Myozenin-2 Recombinant Protein Cat

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Myozenin-2 Recombinant Protein Cat. No.: 92-145 Myozenin-2 Recombinant Protein Specifications SPECIES: Human SOURCE SPECIES: E. coli SEQUENCE: Met1-Leu264 FUSION TAG: C-6 His tag TESTED APPLICATIONS: APPLICATIONS: This recombinant protein can be used for biological assays. For research use only. PREDICTED MOLECULAR 30.9 kD WEIGHT: Properties Greater than 95% as determined by reducing SDS-PAGE. PURITY: Endotoxin level less than 0.1 ng/ug (1 IEU/ug) as determined by LAL test. PHYSICAL STATE: Lyophilized Lyophilized from a 0.2 um filtered solution of 10mM Tris, pH 8.0. It is not recommended BUFFER: to reconstitute to a concentration less than 100 ug/ml. Dissolve the lyophilized protein in ddH2O. September 24, 2021 1 https://www.prosci-inc.com/myozenin-2-recombinant-protein-92-145.html Lyophilized protein should be stored at -20˚C, though stable at room temperature for 3 weeks. STORAGE CONDITIONS: Reconstituted protein solution can be stored at 4-7˚C for 2-7 days. Aliquots of reconstituted samples are stable at -20˚C for 3 months. Additional Info OFFICIAL SYMBOL: MYOZ2 ALTERNATE NAMES: Myozenin-2, Calsarcin-1, FATZ-Related Protein 2, MYOZ2, C4orf5 ACCESSION NO.: Q9NPC6 PROTEIN GI NO.: 78070603 GENE ID: 51778 Background and References Myozenin 2 (MYOZ2) is a 264 amino acid protein that belongs to the myozenin family. MYOZ2 binds to Calcineurin, a phosphatase that is involved in calcium-dependent signal transduction in diverse cell types. MYOZ2 is one of the sarcomeric proteins and plays an important role in myofibrillogenesis and the modulation of calcineurin signaling. It may BACKGROUND: serve as intracellular binding proteins involved in linking Z line proteins such as alpha- actinin, gamma-filamin, TCAP/telethonin, LDB3/ZASP and plays an important role in the modulation of calcineurin signaling. Defects in MYOZ2 are the cause of familial hypertrophic cardiomyopathy type 16 (CMH16), a hereditary heart disorder. ANTIBODIES FOR RESEARCH USE ONLY. For additional information, visit ProSci's Terms & Conditions Page. September 24, 2021 2 https://www.prosci-inc.com/myozenin-2-recombinant-protein-92-145.html.

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Anti-MYOZ2 (GW22350F)
3050 Spruce Street, Saint Louis, MO 63103 USA Tel: (800) 521-8956 (314) 771-5765 Fax: (800) 325-5052 (314) 771-5757 email: [email protected] Product Information Anti-MYOZ2 antibody produced in chicken, affinity isolated antibody Catalog Number GW22350F Formerly listed as GenWay Catalog Number 15-288-22350F, Myozenin-2 Antibody. – Storage Temperature Store at 20 °C The product is a clear, colorless solution in phosphate buffered saline, pH 7.2, containing 0.02% sodium azide. Synonyms: Myozenin 2, Calsarcin-1; FATZ-related protein 2 Species Reactivity: Human Product Description Myozenins may serve as intracellular binding proteins Tested Applications: WB involved in linking Z-disk proteins such as alpha-actinin. Recommended Dilutions: Recommended starting dilution gamma-filamin. TCAP/telethonin. LDB3/ZASP and localizing for Western blot analysis is 1:500, for tissue or cell staining calcineurin signaling to the sarcomere. Plays an important 1:200. role in the modulation of calcineurin signaling. May play a role in myofibrillogenesis. Note: Optimal concentrations and conditions for each application should be determined by the user. NCBI Accession number: NP_057683.1 Swiss Prot Accession number: Q9NPC6 Precautions and Disclaimer This product is for R&D use only, not for drug, household, or Gene Information: Human .. MYOZ2 (51778) other uses. Due to the sodium azide content a material Immunogen: Recombinant protein Myozenin 2 safety data sheet (MSDS) for this product has been sent to the attention of the safety officer of your institution. Please Immunogen Sequence: GI # 7706595, sequence 1 - 264 consult the Material Safety Data Sheet for information regarding hazards and safe handling practices.
