Produktinformation

Total Page：16

File Type：pdf, Size：1020Kb

Produktinformation Diagnostik & molekulare Diagnostik Laborgeräte & Service Zellkultur & Verbrauchsmaterial Forschungsprodukte & Biochemikalien Weitere Information auf den folgenden Seiten! See the following pages for more information! Lieferung & Zahlungsart Lieferung: frei Haus Bestellung auf Rechnung SZABO-SCANDIC Lieferung: € 10,- HandelsgmbH & Co KG Erstbestellung Vorauskassa Quellenstraße 110, A-1100 Wien T. +43(0)1 489 3961-0 Zuschläge F. +43(0)1 489 3961-7 [email protected] • Mindermengenzuschlag www.szabo-scandic.com • Trockeneiszuschlag • Gefahrgutzuschlag linkedin.com/company/szaboscandic • Expressversand facebook.com/szaboscandic MYCBP monoclonal antibody (M13), clone 1B12 Catalog # : H00026292-M13 規格 : [ 100 ug ] List All Specification Application Image Product Mouse monoclonal antibody raised against a partial recombinant Western Blot (Transfected lysate) Description: MYCBP. Immunogen: MYCBP (NP_036465.2, 34 a.a. ~ 103 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa. Sequence: LYEEPEKPNSALDFLKHHLGAATPENPEIELLRLELAEMKEKYEAIVEENK KLKAKLAQYEPPQEEKRAE enlarge Host: Mouse Western Blot (Recombinant protein) Reactivity: Human Sandwich ELISA (Recombinant Isotype: IgG2a Kappa protein) Quality Control Antibody Reactive Against Recombinant Protein. Testing: enlarge ELISA Western Blot detection against Immunogen (33.44 KDa) . Storage Buffer: In 1x PBS, pH 7.4 Storage Store at -20°C or lower. Aliquot to avoid repeated freezing and thawing. Instruction: MSDS: Download Datasheet: Download Applications Western Blot (Transfected lysate) Page 1 of 3 2016/5/23 Western Blot analysis of MYCBP expression in transfected 293T cell line by MYCBP monoclonal antibody (M13), clone 1B12. Lane 1: MYCBP transfected lysate(12 KDa). Lane 2: Non-transfected lysate. Protocol Download Western Blot (Recombinant protein) Protocol Download Sandwich ELISA (Recombinant protein) Detection limit for recombinant GST tagged MYCBP is 0.1 ng/ml as a capture antibody. Protocol Download ELISA Gene Information Entrez GeneID: 26292 GeneBank NM_012333 Accession#: Protein NP_036465.2 Accession#: Gene Name: MYCBP Gene Alias: AMY-1 Gene c-myc binding protein Description: Omim ID: 606535 Gene Ontology: Hyperlink Gene Summary: The MYCBP gene encodes a protein that binds to the N-terminal region of MYC (MIM 190080) and stimulates the activation of E box-dependent transcription by MYC.[supplied by OMIM Other OTTHUMP00000000543,associate of myc-1 Designations: Page 2 of 3 2016/5/23 Related Disease Tobacco Use Disorder 服務條款 | 隱私權政策 | 著作及商標 | 網站地圖 ©2016 亞諾法生技股份有限公司 Abnova Corporation. 版權所有. Page 3 of 3 2016/5/23.

Copy Link

Recommended publications

Astrin-SKAP Complex Reconstitution Reveals Its Kinetochore
RESEARCH ARTICLE Astrin-SKAP complex reconstitution reveals its kinetochore interaction with microtubule-bound Ndc80 David M Kern1,2, Julie K Monda1,2†, Kuan-Chung Su1†, Elizabeth M Wilson-Kubalek3, Iain M Cheeseman1,2* 1Whitehead Institute for Biomedical Research, Cambridge, United States; 2Department of Biology, Massachusetts Institute of Technology, Cambridge, United States; 3Department of Cell Biology, The Scripps Research Institute, La Jolla, United States Abstract Chromosome segregation requires robust interactions between the macromolecular kinetochore structure and dynamic microtubule polymers. A key outstanding question is how kinetochore-microtubule attachments are modulated to ensure that bi-oriented attachments are selectively stabilized and maintained. The Astrin-SKAP complex localizes preferentially to properly bi-oriented sister kinetochores, representing the final outer kinetochore component recruited prior to anaphase onset. Here, we reconstitute the 4-subunit Astrin-SKAP complex, including a novel MYCBP subunit. Our work demonstrates that the Astrin-SKAP complex contains separable kinetochore localization and microtubule binding domains. In addition, through cross-linking analysis in human cells and biochemical reconstitution, we show that the Astrin-SKAP complex binds synergistically to microtubules with the Ndc80 complex to form an integrated interface. We propose a model in which the Astrin-SKAP complex acts together with the Ndc80 complex to stabilize correctly formed kinetochore-microtubule interactions. *For correspondence: DOI: https://doi.org/10.7554/eLife.26866.001 [email protected] †These authors contributed equally to this work Introduction Competing interests: The The macromolecular kinetochore complex links chromosomes to dynamic microtubule polymers and authors declare that no harnesses the forces generated by microtubule growth and depolymerization to facilitate accurate competing interests exist.
