary Tables Supplementary Table 1. Response and activity in 22 non-small-cell lung cancer (NSCLC) xenograft models after treatment with Sagopilone and other cytotoxic agents commonly used in the management of NSCLC Tumor Model Response type
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Mclean, Chelsea.Pdf
COMPUTATIONAL PREDICTION AND EXPERIMENTAL VALIDATION OF NOVEL MOUSE IMPRINTED GENES A Dissertation Presented to the Faculty of the Graduate School of Cornell University In Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy by Chelsea Marie McLean August 2009 © 2009 Chelsea Marie McLean COMPUTATIONAL PREDICTION AND EXPERIMENTAL VALIDATION OF NOVEL MOUSE IMPRINTED GENES Chelsea Marie McLean, Ph.D. Cornell University 2009 Epigenetic modifications, including DNA methylation and covalent modifications to histone tails, are major contributors to the regulation of gene expression. These changes are reversible, yet can be stably inherited, and may last for multiple generations without change to the underlying DNA sequence. Genomic imprinting results in expression from one of the two parental alleles and is one example of epigenetic control of gene expression. So far, 60 to 100 imprinted genes have been identified in the human and mouse genomes, respectively. Identification of additional imprinted genes has become increasingly important with the realization that imprinting defects are associated with complex disorders ranging from obesity to diabetes and behavioral disorders. Despite the importance imprinted genes play in human health, few studies have undertaken genome-wide searches for new imprinted genes. These have used empirical approaches, with some success. However, computational prediction of novel imprinted genes has recently come to the forefront. I have developed generalized linear models using data on a variety of sequence and epigenetic features within a training set of known imprinted genes. The resulting models were used to predict novel imprinted genes in the mouse genome. After imposing a stringency threshold, I compiled an initial candidate list of 155 genes.
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Construction of a Radiation Hybrid Map of Chicken Chromosome 2 And
Construction of a radiation hybrid map of chicken chromosome 2 and alignment to the chicken draft sequence Sophie Leroux, Mélanie Dottax, Suzanne Bardes, Florence Vignoles, Katia Feve, Frédérique Pitel, Mireille Morisson, Alain Vignal To cite this version: Sophie Leroux, Mélanie Dottax, Suzanne Bardes, Florence Vignoles, Katia Feve, et al.. Construction of a radiation hybrid map of chicken chromosome 2 and alignment to the chicken draft sequence. BMC Genomics, BioMed Central, 2005, 6, pp.12. 10.1186/1471-2164-6-12. hal-02682366 HAL Id: hal-02682366 https://hal.inrae.fr/hal-02682366 Submitted on 1 Jun 2020 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. BMC Genomics BioMed Central Research article Open Access Construction of a radiation hybrid map of chicken chromosome 2 and alignment to the chicken draft sequence Sophie Leroux*, Mélanie Dottax, Suzanne Bardes, Florence Vignoles, Katia Fève, Frédérique Pitel, Mireille Morisson and Alain Vignal Address: Laboratoire de Génétique Cellulaire, INRA, Castanet-Tolosan, 31326, France Email: Sophie Leroux*
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Ep 2301948 B1
(19) & (11) EP 2 301 948 B1 (12) EUROPEAN PATENT SPECIFICATION (45) Date of publication and mention (51) Int Cl.: of the grant of the patent: C07H 21/04 (2006.01) C12N 15/82 (2006.01) 09.05.2012 Bulletin 2012/19 A01H 5/00 (2006.01) A01H 5/10 (2006.01) (21) Application number: 10172501.8 (22) Date of filing: 04.11.2002 (54) Promoters for regulation of gene expression in plant roots Promotoren zur Regulierung der Genexpression in Pflanzenwurzeln Promoteurs régulant l’expression génique dans les racines de plante (84) Designated Contracting States: (74) Representative: Radkov, Stoyan Atanassov AT BE BG CH CY CZ DE DK EE ES FI FR GB GR Syngenta International AG IE IT LI LU MC NL PT SE SK TR WRO-1004.8.15 Schwarzwaldallee 215 (30) Priority: 07.11.2001 US 337026 P 4058 Basel (CH) (43) Date of publication of application: (56) References cited: 30.03.2011 Bulletin 2011/13 WO-A-00/29594 US-A- 5 837 848 US-B1- 6 207 879 US-B1- 6 232 526 (62) Document number(s) of the earlier application(s) in accordance with Art. 76 EPC: • DATABASE EMBL [Online] 29 March 2002 02789419.5 / 1 537 136 (2002-03-29), "fzmb011f011b09f0 fzmb filtered library Zea mays genomic clone fzmb011f011b09 (73) Proprietor: Syngenta Participations AG 5’, DNA sequence.", XP002602534, retrieved from 4058 Basel (CH) EBI accession no. EMBL:BH775378 Database accession no. BH775378 (72) Inventors: • LU GUIHUA ET AL: "A novel cis-acting element • Milligan, Stephen, B. conferring root-preferred gene expression in Kirkland, WA 98034 (US) maize", JOURNAL OF PLANT PHYSIOLOGY, vol.
