PPP1R12B Rabbit Pab

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Leader in Biomolecular Solutions for Life Science PPP1R12B Rabbit pAb Catalog No.: A17510 Basic Information Background Catalog No. Myosin phosphatase is a protein complex comprised of three subunits: a catalytic A17510 subunit (PP1c-delta, protein phosphatase 1, catalytic subunit delta), a large regulatory subunit (MYPT, myosin phosphatase target) and small regulatory subunit (sm-M20). Two Observed MW isoforms of MYPT have been isolated--MYPT1 and MYPT2, the first of which is widely 110kDa expressed, and the second of which may be specific to heart, skeletal muscle, and brain. Each of the MYPT isoforms functions to bind PP1c-delta and increase phosphatase Calculated MW activity. This locus encodes both MYTP2 and M20. Alternatively spliced transcript variants encoding different isoforms have been identified. Related pseudogenes have been Category defined on the Y chromosome. [provided by RefSeq, Oct 2011] Primary antibody Applications WB Cross-Reactivity Human Recommended Dilutions Immunogen Information WB 1:500 - 1:2000 Gene ID Swiss Prot 4660 O60237 Immunogen Recombinant fusion protein containing a sequence corresponding to amino acids 660-930 of human PPP1R12B (NP_002472.2). Synonyms MYPT2;PP1bp55;PPP1R12B Contact Product Information www.abclonal.com Source Isotype Purification Rabbit IgG Affinity purification Storage Store at -20℃. Avoid freeze / thaw cycles. Buffer: PBS with 0.02% sodium azide,50% glycerol,pH7.3. Validation Data Western blot analysis of extracts of various cell lines, using PPP1R12B antibody (A17510) at 1:1000 dilution. Secondary antibody: HRP Goat Anti-Rabbit IgG (H+L) (AS014) at 1:10000 dilution. Lysates/proteins: 25ug per lane. Blocking buffer: 3% nonfat dry milk in TBST. Detection: ECL Basic Kit (RM00020). Exposure time: 90s. Antibody | Protein | ELISA Kits | Enzyme | NGS | Service For research use only. Not for therapeutic or diagnostic purposes. Please visit http://abclonal.com for a complete listing of recommended products..

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Pathway-Based Genome-Wide Association Analysis of Coronary Heart Disease Identifies Biologically Important Gene Sets
European Journal of Human Genetics (2012) 20, 1168–1173 & 2012 Macmillan Publishers Limited All rights reserved 1018-4813/12 www.nature.com/ejhg ARTICLE Pathway-based genome-wide association analysis of coronary heart disease identifies biologically important gene sets Lisa de las Fuentes1,4, Wei Yang2,4, Victor G Da´vila-Romań1 and C Charles Gu*,2,3 Genome-wide association (GWA) studies of complex diseases including coronary heart disease (CHD) challenge investigators attempting to identify relevant genetic variants among hundreds of thousands of markers being tested. A selection strategy based purely on statistical significance will result in many false negative findings after adjustment for multiple testing. Thus, an integrated analysis using information from the learned genetic pathways, molecular functions, and biological processes is desirable. In this study, we applied a customized method, variable set enrichment analysis (VSEA), to the Framingham Heart Study data (404 467 variants, n ¼ 6421) to evaluate enrichment of genetic association in 1395 gene sets for their contribution to CHD. We identified 25 gene sets with nominal Po0.01; at least four sets are previously known for their roles in CHD: vascular genesis (GO:0001570), fatty-acid biosynthetic process (GO:0006633), fatty-acid metabolic process (GO:0006631), and glycerolipid metabolic process (GO:0046486). Although the four gene sets include 170 genes, only three of the genes contain a variant ranked among the top 100 in single-variant association tests of the 404 467 variants tested. Significant enrichment for novel gene sets less known for their importance to CHD were also identified: Rac 1 cell-motility signaling pathway (h_rac1 Pathway, Po0.001) and sulfur amino-acid metabolic process (GO:0000096, Po0.001).