[Show full text]
Aneuploidy: Using Genetic Instability to Preserve a Haploid Genome?
Health Science Campus FINAL APPROVAL OF DISSERTATION Doctor of Philosophy in Biomedical Science (Cancer Biology) Aneuploidy: Using genetic instability to preserve a haploid genome? Submitted by: Ramona Ramdath In partial fulfillment of the requirements for the degree of Doctor of Philosophy in Biomedical Science Examination Committee Signature/Date Major Advisor: David Allison, M.D., Ph.D. Academic James Trempe, Ph.D. Advisory Committee: David Giovanucci, Ph.D. Randall Ruch, Ph.D. Ronald Mellgren, Ph.D. Senior Associate Dean College of Graduate Studies Michael S. Bisesi, Ph.D. Date of Defense: April 10, 2009 Aneuploidy: Using genetic instability to preserve a haploid genome? Ramona Ramdath University of Toledo, Health Science Campus 2009 Dedication I dedicate this dissertation to my grandfather who died of lung cancer two years ago, but who always instilled in us the value and importance of education. And to my mom and sister, both of whom have been pillars of support and stimulating conversations. To my sister, Rehanna, especially- I hope this inspires you to achieve all that you want to in life, academically and otherwise. ii Acknowledgements As we go through these academic journeys, there are so many along the way that make an impact not only on our work, but on our lives as well, and I would like to say a heartfelt thank you to all of those people: My Committee members- Dr. James Trempe, Dr. David Giovanucchi, Dr. Ronald Mellgren and Dr. Randall Ruch for their guidance, suggestions, support and confidence in me. My major advisor- Dr. David Allison, for his constructive criticism and positive reinforcement.
[Show full text]
Structural Capacitance in Protein Evolution and Human Diseases
Structural Capacitance in Protein Evolution and Human Diseases Adrian Woolfson, Ashley Buckle, Natalie Borg, Geoffrey Webb, Itamar Kass, Malcolm Buckle, Jiangning Song, Chen Li, Liah Clark, Rory Zhang, et al. To cite this version: Adrian Woolfson, Ashley Buckle, Natalie Borg, Geoffrey Webb, Itamar Kass, et al.. Structural Ca- pacitance in Protein Evolution and Human Diseases. Journal of Molecular Biology, Elsevier, 2018, 10.1016/j.jmb.2018.06.051. hal-02368321 HAL Id: hal-02368321 https://hal.archives-ouvertes.fr/hal-02368321 Submitted on 20 Nov 2019 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. Structural Capacitance in Protein Evolution and Human Diseases Chen Li, Liah Clark, Rory Zhang, Benjamin Porebski, Julia Mccoey, Natalie Borg, Geoffrey Webb, Itamar Kass, Malcolm Buckle, Jiangning Song, etal. To cite this version: Chen Li, Liah Clark, Rory Zhang, Benjamin Porebski, Julia Mccoey, et al.. Structural Capaci- tance in Protein Evolution and Human Diseases. Journal of Molecular Biology, Elsevier, 2018, 10.1016/j.jmb.2018.06.051. hal-02368321 HAL Id: hal-02368321 https://hal.archives-ouvertes.fr/hal-02368321 Submitted on 20 Nov 2019 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.