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MRS2 Rabbit Polyclonal Antibody – TA338429 | Origene
OriGene Technologies, Inc. 9620 Medical Center Drive, Ste 200 Rockville, MD 20850, US Phone: +1-888-267-4436 [email protected] EU: [email protected] CN: [email protected] Product datasheet for TA338429 MRS2 Rabbit Polyclonal Antibody Product data: Product Type: Primary Antibodies Applications: WB Recommended Dilution: WB Reactivity: Human Host: Rabbit Isotype: IgG Clonality: Polyclonal Immunogen: The immunogen for anti-MRS2 antibody: synthetic peptide directed towards the middle region of human MRS2. Synthetic peptide located within the following region: LDALVDPKHSSVDRSKLHILLQNGKSLSELETDIKIFKESILEILDEEEL Formulation: Liquid. Purified antibody supplied in 1x PBS buffer with 0.09% (w/v) sodium azide and 2% sucrose. Note that this product is shipped as lyophilized powder to China customers. Purification: Affinity Purified Conjugation: Unconjugated Storage: Store at -20°C as received. Stability: Stable for 12 months from date of receipt. Predicted Protein Size: 50 kDa Gene Name: MRS2, magnesium transporter Database Link: NP_065713 Entrez Gene 57380 Human Q9HD23 Background: MRS2 is a magnesium transporter that may mediate the influx of magnesium into the mitochondrial matrix. Synonyms: HPT; MRS2L Note: Immunogen Sequence Homology: Pig: 100%; Rat: 100%; Horse: 100%; Human: 100%; Mouse: 100%; Bovine: 100%; Dog: 93%; Goat: 93%; Rabbit: 93%; Guinea pig: 93% This product is to be used for laboratory only. Not for diagnostic or therapeutic use. View online » ©2021 OriGene Technologies, Inc., 9620 Medical Center Drive, Ste 200, Rockville, MD 20850, US 1 / 2 MRS2 Rabbit Polyclonal Antibody – TA338429 Protein Families: Transcription Factors, Transmembrane Product images: WB Suggested Anti-MRS2 Antibody Titration: 0.2- 1 ug/ml; ELISA Titer: 1: 312500; Positive Control: PANC1 cell lysate This product is to be used for laboratory only.
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MRS2L CRISPR/Cas9 KO Plasmid (M): Sc-436212
SANTA CRUZ BIOTECHNOLOGY, INC. MRS2L CRISPR/Cas9 KO Plasmid (m): sc-436212 BACKGROUND APPLICATIONS The clustered regularly interspaced short palindromic repeats (CRISPR) and MRS2L 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 systems. Science 339: 819-823. 2A peptide: expression of Cas9 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.
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Comparative Gene Expression Analysis to Identify Common Factors in Multiple Cancers
COMPARATIVE GENE EXPRESSION ANALYSIS TO IDENTIFY COMMON FACTORS IN MULTIPLE CANCERS DISSERTATION Presented in Partial Fulfillment of the Requirements for the Degree Doctor of Philosophy in the Graduate School of The Ohio State University By Leszek A. Rybaczyk, B.A. ***** The Ohio State University 2008 Dissertation Committee: Professor Kun Huang, Adviser Professor Jeffery Kuret Approved by Professor Randy Nelson Professor Daniel Janies ------------------------------------------- Adviser Integrated Biomedical Science Graduate Program ABSTRACT Most current cancer research is focused on tissue-specific genetic mutations. Familial inheritance (e.g., APC in colon cancer), genetic mutation (e.g., p53), and overexpression of growth receptors (e.g., Her2-neu in breast cancer) can potentially lead to aberrant replication of a cell. Studies of these changes provide tremendous information about tissue-specific effects but are less informative about common changes that occur in multiple tissues. The similarity in the behavior of cancers from different organ systems and species suggests that a pervasive mechanism drives carcinogenesis, regardless of the specific tissue or species. In order to detect this mechanism, I applied three tiers of analysis at different levels: hypothesis testing on individual pathways to identify significant expression changes within each dataset, intersection of results between different datasets to find common themes across experiments, and Pearson correlations between individual genes to identify correlated genes within each dataset. By comparing a variety of cancers from different tissues and species, I was able to separate tissue and species specific effects from cancer specific effects. I found that downregulation of Monoamine Oxidase A is an indicator of this pervasive mechanism and can potentially be used to detect pathways and functions related to the initiation, promotion, and progression of cancer.