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PPP1R12B Rabbit Pab
Leader in Biomolecular Solutions for Life Science PPP1R12B Rabbit pAb Catalog No.: A17510 Basic Information Background Catalog No. Myosin phosphatase is a protein complex comprised of three subunits: a catalytic A17510 subunit (PP1c-delta, protein phosphatase 1, catalytic subunit delta), a large regulatory subunit (MYPT, myosin phosphatase target) and small regulatory subunit (sm-M20). Two Observed MW isoforms of MYPT have been isolated--MYPT1 and MYPT2, the first of which is widely 110kDa expressed, and the second of which may be specific to heart, skeletal muscle, and brain. Each of the MYPT isoforms functions to bind PP1c-delta and increase phosphatase Calculated MW activity. This locus encodes both MYTP2 and M20. Alternatively spliced transcript variants encoding different isoforms have been identified. Related pseudogenes have been Category defined on the Y chromosome. [provided by RefSeq, Oct 2011] Primary antibody Applications WB Cross-Reactivity Human Recommended Dilutions Immunogen Information WB 1:500 - 1:2000 Gene ID Swiss Prot 4660 O60237 Immunogen Recombinant fusion protein containing a sequence corresponding to amino acids 660-930 of human PPP1R12B (NP_002472.2). Synonyms MYPT2;PP1bp55;PPP1R12B Contact Product Information 400-999-6126 Source Isotype Purification Rabbit IgG Affinity purification [email protected] www.abclonal.com.cn Storage Store at -20℃. Avoid freeze / thaw cycles. Buffer: PBS with 0.02% sodium azide,50% glycerol,pH7.3. Validation Data Western blot analysis of extracts of various cell lines, using PPP1R12B antibody (A17510) at 1:1000 dilution. Secondary antibody: HRP Goat Anti-Rabbit IgG (H+L) (AS014) at 1:10000 dilution. Lysates/proteins: 25ug per lane. Blocking buffer: 3% nonfat dry milk in TBST.
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bioRxiv preprint doi: https://doi.org/10.1101/780122; this version posted September 24, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. 1 Disease swamps molecular signatures of genetic-environmental associations to abiotic 2 factors in Tasmanian devil (Sarcophilus harrisii) populations 3 4 Alexandra K. Fraik1, Mark J. Margres1, Brendan Epstein1,2, Soraia Barbosa3, Menna Jones4, 5 Sarah Hendricks3, Barbara Schönfeld 4, Amanda R. Stahlke3, Anne Veillet3, Rodrigo Hamede4, 6 Hamish McCallum5, Elisa Lopez-Contreras1, Samantha J. Kallinen1, Paul A. Hohenlohe3, Joanna 7 L. Kelley1, Andrew Storfer1 8 9 Affiliations: 1School of Biological Sciences, Washington State University Pullman, WA 99164, 10 USA; 2Plant Biology, University of Minnesota, Minneapolis, MN 55455, USA; 3Department of 11 Biological Sciences, University of Idaho, Institute for Bioinformatics and Evolutionary Studies, 12 University of Idaho, 875 Perimeter Drive, Moscow, Idaho 83844, USA;4School of Biological 13 Sciences, Hobart, TAS 7004, Australia; 5School of Environment, Griffith University Nathan, QLD 14 4111, Australia 15 Emails for correspondence: Alexandra Fraik, School of Biological Sciences, Washington State 16 University, Pullman, WA, [email protected]; Andrew Storfer, School of Biological 17 Sciences, Washington State University, Pullman, WA, [email protected] 18 Keywords: landscape genomics, genetic-environmental associations, Tasmanian devils, devil 19 facial tumor disease, population genetics, local adaptation bioRxiv preprint doi: https://doi.org/10.1101/780122; this version posted September 24, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved.
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DNA methylation changes in glial cells of the normal-appearing white matter in Multiple Sclerosis patients Lara Kular1*, Ewoud Ewing1, Maria Needhamsen1, Majid Pahlevan Kakhki1, Ruxandra Covacu1, David Gomez-Cabrero2,3,4, Lou Brundin1,2 and Maja Jagodic1*. 1Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden. 2Department of Medicine, Unit of Computational Medicine, Center for Molecular Medicine, Karolinska Institutet, Solna, Sweden. 3Mucosal and Salivary Biology Division, King's College London Dental Institute, London, SE1 9RT, UK. 4Translational Bioinformatics Unit, Navarrabiomed, Complejo Hospitalario de Navarra (CHN), Universidad Pública de Navarra (UPNA), IdiSNA, Pamplona, Spain. 5Department of Neurology, Karolinska University Hospital, Stockholm, Sweden. *To whom correspondence should be addressed: Maja Jagodic and Lara Kular, Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden, [email protected] and [email protected]. Abstract Background Multiple Sclerosis (MS), the leading cause of non-traumatic neurological disability in young adults, is a chronic inflammatory and neurodegenerative disease of the central nervous system (CNS). Due to the poor accessibility to the target organ, CNS-confined processes underpinning the later progressive form of MS remain elusive thereby limiting treatment options. We aim to examine DNA methylation, a stable epigenetic mark of genome activity, in glial cells to capture relevant molecular changes underlying MS neuropathology. Methods We profiled DNA methylation in nuclei of glial cells, isolated from 38 post-mortem normal-appearing white matter (NAWM) specimens of MS patients (n=8) in comparison to white matter of control individuals (n=14), using Infinium MethylationEPIC BeadChip. Findings We identified 1,226 significant (genome-wide adjusted P-value < 0.05) differentially methylated positions (DMPs) between MS patients and controls.
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