[Show full text]
Lncrna LUNAR1 Accelerates Colorectal Cancer Progression by Targeting the Mir‑495‑3P/MYCBP Axis
INTERNATIONAL JOURNAL OF ONCOLOGY 57: 1157-1168, 2020 lncRNA LUNAR1 accelerates colorectal cancer progression by targeting the miR‑495‑3p/MYCBP axis JIAJIE QIAN1, ALOK GARG2, FUQIANG LI3, QIANYUN SHEN1 and KE XIAO4 1Department of Gastrointestinal Surgery, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China; 2Department of Surgery, City Hospital Braunschweig, D-38118 Braunschweig, Germany; 3Department of Thyroid Surgery, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China; 4Institute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, D-30625 Hannover, Lower Saxony, Germany Received April 16, 2020; Accepted September 14, 2020 DOI: 10.3892/ijo.2020.5128 Abstract. Colorectal cancer (CRC) is a tumor type and functional research showed that LUNAR1 accelerated characterized by high patient morbidity and mortality. It has CRC progression via the miR-495-3p/MYCBP axis. In been reported that long non-coding (lncRNA) LUNAR1 conclusion, LUNAR1 accelerates CRC progression via the (LUNAR1) participates in the regulation of tumor progression, miR-495-3p/MYCBP axis, indicating that LUNAR1 may such as diffuse large B-cell lymphoma. However, its role and serve as a prognostic biomarker for CRC patients. underlying mechanisms in CRC progression have not been elucidated. The present study was designed to investigate Introduction the underlying mechanisms by which LUNAR1 regulates CRC progression. RT-qPCR and Pearson's correlation Colorectal cancer (CRC) is a tumor type characterized by analysis revealed that LUNAR1 was highly expressed and high patient morbidity and mortality (1). At present, surgery, was negatively associated with the overall survival of CRC radiotherapy and chemotherapy are the primary strategies for patients.
[Show full text]
Novel Gene Discovery in Primary Ciliary Dyskinesia
Novel Gene Discovery in Primary Ciliary Dyskinesia Mahmoud Raafat Fassad Genetics and Genomic Medicine Programme Great Ormond Street Institute of Child Health University College London A thesis submitted in conformity with the requirements for the degree of Doctor of Philosophy University College London 1 Declaration I, Mahmoud Raafat Fassad, confirm that the work presented in this thesis is my own. Where information has been derived from other sources, I confirm that this has been indicated in the thesis. 2 Abstract Primary Ciliary Dyskinesia (PCD) is one of the ‘ciliopathies’, genetic disorders affecting either cilia structure or function. PCD is a rare recessive disease caused by defective motile cilia. Affected individuals manifest with neonatal respiratory distress, chronic wet cough, upper respiratory tract problems, progressive lung disease resulting in bronchiectasis, laterality problems including heart defects and adult infertility. Early diagnosis and management are essential for better respiratory disease prognosis. PCD is a highly genetically heterogeneous disorder with causal mutations identified in 36 genes that account for the disease in about 70% of PCD cases, suggesting that additional genes remain to be discovered. Targeted next generation sequencing was used for genetic screening of a cohort of patients with confirmed or suggestive PCD diagnosis. The use of multi-gene panel sequencing yielded a high diagnostic output (> 70%) with mutations identified in known PCD genes. Over half of these mutations were novel alleles, expanding the mutation spectrum in PCD genes. The inclusion of patients from various ethnic backgrounds revealed a striking impact of ethnicity on the composition of disease alleles uncovering a significant genetic stratification of PCD in different populations.