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Mutations in MYOZ1 As Well As MYOZ2 Encoding the Calsarcins Are Not Associated with Idiopathic and Familial Dilated Cardiomyopathy
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by MDC Repository Repository of the Max Delbrück Center for Molecular Medicine (MDC) Berlin (Germany) http://edoc.mdc-berlin.de/8815/ Mutations in MYOZ1 as well as MYOZ2 encoding the calsarcins are not associated with idiopathic and familial dilated cardiomyopathy Maximilian G. Posch, Andreas Perrot, Rainer Dietz, Cemil Özcelik, Sabine Pankuweit, Volker Ruppert, Anette Richter, and Bernhard Maisch Published in final edited form as: Molecular Genetics and Metabolism. 2007 Jun; 91(2): 207-208 doi: 10.1016/j.ymgme.2007.02.014 Elsevier (The Netherlands) ► Letter to the editor Mutations in MYOZ1 as well as MYOZ2 encoding the calsarcins are not associated with idiopathic and familial dilated cardiomyopathy Maximilian G. Posch, Andreas Perrot, Rainer Dietz, Cemil Özcelik, Sabine Pankuweit, Volker Ruppert, Anette Richter, and Bernhard Maisch 1 Charité – Universitätsmedizin Berlin/Cardiology at Campus Buch & Virchow Klinikum, Helios-Kliniken and Max- Delbrück Center for Molecular Medicine, Wiltbergstrasse 50, 13125 Berlin, Germany 2 Department of Internal Medicine and Cardiology, Philipps University Marburg, Baldingerstrasse, 35043 Marburg, Germany a very weak mRNA expression of MYOZ1 [5]. Conversely, Dear Editor, MYOZ2 encoding calsarcin-1 is predominantly expressed We have read the article of Arola and colleagues [1] with in cardiomyocytes and to lesser extends in skeletal great interest. The authors report a candidate gene muscle [5,6]. Calsarcin-1 is located at the sarcomeric Z- approach in the MYOZ1 gene encoding calsarcin-2 in 185 disk and interacts with DCM disease genes like telethonin patients with idiopathic dilated cardiomyopathy (iDCM).
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Discovery and Systematic Characterization of Risk Variants and Genes For
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Table SI. Differentially Expressed Genes. Gene Logfc Aveexpr T Value
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Hypertrophic Cardiomyopathy: Genetics, Pathogenesis, Clinical Manifestations, Diagnosis, and Therapy
HHS Public Access Author manuscript Author ManuscriptAuthor Manuscript Author Circ Res Manuscript Author . Author manuscript; Manuscript Author available in PMC 2018 September 15. Published in final edited form as: Circ Res. 2017 September 15; 121(7): 749–770. doi:10.1161/CIRCRESAHA.117.311059. Hypertrophic Cardiomyopathy: Genetics, Pathogenesis, Clinical Manifestations, Diagnosis, and Therapy Ali J. Marian, M.D.* and Eugene Braunwald, M.D.† *Center for Cardiovascular Genetics, Institute of Molecular Medicine and Department of Medicine, University of Texas Health Sciences Center at Houston, and Texas Heart Institute, Houston, TX †TIMI Study Group, Cardiovascular Division, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA Abstract Hypertrophic cardiomyopathy (HCM) is a genetic disorder that is characterized by left ventricular hypertrophy unexplained by secondary causes, and a non-dilated left ventricle with preserved or increased ejection fraction. It is commonly asymmetric with the most severe hypertrophy involving the basal interventricular septum. Left ventricular outflow tract obstruction is present at rest in about one third of the patients, and can be provoked in another third. The histologic features of HCM include myocyte hypertrophy and disarray, as well as interstitial fibrosis. The hypertrophy is also frequently associated with left ventricular diastolic dysfunction. In the majority of patients, HCM has a relatively benign course. However, HCM is also an important cause of sudden cardiac death, particularly in adolescents and young adults. Nonsustained ventricular tachycardia, syncope, a family history of sudden cardiac death, and severe cardiac hypertrophy are major risk factors for sudden cardiac death. This complication can usually be averted by implantation of a cardioverter-defibrillator in appropriate high-risk patients.
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Hypertrophic Cardiomyopathy (Type 1–14)
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Mono- and Bi-Allelic Protein Truncating Variants in Alpha-Actinin 2 Cause Cardiomyopathy Through Distinct Mechanisms
bioRxiv preprint doi: https://doi.org/10.1101/2020.11.19.389064; this version posted November 20, 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 4.0 International license. Mono- and bi-allelic protein truncating variants in alpha-actinin 2 cause cardiomyopathy through distinct mechanisms Malene E Lindholm1, David Jimenez-Morales1, Han Zhu1, Kinya Seo1, David Amar1, Chunli Zhao1, Archana Raja1, Roshni Madhvani1*, Cedric Espenel4, Shirley Sutton1, Colleen Caleshu1,6, Gerald J Berry5, Kara S. Motonaga2,3, Kyla Dunn2,3, Julia Platt1,2, Euan A Ashley1,2, Matthew T Wheeler1,2 1. Division of Cardiovascular Medicine, Department of Medicine, Stanford University School of Medicine, Stanford University, Stanford, USA. 2. Center for Inherited Cardiovascular Diseases, Stanford University School of Medicine, Stanford University, Stanford, USA 3. Division of Pediatric Cardiology, Department of Pediatrics, Stanford University School of Medicine, Stanford, USA 4. Cell Sciences Imaging Facility, Stanford University School of Medicine, Stanford, USA 5. Department of Pathology, Stanford University School of Medicine, Stanford, USA. 6. GeneMatters bioRxiv preprint doi: https://doi.org/10.1101/2020.11.19.389064; this version posted November 20, 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 4.0 International license. Abstract Alpha-actinin 2 (ACTN2) anchors actin within cardiac sarcomeres.
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