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Breakthroughs in the Search for Dyslexia Candidate Genes
McGrath, L. M., Smith, S. D., Pennington, B. F. (2006). Breakthroughs in the search for dyslexia candidate genes. Trends in Molecular Medicine, 12, 333-341. Breakthroughs in the Search for Dyslexia Candidate Genes Lauren M. McGrath1, Shelley D. Smith2, and Bruce F. Pennington1 1 University of Denver, Department of Psychology, Frontier Hall, 2155 S. Race St., Denver, CO 80208, USA 2 University of Nebraska Medical Center, 985456 Nebraska Medical Center, Omaha, NE 68198-5456, USA Corresponding author: McGrath, L. M. ([email protected]) Keywords: dyslexia, reading disability, candidate genes, linkage, association, DYX1C1, EKN1, ROBO1, DCDC2, KIAA0319. 1 Abstract Four candidate genes for dyslexia, or reading disability (RD), have recently been proposed: DYX1C1, ROBO1, DCDC2, and KIAA0319. Each of the genes is implicated in brain development processes, such as neural migration and axonal guidance, with the exception of DYX1C1 whose function is still unknown. The most immediate clinical prospect of these gene identifications is the possibility of early identification via genetic screening. However, the field has yet to identify a functional mutation in any of the genes, which currently limits this future prospect. When causal variants are identified, they will need to be considered within a multifactorial framework, likely involving gene x gene and gene x environment interactions, in order to make accurate predictions of diagnostic status. 2 Breakthroughs in the Search for Dyslexia Candidate Genes Background Dyslexia, or reading disability (RD), is a complex neurobehavioral disorder affecting approximately 5-10% of school-aged children [1]. A consensus definition of RD was developed in 2002 by the International Dyslexia Association and adopted by the National Institute of Child Health and Human Development (NICHD) (www.interdys.org): “Dyslexia is a specific learning disability that is neurological in origin.
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UC San Francisco Electronic Theses and Dissertations
UCSF UC San Francisco Electronic Theses and Dissertations Title Uncovering virulence pathways facilitated by proteolysis in HIV and a HIV associated fungal pathogen, Cryptococcus neoformans Permalink https://escholarship.org/uc/item/7vv2p2fh Author Clarke, Starlynn Cascade Publication Date 2015 Peer reviewed|Thesis/dissertation eScholarship.org Powered by the California Digital Library University of California ii Acknowledgments I would first like to thank my thesis advisor, Dr. Charles Craik. Throughout my PhD Charly has been unfailingly optimistic and enthusiastic about my projects, but most importantly, he has always had confidence in my abilities. During the course of graduate school I have doubted myself and my capabilities almost daily, but Charly has always believed that I would be successful in my scientific endeavors and I cannot thank him enough for that. Charly is the most enthusiastic scientist that I have ever met and he has the capacity to find a silver lining to almost any event. He also understands the importance of presentation and has the resourcefulness to transform almost any situation into an opportunity. These are all traits that do not come naturally to me, but having Charly as a mentor has helped me to learn some of these important skills. I would also like to thank my thesis committee members, Dr. Raul Andino and Dr. John Gross who have both been incredibly supportive over the years. Despite the fact that my research ended up veering away from the original focus that was more in line with their expertise, they have continued to provide me with encouragement and thoughtful feedback during my thesis committee meetings as well as at other times that I sought their advice.
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DCDC2 Is Associated with Reading Disability and Modulates Neuronal Development in the Brain
Corrections GENETICS. For the article ‘‘DCDC2 is associated with reading NEUROSCIENCE. For the article ‘‘Early age-related cognitive im- disability and modulates neuronal development in the brain,’’ by pairment in mice lacking cannabinoid CB1 receptors,’’ by A. Haiying Meng, Shelley D. Smith, Karl Hager, Matthew Held, Bilkei-Gorzo, I. Racz, O. Valverde, M. Otto, K. Michel, M. Jonathan Liu, Richard K. Olson, Bruce F. Pennington, John C. Sarstre, and A. Zimmer, which appeared in issue 43, October 25, DeFries, Joel Gelernter, Thomas O’Reilly-Pol, Stefan Somlo, 2005, of Proc. Natl. Acad. Sci. USA (102, 15670–15675; first Pawel Skudlarski, Sally E. Shaywitz, Bennett A. Shaywitz, Karen published October 12, 2005; 10.1073͞pnas.0504640102), the Marchione, Yu Wang, Murugan Paramasivam, Joseph J. Lo- author name M. Sarstre should have appeared as M. Sastre. The Turco, Grier P. Page, and Jeffrey R. Gruen, which appeared in online version has been corrected. The corrected author line issue 47, November 22, 2005, of Proc. Natl. Acad. Sci. USA (102, appears below. 17053–17058; first published November 8, 2005; 10.1073͞ pnas.0508591102), the authors note that the data for compound A. Bilkei-Gorzo, I. Racz, O. Valverde, M. Otto, K. Michel, STR have been deposited in the GenBank database (accession M. Sastre, and A. Zimmer no. BV677278). www.pnas.org͞cgi͞doi͞10.1073͞pnas.0509848102 www.pnas.org͞cgi͞doi͞10.1073͞pnas.0509997102 CORRECTIONS www.pnas.org PNAS ͉ December 20, 2005 ͉ vol. 102 ͉ no. 51 ͉ 18763 Downloaded by guest on September 26, 2021 DCDC2 is associated with reading disability and modulates neuronal development in the brain Haiying Menga, Shelley D.
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