[Show full text]
ALK Is a Critical Regulator of the MYC-Signaling Axis in ALK Positive Lung Cancer
Henry Ford Health System Henry Ford Health System Scholarly Commons Hematology Oncology Articles Hematology-Oncology 2-6-2018 ALK is a critical regulator of the MYC-signaling axis in ALK positive lung cancer Amanda B. Pilling Henry Ford Health System, [email protected] Jihye Kim Adriana Estrada-Bernal Qiong Zhou Anh T. Le See next page for additional authors Follow this and additional works at: https://scholarlycommons.henryford.com/ hematologyoncology_articles Recommended Citation Pilling AB, Kim J, Estrada-Bernal A, Zhou Q, Le AT, Singleton KR, Heasley LE, Tan AC, DeGregori J, and Doebele RC. ALK is a critical regulator of the MYC-signaling axis in ALK positive lung cancer. Oncotarget 2018; 9(10):8823-8835. This Article is brought to you for free and open access by the Hematology-Oncology at Henry Ford Health System Scholarly Commons. It has been accepted for inclusion in Hematology Oncology Articles by an authorized administrator of Henry Ford Health System Scholarly Commons. Authors Amanda B. Pilling, Jihye Kim, Adriana Estrada-Bernal, Qiong Zhou, Anh T. Le, Katherine R. Singleton, Lynn E. Heasley, Aik C. Tan, James DeGregori, and Robert C. Doebele This article is available at Henry Ford Health System Scholarly Commons: https://scholarlycommons.henryford.com/ hematologyoncology_articles/14 www.impactjournals.com/oncotarget/ Oncotarget, 2018, Vol. 9, (No. 10), pp: 8823-8835 Priority Research Paper ALK is a critical regulator of the MYC-signaling axis in ALK positive lung cancer Amanda B. Pilling1,2, Jihye Kim1, Adriana Estrada-Bernal1, Qiong Zhou1, Anh T. Le1, Katherine R. Singleton1, Lynn E. Heasley1, Aik Choon Tan1, James DeGregori1 and Robert C.
[Show full text]
Differential Expression of Skin Cancer and Hair-Follicle Cycle Regulated Genes in Tumor Susceptible K14-Agouti Mice
University of Tennessee, Knoxville TRACE: Tennessee Research and Creative Exchange Doctoral Dissertations Graduate School 8-2006 Differential Expression of Skin Cancer and Hair-Follicle Cycle Regulated Genes in Tumor Susceptible K14-Agouti Mice Yesim Aydin Son University of Tennessee - Knoxville Follow this and additional works at: https://trace.tennessee.edu/utk_graddiss Part of the Life Sciences Commons Recommended Citation Son, Yesim Aydin, "Differential Expression of Skin Cancer and Hair-Follicle Cycle Regulated Genes in Tumor Susceptible K14-Agouti Mice. " PhD diss., University of Tennessee, 2006. https://trace.tennessee.edu/utk_graddiss/1636 This Dissertation is brought to you for free and open access by the Graduate School at TRACE: Tennessee Research and Creative Exchange. It has been accepted for inclusion in Doctoral Dissertations by an authorized administrator of TRACE: Tennessee Research and Creative Exchange. For more information, please contact [email protected]. To the Graduate Council: I am submitting herewith a dissertation written by Yesim Aydin Son entitled "Differential Expression of Skin Cancer and Hair-Follicle Cycle Regulated Genes in Tumor Susceptible K14-Agouti Mice." I have examined the final electronic copy of this dissertation for form and content and recommend that it be accepted in partial fulfillment of the equirr ements for the degree of Doctor of Philosophy, with a major in Life Sciences. Edward J. Michaud, Major Professor We have read this dissertation and recommend its acceptance: Cymbeline T. Culiat, Mitchel
[Show full text]
Renoprotective Effect of Combined Inhibition of Angiotensin-Converting Enzyme and Histone Deacetylase
BASIC RESEARCH www.jasn.org Renoprotective Effect of Combined Inhibition of Angiotensin-Converting Enzyme and Histone Deacetylase † ‡ Yifei Zhong,* Edward Y. Chen, § Ruijie Liu,*¶ Peter Y. Chuang,* Sandeep K. Mallipattu,* ‡ ‡ † | ‡ Christopher M. Tan, § Neil R. Clark, § Yueyi Deng, Paul E. Klotman, Avi Ma’ayan, § and ‡ John Cijiang He* ¶ *Department of Medicine, Mount Sinai School of Medicine, New York, New York; †Department of Nephrology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China; ‡Department of Pharmacology and Systems Therapeutics and §Systems Biology Center New York, Mount Sinai School of Medicine, New York, New York; |Baylor College of Medicine, Houston, Texas; and ¶Renal Section, James J. Peters Veterans Affairs Medical Center, New York, New York ABSTRACT The Connectivity Map database contains microarray signatures of gene expression derived from approximately 6000 experiments that examined the effects of approximately 1300 single drugs on several human cancer cell lines. We used these data to prioritize pairs of drugs expected to reverse the changes in gene expression observed in the kidneys of a mouse model of HIV-associated nephropathy (Tg26 mice). We predicted that the combination of an angiotensin-converting enzyme (ACE) inhibitor and a histone deacetylase inhibitor would maximally reverse the disease-associated expression of genes in the kidneys of these mice. Testing the combination of these inhibitors in Tg26 mice revealed an additive renoprotective effect, as suggested by reduction of proteinuria, improvement of renal function, and attenuation of kidney injury. Furthermore, we observed the predicted treatment-associated changes in the expression of selected genes and pathway components. In summary, these data suggest that the combination of an ACE inhibitor and a histone deacetylase inhibitor could have therapeutic potential for various kidney diseases.
