BF0433-DLK1 Antibody

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Affinity Biosciences website:www.affbiotech.com order:[email protected] DLK1 Antibody Cat.#: BF0433 Concn.: 1mg/ml Mol.Wt.: 41kDa Size: 50ul,100ul,200ul Source: Mouse Clonality: Monoclonal Application: ELISA 1:10000, WB 1:500-1:2000, IF/ICC 1:200-1:1000, FCM 1:200-1:400 *The optimal dilutions should be determined by the end user. Reactivity: Human Purification: Affinity-chromatography. Specificity: DLK1 antibody detects endogenous levels of total DLK1. Immunogen: Purified recombinant fragment of human DLK1 expressed in E. Coli. Uniprot: P80370 Description: This gene encodes a transmembrane protein containing six epidermal growth factor repeats. The protein is involved in the differentiation of several cell types, including adipocytes; it is also thought to be a tumor suppressor. It is one of several imprinted genes located in a region of on chr 14q32. Certain mutations in this imprinted region can cause phenotypes similar to maternal and paternal uniparental disomy of chromosome 14 (UPD14). This gene is expressed from the paternal allele. A polymorphism within this gene has been associated with child and adolescent obesity. The mode of inheritance for this polymorphism is polar overdominance; this non-Mendelian inheritance pattern was first described in sheep with the callipyge phenotype, which is characterized by muscle hypertrophy and decreased fat mass. Storage Condition and Mouse IgG1 in phosphate buffered saline (without Mg2+ and Buffer: Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.Store at -20 °C.Stable for 12 months from date of receipt. Figure 1: Western blot analysis using DLK1 mAb against human DLK1 (AA: 174-349) recombinant protein. (Expected MW is 44.9 kDa) 1 / 2 Affinity Biosciences website:www.affbiotech.com order:[email protected] IMPORTANT: For western blot, incubate membrane with diluted primary Ab in 5% w/v milk , 1X TBS, 0.1% Tween®20 at 4°C with gentle shaking, overnight. For Research Use Only. Not for use in diagnostic and therapeutic procedures. Not for resale without express authorization. 2 / 2 Powered by TCPDF (www.tcpdf.org).

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Biochemical Mechanisms of Thyroid Hormone Deiodination
THYROID Volume 15, Number 8, 2005 © Mary Ann Liebert, Inc. Biochemical Mechanisms of Thyroid Hormone Deiodination George G.J.M. Kuiper, Monique H.A. Kester, Robin P. Peeters, and Theo J. Visser Deiodination is the foremost pathway of thyroid hormone metabolism not only in quantitative terms but also because thyroxine (T4) is activated by outer ring deiodination (ORD) to 3,3’,5-triiodothyronine (T3), whereas both T4 and T3 are inactivated by inner ring deiodination (IRD) to 3,3’,5-triiodothyronine and 3,3’- diiodothyronine, respectively. These reactions are catalyzed by three iodothyronine deiodinases, D1-3. Although they are homologous selenoproteins, they differ in important respects such as catalysis of ORD and/or IRD, deiodination of sulfated iodothyronines, inhibition by the thyrostatic drug propylthiouracil, and regulation during fetal and neonatal development, by thyroid state, and during illness. In this review we will briefly discuss recent developments in these different areas. These have resulted in the emerging view that the biological activity of thyroid hormone is regulated locally by tissue-specific regulation of the different deiodinases. HYROID HORMONE is essential for growth, development, thyrostatic drug 6-propyl-2-thiouracil (PTU). D1 activity is Tand regulation of energy metabolism (1–3). Amphibian positively regulated by T3, reflecting regulation of D1 ex- metamorphosis is an important example of thyroid hormone pression by T3 at the pretranslational level. actions on development (4). Equally well known is the crit- In humans, D2 activity is found in brain, anterior pitu- ical role of thyroid hormone in development and function itary, placenta, thyroid and skeletal muscle, and D2 mRNA of the human central nervous system (5,6).
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The Imprinted DLK1-MEG3 Gene Region on Chromosome 14Q32.2 Alters Susceptibility to Type 1 Diabetes
LETTERS The imprinted DLK1-MEG3 gene region on chromosome 14q32.2 alters susceptibility to type 1 diabetes Chris Wallace, Deborah J Smyth, Meeta Maisuria-Armer, Neil M Walker, John A Todd & David G Clayton Genome-wide association (GWA) studies to map common score tests were based on the Cochran-Armitage test, with a Mantel disease susceptibility loci have been hugely successful, with extension to allow combination over different strata (UK region in over 300 reproducibly associated loci reported to date1. the case of the WTCCC and T1DGC samples, and estimated ancestry However, these studies have not yet provided convincing score derived from principal components in the case of the GoKinD- evidence for any susceptibility locus subject to parent-of-origin NIMH samples3). For imputed SNPs, we calculated the score statistics effects. Using imputation to extend existing GWA datasets2–4, using the expected value of the imputed SNP, given observed SNPs, we have obtained robust evidence at rs941576 for paternally with the expectation calculated under the null hypothesis. inherited risk of type 1 diabetes (T1D; ratio of allelic effects for Overall, there was some overdispersion of test statistics (λ = 1.14 and paternal versus maternal transmissions = 0.75; 95% confidence 1.09 for 1 and 2 degrees of freedom, respectively). This was consistent interval (CI) = 0.71–0.79). This marker is in the imprinted with the large sample size (almost 17,000 samples) and the overdisper- region of chromosome 14q32.2, which contains the functional sion observed in earlier analysis of these data without HapMap imputa- candidate gene DLK1. Our meta-analysis also provided support tion4.
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REVIEW Iodothyronine Deiodinase Structure and Function
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Imprinted Gene Expression at the Dlk1-Dio3 Cluster Is Controlled by Both Maternal and Paternal
bioRxiv preprint doi: https://doi.org/10.1101/536102; this version posted January 31, 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. Imprinted gene expression at the Dlk1-Dio3 cluster is controlled by both maternal and paternal IG-DMRs in a tissue-specific fashion. Katherine A. Alexander 2 and María J. García-García 1* 1 Department of Molecular Biology and Genetics, Cornell University. Ithaca. NY. 14853. USA 2 Current address: Department of Cellular and Developmental Biology, University of Pennsylvania. Philadelphia PA, 19103, USA * corresponding author: [email protected] Short title: Tissue-specific imprinting control Keywords: imprinting, TRIM28, IG-DMR, Dlk1, Gtl2, PRO-seq 1 bioRxiv preprint doi: https://doi.org/10.1101/536102; this version posted January 31, 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. ABSTRACT Imprinting at the Dlk1-Dio3 cluster is controlled by the IG-DMR, an imprinting control region differentially methylated between maternal and paternal chromosomes. The maternal IG-DMR is essential for imprinting control, functioning as a cis enhancer element. Meanwhile, DNA methylation at the paternal IG-DMR is thought to prevent enhancer activity. To explore whether suppression of enhancer activity at the methylated IG-DMR requires the transcriptional repressor TRIM28, we analyzed Trim28chatwo embryos and performed epistatic experiments with IG-DMR deletion mutants. We found that while TRIM28 regulates the enhancer properties of the paternal IG-DMR, it also controls imprinting through other mechanisms.
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Downloaded from genesdev.cshlp.org on September 27, 2021 - Published by Cold Spring Harbor Laboratory Press RESEARCH COMMUNICATION entially methylated cis-acting imprinting control ele- The Dlk1 and Gtl2 genes are ment (Thorvaldson et al. 1998). Third, a majority of im- linked and reciprocally printed genes for which a function has been identified imprinted code for proteins involved in the control of embryonic growth (Tilghman 1999). Jennifer V. Schmidt,1,2 Paul G. Matteson,2 Given the role of imprinted genes in fetal growth it is Beverly K. Jones, Xiao-Juan Guan, not surprising that they are often expressed in the pla- and Shirley M. Tilghman3 centa, the primary tissue regulating nutrient transfer be- tween mother and fetus. To identify new imprinted Howard Hughes Medical Institute and Department genes, we designed an allelic differential display strategy of Molecular Biology, Princeton University, Princeton, (Hagiwara et al. 1997) using placental mRNA derived New Jersey 08544 USA from two closely related species of North American deer mice, Peromyscus maniculatus (BW) and Peromyscus Genes subject to genomic imprinting exist in large chro- polionotus (PO). These mice display a high degree of mosomal domains, probably reflecting coordinate regu- polymorphism (Vrana et al. 1998), making them useful lation of the genes within a cluster. Such regulation has for screens that depend on allelic differences. been demonstrated for the H19, Igf2, and Ins2 genes that We report here the paternal-specific expression of the share a bifunctional imprinting control region. We have Delta-like (Dlk1) gene in both Peromyscus and the labo- identified the Dlk1 gene as a new imprinted gene that is ratory mouse genus Mus.
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Epigenetic Regulation of the Dlk1-Meg3 Imprinted Locus in Human Islets
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Expression of Mirnas from the Imprinted DLK1/DIO3 Locus Signals the Osteogenic Potential of Human Pluripotent Stem Cells
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bioRxiv preprint doi: https://doi.org/10.1101/2020.08.07.241034; this version posted August 7, 2020. 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. Epigenetic change induced by in utero dietary challenge provokes phenotypic variability across multiple generations of mice Mathew Van de Pette1, Antonio Galvao2,3,4, Steven J. Millership5, Wilson To1, Andrew Dimond1, Chiara Prodani1, Grainne McNamara1, Ludovica Bruno1, Alessandro Sardini6, Zoe Webster7, James McGinty8, Paul French8, Anthony G. Uren9, Juan Castillo-Fernandez2, Rosalind M. John10, Anne C. Ferguson-Smith11, Matthias Merkenschlager1, Gavin Kelsey2,4 and Amanda G. Fisher1* 1 Lymphocyte Development Group, MRC London Institute of Medical Sciences, Imperial College London Hammersmith Hospital Campus, Du Cane Road, London, W12 0NN, UK. 2 Epigenetics Programme, The Babraham Institute, Cambridge, CB22 3AT, UK. 3 Institute of Animal Reproduction and Food Research of PAS, Department of Reproductive Immunology and Pathology, Olsztyn, Poland. 4 Centre for Trophoblast Research, University of Cambridge, Cambridge, CB2 3EG, UK. 5 Department of Medicine, Imperial College London, Hammersmith Hospital, Du Cane Road, London, W12 0NN, UK. 6 Whole Animal Physiology and Imaging, London Institute of Medical Sciences, Imperial College London, Hammersmith Hospital Campus, Du Cane Road, London, W12 0NN, UK. 7 Transgenics and Embryonic Stem Cell Laboratory, London Institute of Medical Sciences, Imperial College London, Hammersmith Hospital Campus, Du Cane Road, London, W12 0NN, UK. 8 Photonics Group, Department of Physics, Imperial College London, London, UK. 9 Cancer Genomics Group, MRC Institute of Clinical Sciences, Imperial College London, Hammersmith Hospital Campus, Du Cane Road, London, W12 0NN, UK.
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