[Show full text]
Seh1 Targets GATOR2 and Nup153 to Mitotic Chromosomes Melpomeni Platani1,*, Itaru Samejima1, Kumiko Samejima1, Masato T
© 2018. Published by The Company of Biologists Ltd | Journal of Cell Science (2018) 131, jcs213140. doi:10.1242/jcs.213140 RESEARCH ARTICLE Seh1 targets GATOR2 and Nup153 to mitotic chromosomes Melpomeni Platani1,*, Itaru Samejima1, Kumiko Samejima1, Masato T. Kanemaki2 and William C. Earnshaw1,* ABSTRACT Nup107 complex (also known as the Y complex), a core structural In metazoa, the Nup107 complex (also known as the nucleoporin scaffold of nuclear pores in interphase located on both faces of the Y-complex) plays a major role in formation of the nuclear pore NPC. In vertebrates, the Nup107 complex is composed of ten complex in interphase and is localised to kinetochores in mitosis. The different nucleoporins: Nup160, Nup133, Nup107, Nup96, Nup85, Nup107 complex shares a single highly conserved subunit, Seh1 Nup43, Nup37, Sec13, Seh1 (also known as SEH1L) and Elys (also (also known as SEH1L in mammals) with the GATOR2 complex, an known as AHCTF1) (Knockenhauer and Schwartz, 2016). The essential activator of mTORC1 kinase. mTORC1/GATOR2 has a Nup107 complex plays a crucial role in NPC assembly, mRNA central role in the coordination of cell growth and proliferation. Here, export and cell differentiation (González-Aguilera and Askjaer, 2012; we use chemical genetics and quantitative chromosome proteomics Harel et al., 2003; Vasu et al., 2001; Walther et al., 2003). Nup107 to study the role of the Seh1 protein in mitosis. Surprisingly, Seh1 is complex components remain associated together throughout mitosis not required for the association of the Nup107 complex with mitotic and are among the earliest nucleoporins recruited onto chromatin chromosomes, but it is essential for the association of both during nuclear envelope reformation at the end of cell division the GATOR2 complex and nucleoporin Nup153 with mitotic (Belgareh et al., 2001).
[Show full text]
Bioinformatics Mining of the Dark Matter Proteome For
BIOINFORMATICS MINING OF THE DARK MATTER PROTEOME FOR CANCER TARGETS DISCOVERY by Ana Paula Delgado A Thesis Submitted to the Faculty of The Charles E. Schmidt College of Science In Partial Fulfillment of the Requirements for the Degree of Master of Science Florida Atlantic University Boca Raton, Florida May 2015 Copyright 2015 by Ana Paula Delgado ii ACKNOWLEDGEMENTS I would first like to thank Dr. Narayanan for his continuous encouragement, guidance, and support during the past two years of my graduate education. It has truly been an unforgettable experience working in his laboratory. I also want to express gratitude to my external advisor Professor Van de Ven from the University of Leuven, Belgium for his constant involvement and assistance on my project. Moreover, I would like to thank Dr. Binninger and Dr. Dawson-Scully for their advice and for agreeing to serve on my thesis committee. I also thank provost Dr. Perry for his involvement in my project. I thank Jeanine Narayanan for editorial assistance with the publications and with this dissertation. It has been a pleasure working with various undergraduate students some of whom became lab mates including Pamela Brandao, Maria Julia Chapado and Sheilin Hamid. I thank them for their expert help in the projects we were involved in. Lastly, I want to express my profound thanks to my parents and brother for their unconditional love, support and guidance over the last couple of years. They were my rock when I was in doubt and never let me give up. I would also like to thank my boyfriend Spencer Daniel and best friends for being part of an incredible support system.
[Show full text]
Dema and Faust Et Al., Suppl. Material 2020.02.03
Supplementary Materials Cyclin-dependent kinase 18 controls trafficking of aquaporin-2 and its abundance through ubiquitin ligase STUB1, which functions as an AKAP Dema Alessandro1,2¶, Dörte Faust1¶, Katina Lazarow3, Marc Wippich3, Martin Neuenschwander3, Kerstin Zühlke1, Andrea Geelhaar1, Tamara Pallien1, Eileen Hallscheidt1, Jenny Eichhorst3, Burkhard Wiesner3, Hana Černecká1, Oliver Popp1, Philipp Mertins1, Gunnar Dittmar1, Jens Peter von Kries3, Enno Klussmann1,4* ¶These authors contributed equally to this work 1Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Robert- Rössle-Strasse 10, 13125 Berlin, Germany 2current address: University of California, San Francisco, 513 Parnassus Avenue, CA 94122 USA 3Leibniz-Forschungsinstitut für Molekulare Pharmakologie (FMP), Robert-Rössle-Strasse 10, 13125 Berlin, Germany 4DZHK (German Centre for Cardiovascular Research), Partner Site Berlin, Oudenarder Strasse 16, 13347 Berlin, Germany *Corresponding author Enno Klussmann Max Delbrück Center for Molecular Medicine Berlin in the Helmholtz Association (MDC) Robert-Rössle-Str. 10, 13125 Berlin Germany Tel. +49-30-9406 2596 FAX +49-30-9406 2593 E-mail: [email protected] 1 Content 1. CELL-BASED SCREENING BY AUTOMATED IMMUNOFLUORESCENCE MICROSCOPY 3 1.1 Screening plates 3 1.2 Image analysis using CellProfiler 17 1.4 Identification of siRNA affecting cell viability 18 1.7 Hits 18 2. SUPPLEMENTARY TABLE S4, FIGURES S2-S4 20 2 1. Cell-based screening by automated immunofluorescence microscopy 1.1 Screening plates Table S1. Genes targeted with the Mouse Protein Kinases siRNA sub-library. Genes are sorted by plate and well. Accessions refer to National Center for Biotechnology Information (NCBI, BLA) entries. The siRNAs were arranged on three 384-well microtitre platres.
[Show full text]
Mouse Maats1 Conditional Knockout Project (CRISPR/Cas9)
https://www.alphaknockout.com Mouse Maats1 Conditional Knockout Project (CRISPR/Cas9) Objective: To create a Maats1 conditional knockout Mouse model (C57BL/6J) by CRISPR/Cas-mediated genome engineering. Strategy summary: The Maats1 gene (NCBI Reference Sequence: NM_001081025 ; Ensembl: ENSMUSG00000022805 ) is located on Mouse chromosome 16. 17 exons are identified, with the ATG start codon in exon 1 and the TAG stop codon in exon 17 (Transcript: ENSMUST00000023501). Exon 5~6 will be selected as conditional knockout region (cKO region). Deletion of this region should result in the loss of function of the Mouse Maats1 gene. To engineer the targeting vector, homologous arms and cKO region will be generated by PCR using BAC clone RP23-351P21 as template. Cas9, gRNA and targeting vector will be co-injected into fertilized eggs for cKO Mouse production. The pups will be genotyped by PCR followed by sequencing analysis. Note: Exon 5 starts from about 18.77% of the coding region. The knockout of Exon 5~6 will result in frameshift of the gene. The size of intron 4 for 5'-loxP site insertion: 931 bp, and the size of intron 6 for 3'-loxP site insertion: 3782 bp. The size of effective cKO region: ~1143 bp. The cKO region does not have any other known gene. Page 1 of 7 https://www.alphaknockout.com Overview of the Targeting Strategy Wildtype allele 5' gRNA region gRNA region 3' 1 4 5 6 17 Targeting vector Targeted allele Constitutive KO allele (After Cre recombination) Legends Exon of mouse Maats1 Homology arm cKO region loxP site Page 2 of 7 https://www.alphaknockout.com Overview of the Dot Plot Window size: 10 bp Forward Reverse Complement Sequence 12 Note: The sequence of homologous arms and cKO region is aligned with itself to determine if there are tandem repeats.
[Show full text]